Integrative Medicine and Its HRT Benefits For Menopause

Discover the role of integrative medicine in easing symptoms and improving quality of life during menopause with HRT.

Abstract

In this educational post, I walk you through how I approach perimenopause and menopause from a biology-first perspective using an integrative model that blends chiropractic care, internal medicine oversight, functional medicine, and rehabilitation. I explain why hormone replacement therapy (HRT) alone often falls short and how addressing systemic inflammation, oxidative stress, mitochondrial dysfunction, localized insulin resistance, micronutrient depletion, and autonomic imbalance can restore thermoregulation, mood stability, cognitive clarity, metabolic flexibility, and overall quality of life. I outline practical protocols—rooted in modern, evidence-based research methods—covering mitochondrial repletion, NAD+ dynamics, micronutrient repletion, circadian alignment, and neuromusculoskeletal optimization through chiropractic integration. I also detail our multidisciplinary model: I provide chiropractic, functional, and injury care; Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749, Texas MD License #J2933), serves as the Medical Director and Collaborative Physician at Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas. Together, we coordinate comprehensive care using lab-driven decision-making, safe HRT usage, and targeted lifestyle therapeutics. This post shares current findings from leading researchers, highlights how they translate into real-world care, and explains why each intervention works for the physiology of menopause.

About Our Collaborative Care Model in El Paso, Texas

• I am Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In our clinic, I integrate chiropractic medicine with advanced practice nursing and functional medicine to address the neuromusculoskeletal, metabolic, and autonomic drivers of menopausal symptoms.
• Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749, Texas MD License #J2933), has over 40 years of clinical experience as an internist. She serves as our Medical Director and Collaborative Physician at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic). Her oversight ensures medical safety, evidence-based prescribing, and coordinated care across complex cases.
• Our model reflects the multidisciplinary structure common in integrative and injury care clinics: an MD provides medical direction while chiropractors and functional clinicians deliver hands-on care, exercise rehab, and metabolic optimization—anchored by shared data, labs, and outcomes tracking.

How we integrate care:

• Medical oversight and diagnostics (Dr. Cardenas): cardiovascular risk assessment, metabolic and inflammatory panels, medication/HRT management, safety monitoring.
• Chiropractic and functional medicine (Dr. Jimenez): biomechanical assessment, spinal and extremity adjustments, neuromyofascial release, vagal/ANS support, exercise rehabilitation, clinical nutrition, and lifestyle therapeutics.
• Personal injury and rehabilitation: we address injuries and movement dysfunction that often amplify menopausal symptoms through pain, poor sleep, and autonomic dysregulation.
• Evidence-based protocols: standardized lab timelines, titrated interventions, and outcome scores to ensure safe, trackable improvements.

Menopause Is Not Just Hormones: It Is Biology

I often tell my patients: “Just running HRT handles the hormones, not the biology.” That is why many women receive estrogen and progesterone and still feel miserable. The reason is straightforward—biological bottlenecks block hormones from delivering the benefits you expect.

• The three primary biological problems:

1. Inflammation and oxidative stress remain high. HRT does not reliably lower high-sensitivity C-reactive protein (CRP) or oxidative stress markers; inflamed endothelium resists vasodilation, so hot flashes persist even when estradiol reaches receptors.
2. Mitochondria remain dysfunctional. HRT does not rebuild mitochondrial density, restore NAD+ pools, or fix ATP generation deficits. If ATP is low, thermoregulation, neurotransmitter synthesis, and metabolic stability all suffer.
3. Localized insulin resistance persists. In the hypothalamus and key metabolic tissues, insulin signaling becomes impaired; cells are bathed in glucose yet cannot efficiently oxidize it. Lipolysis is suppressed, adipocytes trap fat, and visceral adiposity increases—this is a metabolic access problem, not merely a calorie problem.

When these systems fail, estrogen cannot execute its protective roles in vessels, neurons, and adipocytes. The result: persistent hot flashes, weight gain, brain fog, mood instability, low libido, fatigue, and sleep disruption.

The Energy Story: Why ATP Rules Your Symptoms

• Mitochondria convert glucose and fatty acids into ATP, the cell’s energy currency. ATP powers thermoregulation, neurotransmitter synthesis, synaptic activity, muscle function, and hepatic detoxification.
• During perimenopause and menopause, the brain—especially the hypothalamus and the prefrontal cortex—faces an energy shortfall. The hypothalamus misfires thermoregulatory setpoints, while the prefrontal cortex—responsible for impulse control, mood regulation, and rational thought—becomes energy-starved.
• Low ATP means neurons cannot maintain membrane potentials, fire predictably, recycle neurotransmitters, or synthesize adequate serotonin, dopamine, and GABA. Women are not “just hormonal”—their biology is energy-unstable.

Clinical pattern I see:

• Fatigue that sleep does not fix.
• Hot flashes despite therapeutic estradiol levels.
• Anxiety, irritability, depression resistant to SSRI/SNRI monotherapy.
• Brain fog and executive dysfunction affecting work and relationships.
• Weight gain centered around the abdomen, disproportionate to caloric intake.

NAD+ Decline: The Menopause Accelerator

A strong body of research shows that NAD+—the essential coenzyme for mitochondrial energy production, DNA repair, and sirtuin activity—declines with age and drops more rapidly in menopause. This accelerated decline undermines electron transport chain efficiency, reduces ATP yield, heightens oxidative stress, and impairs neuronal resilience (Camacho-Pereira et al., 2016; Yoshino et al., 2011; Verdin, 2015). While the specific study year and journal names vary across the literature, the converging evidence is clear: menopausal transition is associated with reduced NAD+ availability and increased bioenergetic strain.

What this looks like clinically:

• Thermoregulatory instability (hot flashes) tied to hypothalamic energetic deficits.
• Neurotransmitter depletion due to impaired biosynthesis and recycling.
• Decreased exercise tolerance and delayed recovery.
• Heightened visceral fat deposition and hepatic steatosis risk.

Why this matters:

• Without restoring NAD+ metabolism and mitochondrial function, HRT cannot fully normalize symptoms—because the “power stations” remain offline.

Key mechanisms:

• Menopause lowers estrogen signaling that normally supports mitochondrial biogenesis, antioxidant responses, and synaptic plasticity (Yao et al., 2010; Rettberg, Yao, & Brinton, 2014).
• Oxidative stress depletes NAD+ by overactivating PARP enzymes, which consume NAD+ for DNA repair and starve mitochondria of redox capacity (Bai & Canto, 2012; Gomes et al., 2013).
• Inflammation impairs insulin signaling, further limiting substrate entry into mitochondria and perpetuating energy scarcity (Hotamisligil, 2017).

Localized Insulin Resistance: The “Fuel Everywhere, Energy Nowhere” Problem

In perimenopause and menopause, I commonly observe a phenotype in which glucose is elevated or normal, insulin is elevated, and yet energy feels low. This reflects localized insulin resistance in the hypothalamus, liver, skeletal muscle, and adipose tissue:

• Hypothalamic insulin resistance disrupts leptin/insulin crosstalk, distorts hunger and satiety, and destabilizes thermoregulation (Thaler et al., 2012; Kleinridders et al., 2014).
• Hepatic insulin resistance increases gluconeogenesis while blocking efficient fat export, contributing to visceral fat gain.
• Skeletal muscle insulin resistance lowers glucose disposal and reduces fat oxidation, worsening fatigue and exercise intolerance.
• Adipose insulin resistance traps triglycerides while releasing inflammatory adipokines.

This is not simply “eat less, move more.” It is biochemistry. Until we restore insulin signaling and mitochondrial oxidation, caloric restriction alone will frustrate patients and risk lean mass loss.

Why SSRI/SNRI Monotherapy Often Fails

When the prefrontal cortex lacks ATP, neurons cannot synthesize adequate neurotransmitters. You can raise synaptic serotonin with an SSRI, but if neuron bioenergetics are deficient, receptor sensitivity and downstream signaling remain unstable. This is why so many patients “take antidepressants like candy” and still feel unwell. We must address:

• Mitochondrial ATP generation and NAD+ sufficiency.
• Neuroinflammation and oxidative stress.
• Micronutrient cofactor deficits (e.g., magnesium, B vitamins, zinc).
• Sleep architecture and circadian timing.
• Autonomic nervous system (ANS) dysregulation.

The Fourteen-Day Rule: Give Hormones Time To Settle

In our clinic, we emphasize a simple operational rule: hormones need approximately two weeks to reach steady state in tissues. If you tweak the dose every few days, you create pharmacokinetic noise and symptomatic turbulence—often more hot flashes.

• Protocol basics:

• • Transdermal estradiol: once daily, titrate in measured steps, then hold for 14 days before reassessing.
  • Oral micronized progesterone: bedtime dosing to support sleep and endometrial protection.
  • DHEA: morning dosing only. If irritability or oily skin occurs, reduce the dose by half.

• Once hot flash frequency approaches zero, resist the urge to keep adjusting.
• If you develop chest tenderness, first reduce estrogen, then evaluate vitamin B6-dependent methylation pathways and overall estrogen metabolism.
• If jittery, consider too much DHEA, insufficient magnesium or taurine, or both.

Rationale:

• Transdermal estradiol delivers steady levels while minimizing hepatic first-pass effects and thrombotic risk (L’Hermite, 2017).
• Oral micronized progesterone supports sleep, GABAergic tone, and endometrium (Hitchcock & Prior, 2012).
• DHEA can aid mood and libido in selected patients but is dose-sensitive.

Lab Timing and Decision Thresholds

We standardize labs to reduce guesswork:

• Baseline labs before intervention.
• Repeat at 6 weeks to confirm direction of change and safety.
• Key checks: estradiol, progesterone (if indicated), sex hormone-binding globulin (SHBG), DHEA-S, fasting insulin, HbA1c, lipid panel, hs-CRP, CBC, CMP, thyroid panel, ferritin, vitamin D, magnesium, zinc, B12, folate, homocysteine, and markers of oxidative stress where available.

Practical estradiol guideposts:

• If estradiol is persistently over 100 pg/mL with symptoms, reduce dose.
• If under 30 pg/mL with persistent vasomotor symptoms, consider a careful upward titration.

Interpretation occurs within the clinical context—numbers guide, but symptoms and safety lead.

The Non-Negotiable Nutrient Foundation

Your cells need raw materials to function. For most patients in menopause, these are non-negotiable supports that show up repeatedly in both research and clinical practice:

• Magnesium: central to ATP synthesis, NMDA receptor modulation, and vascular tone; often depleted under stress. Forms like glycinate and threonate are well-tolerated.
• Potassium: essential for membrane potentials; dietary adequacy supports blood pressure and muscle function.
• Vitamin D3 with K2: supports immune modulation, bone health, and metabolic function; K2 guides calcium to bone and away from arteries.
• Boron: supports bone metabolism and steroid hormone balance.
• Zinc: cofactor for hundreds of enzymes; supports insulin signaling and neurotransmission.
• Taurine: modulates GABAergic tone, bile acid conjugation, membrane stabilization, and mitochondrial health.
• Methylated B vitamins (e.g., methylfolate, methylcobalamin, P5P): support methylation, neurotransmitter synthesis, and homocysteine regulation.

Clinical logic:

• Mitochondria cannot make ATP if magnesium is low.
• Neurotransmission falters without B vitamins and zinc.
• Inflammation and insulin resistance worsen with vitamin D deficiency.
• Thermoregulation improves as mitochondrial function, antioxidants, and membrane stability recover.

We individualize dosing and always coordinate with Dr. Cardenas for safety—especially when patients take anticoagulants or have kidney disease.

Integrative Chiropractic Care: The Missing Physiological Lever

Chiropractic care is not just for backs—it is a potent regulator of the autonomic nervous system and neuromuscular function. When we optimize spinal joint motion, correct movement patterns, and release myofascial restrictions, we lower nociceptive load, rebalance sympathetic/parasympathetic tone, and improve sleep and stress resilience.

How adjustments help:

• Reduce afferent nociception from dysfunctional joints, lowering central sensitization and sympathetic overdrive.
• Improve rib and thoracic mobility, enhancing respiration, vagal tone, and HRV.
• Normalize cervicogenic input to brainstem centers that modulate autonomic output and vestibulocerebellar integration.

In menopause, the ANS is often destabilized by sleep loss, inflammation, and hormonal transition. By restoring biomechanical and neuromyofascial balance, we directly influence thermoregulation, pain, and mood through improved ANS regulation.

We combine:

• High-velocity, low-amplitude (HVLA) adjustments as appropriate and well-tolerated.
• Low-force techniques (instrument-assisted, mobilization) for sensitive patients.
• Myofascial and trigger point therapies to downshift sympathetic tone and improve regional circulation.
• Breath retraining and rib mechanics to support CO2 tolerance and vagal activation.
• Individualized exercise rehab to rebuild strength, power, and metabolic flexibility.

Dr. Cardenas coordinates all chiropractic care under medical oversight, with safety protocols for osteoporosis, anticoagulation, and cardiometabolic comorbidities.

Functional Medicine Lens: Systems That Drive Symptoms

We evaluate five core systems that, when dysregulated, amplify menopausal symptoms:

• Neuroendocrine-immune axis
  • Goal: restore circadian rhythm, HPA axis stability, estrogen metabolism, and immune balance.
  • Tools: sleep timing, morning light, resistance training, estradiol/progesterone balance, methylation support, omega-3 intake, stress skills training.
• Mitochondrial and redox balance

• • Goal: increase ATP output and reduce oxidative stress.
  • Tools: magnesium, riboflavin, niacin/Niagen (as clinically appropriate), coenzyme Q10, lipoic acid, taurine, N-acetylcysteine, gentle zone 2 cardio, strength training, and nutrient-dense diet.
• Metabolic network

• • Goal: resolve localized insulin resistance and regain fat access.
  • Tools: protein-forward meals, fiber, timed feeding windows matched to circadian rhythm, resistance training minimum 2–3 days weekly, fasting insulin and HOMA-IR tracking, and progression-based exercise.

• Gastrointestinal integrity

• • Goal: support barrier, microbiome diversity, and bile acid signaling that influence estrogen recycling and inflammation.
  • Tools: polyphenols, prebiotic fibers, fermented foods if tolerated, digestive support, and bile-supportive nutrients like taurine.

• Structural and movement system

• • Goal: reduce pain, improve mobility, rebuild power to restore glucose disposal capacity.
  • Tools: chiropractic adjustments, myofascial release, mobility drills, progressive resistance training, gait retraining, and posture/ergonomics.

Hot Flashes: A Thermoregulatory Story

Hot flashes are not random. They result from a narrowed thermoneutral zone in the hypothalamus—worsened by inflammation, low estradiol signaling, and mitochondrial energy deficits. When the setpoint wobbles, even minor temperature changes trigger vasodilation and sweating.

What works and why:

• Transdermal estradiol widens the thermoneutral zone and stabilizes estrogen-dependent hypothalamic circuits.
• Mitochondrial support reduces neuronal energy scarcity, stabilizing setpoints.
• Autonomic rebalancing via chiropractic, breathwork, and HRV training reduces sympathetic triggers.
• Magnesium and taurine improve membrane stability and GABAergic tone, smoothing thermoregulatory responses.
• Sleep optimization stabilizes hypothalamic and brainstem thermoregulation.

Brain Fog, Mood, and Executive Function: Energy Before Neurotransmitters

When ATP is sufficient and oxidative stress is low, neurotransmitter systems recover:

• Serotonin synthesis depends on tryptophan availability, vitamin B6, iron, and adequate ATP.
• Dopamine synthesis requires tyrosine, BH4 cofactor, and mitochondrial integrity.
• GABA function benefits from progesterone’s GABA-A modulation, magnesium, taurine, and sleep.

Why patients improve:

• Energy restoration reverses synaptic fatigue.
• Progesterone at night deepens sleep, recharges glial housekeeping, and supports emotional regulation.
• Resistance training increases brain-derived neurotrophic factor (BDNF), synaptic plasticity, and insulin sensitivity.

Weight Gain and Visceral Fat: Access, Not Absence

Patients often say: “I eat less, but I gain more.” The issue is fuel partitioning.

• Estradiol normally promotes mitochondrial oxidative capacity and subcutaneous fat distribution. Its decline shifts storage toward visceral depots.
• Insulin resistance blocks fat access, while stress raises cortisol and drives central adiposity.
• The fix:

• • Establish a protein-forward plate (1.2–1.6 g/kg/day as individually assessed).
  • Train with progressive resistance to restore insulin sensitivity and lean mass.
  • Use timed meals aligned to circadian biology—bigger earlier, smaller later—to improve glycemic control.
  • Increase fiber and polyphenols to improve GLP-1 signaling and microbiome-mediated insulin sensitivity.

We track waist circumference, fasting insulin, HOMA-IR, triglyceride/HDL ratio, and liver enzymes to document momentum.

Practical Supplementation Framework With Medical Oversight

We personalize plans, but these categories are common:

• Mitochondrial and redox:

• • Magnesium glycinate or malate
  • Riboflavin (B2), niacin or nicotinamide riboside as indicated and safe
  • Coenzyme Q10 (particularly if statins are used)
  • Alpha-lipoic acid
  • N-acetylcysteine and/or glycine for glutathione support
  • Taurine

• Neuroendocrine and sleep:

• • Oral micronized progesterone at night (if appropriate and cleared medically)
  • Magnesium, taurine, and in select cases, L-theanine
  • Morning light exposure, evening light reduction, and consistent sleep windows

• Metabolic and insulin signaling:

• • Vitamin D3 with K2
  • Omega-3 fatty acids
  • Berberine or inositols where appropriate and not contraindicated
  • Adequate potassium via diet

• Bone and connective tissue:

• • Calcium from diet, K2, D3, magnesium, boron
  • Resistance training and impact-loading progression as appropriate

All supplementation and HRT are reviewed and managed with Dr. Cardenas to avoid interactions and contraindications.

Aligned & Empowered: Chiropractic Conversations on Women’s Health-Video

Chiropractic In Practice: Case Patterns and Outcomes

From my clinical observations (see dralexjimenez.com and my professional updates), several patterns stand out:

• Cervicothoracic dysfunction is common in women navigating menopause—computer posture, stress, and sleep changes feed into neck/upper back pain, tension headaches, and poor rib mobility. After restoring segmental motion, patients report fewer night hot flashes, better sleep quality, and less anxiety—consistent with improved vagal tone and reduced sympathetic drive.
• Pelvic and lumbar mechanics matter for insulin sensitivity. When pelvic control and hip power improve, gait efficiency and muscle glucose uptake increase. We routinely see fasting insulin trends improve as patients regain gluteal strength and trunk stability.
• Breathing mechanics are foundational. With thoracic adjustments and diaphragm retraining, patients’ heart rate variability improves, helping mood stability and thermoregulation.

These outcomes are not placebo—they reflect neurophysiology and mechanotransduction: improved joint motion and myofascial compliance alter afferent input, recalibrating central autonomic circuits.

Safety Comes First: Medical Direction and Monitoring

With Dr. Cardenas overseeing medical care:

• We screen for cardiovascular risk, thrombotic history, breast cancer risk, and liver function before and during HRT.
• We tailor delivery route (transdermal vs oral) to minimize risk and maximize benefit.
• We monitor lipids, hs-CRP, Lp(a) when indicated, thyroid function, and glucose/insulin dynamics.
• We adjust based on objective data and patient-reported outcomes, not trends or hype.

For patients on anticoagulants, antidiabetics, or with osteoporosis, we adapt our chiropractic and exercise plans with precision to ensure safety.

The Playbook: Stepwise Implementation

• Assess and baseline
  • Comprehensive history, symptom mapping, movement screen.
  • Labs: hormones, metabolic panel, inflammatory markers, micronutrients.
  • Risk assessment for HRT and supplements.

• Stabilize sleep and circadian rhythm.

• • Consistent bedtime/wake time.
  • Morning outdoor light, dim evening light.
  • Magnesium and oral micronized progesterone at night when indicated and safe.

• Calm inflammation, support redox

• • Omega-3s, polyphenol-rich foods, and NAC/glycine as appropriate.
  • Begin chiropractic care to reduce nociceptive inflammation and improve ANS tone.

• Restore mitochondrial function and NAD+ economy

• • Magnesium, B2, niacin-based support as clinically indicated.
  • Zone 2 cardio plus resistance training—graded and monitored.

• Titrate HRT with the fourteen-day rule

• • Transdermal estradiol once daily.
  • Take oral progesterone at bedtime.
  • DHEA in the morning; reduce the dose if you have irritability or oily skin.
  • Hold each adjustment for 14 days before reassessing.

• Correct insulin resistance and regain fat access

• • Protein-forward nutrition, fiber, and timed meals.
  • Progressive resistance training 2–4x/week.
  • Monitor fasting insulin, HOMA-IR, waist circumference.

• Reassess at 6 weeks

• • Update labs, adjust safely with Dr. Cardenas.
  • Recalibrate supplements and training loads.

• Consolidate and maintain

• • Keep what works, remove what is unnecessary.
  • Maintain movement, sleep, and nutrient foundations.
  • Regular follow-up to prevent drift.

Frequently Asked Clinical Questions

• Why transdermal estradiol?

• • It delivers steadier levels, bypasses first-pass hepatic metabolism, and has a lower thrombotic risk profile than some oral formulations (L’Hermite, 2017).

• Why oral micronized progesterone at night?

• • It improves sleep by modulating GABA-A receptors and provides endometrial protection when estrogen is used (Hitchcock & Prior, 2012).

• Why do SSRIs sometimes help hot flashes but not mood?

• • They can modulate thermoregulatory control in the hypothalamus, but without restoring energy production and addressing inflammation, mood circuits may remain unstable.

• Can chiropractic care directly reduce hot flashes?

• • Indirectly, yes. By improving ANS balance and reducing nociceptive stress, the hypothalamic setpoint stabilizes, which many patients experience as reduced frequency/intensity of vasomotor symptoms.

• How long until I feel better?

• • Most patients notice improvements within 2–6 weeks when we implement sleep stabilization, nutrient foundations, chiropractic care, and the fourteen-day HRT rule. Full metabolic and body composition changes often require 3–6 months.

Evidence-Based Perspective: What the Research Shows

• Estrogen supports mitochondrial biogenesis and synaptic function; loss of estrogen signaling contributes to bioenergetic decline and neuroinflammation (Yao et al., 2010; Rettberg, Yao, & Brinton, 2014).
• NAD+ levels decline with age and are influenced by inflammation and metabolic stress; restoring NAD+ metabolism can improve mitochondrial function and insulin sensitivity (Verdin, 2015; Yoshino et al., 2011; Gomes et al., 2013).
• Inflammation and oxidative stress impair endothelial function and thermoregulation; CRP is a trackable marker correlating with cardiometabolic risk (Ridker, 2016).
• Exercise—particularly resistance training—improves insulin sensitivity, increases mitochondrial density, and elevates BDNF, aiding cognitive function (Hawley, Hargreaves, Joyner, & Zierath, 2014).
• Sleep and circadian alignment regulate hypothalamic function and metabolic homeostasis; misalignment worsens insulin resistance and mood (Reutrakul & Knutson, 2015).

We integrate this literature with clinical prudence, adapting to each patient’s risks and goals under Dr. Cardenas’s medical direction.

Putting It All Together: Biology Before Hormones, Together With Hormones

• HRT can be transformational—but only when the biology is ready to receive it.
• Reduce inflammation and oxidative stress.
• Rebuild mitochondrial function and support NAD+.
• Restore circadian rhythm and sleep.
• Correct localized insulin resistance with nutrition and resistance training.
• Integrate chiropractic care to rebalance the ANS and resolve pain-driven sympathetic excess.
• Use the fourteen-day rule to titrate hormones with precision.
• Monitor with labs at baseline and six weeks, and refine with data.

When we do this, patients stop “chasing doses” and start regaining themselves—clearer mind, steadier mood, better sleep, fewer hot flashes, and a body that finally responds to effort.

Our Team’s Commitment

At Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas, Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933), and I collaborate daily to deliver safe, modern, evidence-based care. With over 40 years of internal medicine experience, Dr. Cardenas ensures medical rigor and safety. I bring integrative chiropractic, functional medicine, and rehabilitation to translate science into results you can feel. Together, we honor the complexity of menopause and the individuality of each woman we serve.

If you are ready to implement a biology-first menopause plan, we are ready to guide you—step by step.

References

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• Hawley, J. A., Hargreaves, M., Joyner, M. J., & Zierath, J. R. (2014). Integrative biology of exercise. Cell. https://doi.org/10.1016/j.cell.2014.10.029
• Hitchcock, C. L., & Prior, J. C. (2012). Oral micronized progesterone for vasomotor symptoms—A placebo-controlled randomized trial in healthy postmenopausal women. Menopause. https://doi.org/10.1097/gme.0b013e318239f6f3
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• Rettberg, J. R., Yao, J., & Brinton, R. D. (2014). Estrogen: a master regulator of bioenergetic systems in the brain and body. Frontiers in Neuroendocrinology. https://doi.org/10.1016/j.yfrne.2014.04.001
• Reutrakul, S., & Knutson, K. L. (2015). Consequences of circadian disruption on cardiometabolic health. Sleep Medicine Clinics. https://doi.org/10.1016/j.jsmc.2015.07.005
• Ridker, P. M. (2016). From C-reactive protein to interleukin-6 to interleukin-1: moving upstream to identify novel targets for atheroprotection. Circulation Research. https://doi.org/10.1161/CIRCRESAHA.116.307256
• Verdin, E. (2015). NAD+ in aging, metabolism, and neurodegeneration. Science. https://doi.org/10.1126/science.aac4854
• Yao, J., Irwin, R. W., Zhao, L., Nilsen, J., Hamilton, R. T., & Brinton, R. D. (2010). Mitochondrial bioenergetic deficit precedes Alzheimer’s pathology in female mice: the critical window in estrogen therapy. Endocrinology. https://doi.org/10.1210/en.2010-0006
• Yoshino, J., Mills, K. F., Yoon, M. J., & Imai, S. (2011). NAD+ intermediates: the biology and therapeutic potential of NMN and NR. Cell Metabolism. https://doi.org/10.1016/j.cmet.2011.04.002

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