Chiropractic Restoration Techniques for Metabolic Health

Uncover the relationship between chiropractic restoration for metabolic health and effective wellness solutions.

Abstract

Chronic degenerative conditions—from atherosclerotic cardiovascular disease and dilated cardiomyopathy to Type 2 diabetes mellitus, early cognitive decline, and post-traumatic musculoskeletal injuries—share a convergent pathophysiological foundation: systemic inflammation, insulin resistance, and progressive mitochondrial bioenergetic failure. At the center of this cascade sits systemic depletion of nicotinamide adenine dinucleotide (NAD+), the indispensable coenzyme that powers electron transport, activates sirtuin-mediated epigenetic regulation, and supplies substrate for poly(ADP-ribose) polymerase (PARP)-driven DNA repair.

When intracellular NAD+ levels fall under the combined pressures of age, metabolic overload, toxic insult, or physical trauma, enzymatic cascades stall, reactive oxygen species (ROS) surge, and tissue repair slows or stops. At Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, I work in direct collaboration with Medical Director Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine, NPI #1164426749, Texas MD License #J2933), who brings more than 40 years of internal medicine experience. Together, we deploy a multidisciplinary model that integrates functional medicine diagnostics, medical co-management, parenteral and subcutaneous NAD+ and peptide therapies, targeted nutraceutical support, precision laboratory profiling, and advanced biomechanical chiropractic rehabilitation.

By restoring cellular NAD+ pools, reducing oxidative and inflammatory stress, correcting somatic subluxations, and optimizing the neuro-biomechanical axis, this collaborative approach addresses the cellular origins of disease while supporting structural integrity and metabolic flexibility. This educational post walks through the molecular mechanisms, supporting clinical research, practical protocols we use, and the real-world outcomes we observe in our El Paso practice.

Understanding the Molecular Engine: Why NAD+ Is the Universal Cellular Toolkit

Every cell in the human body performs thousands of synchronized biochemical reactions each second. These reactions synthesize structural proteins, transcribe genomic sequences, neutralize toxic intermediates, and—most critically—generate adenosine triphosphate (ATP). Enzymes catalyze these transformations, dramatically lowering the required activation energy. Yet an enzyme cannot function in isolation. It requires its specific coenzymes and cofactors. Without them, the enzyme remains an inactive apoenzyme.

NAD+ is the universal biological toolkit for a vast array of these reactions. In its oxidized form, NAD+ accepts electrons; in its reduced form (NADH), it donates electrons to the mitochondrial electron transport chain (ETC). Beyond its classical role in glycolysis, beta-oxidation, and the tricarboxylic acid (TCA) cycle, NAD+ is an essential consumable substrate for regulatory enzymes that maintain cellular health:

• Sirtuins (SIRT1–SIRT7), class III histone deacetylases that regulate mitochondrial biogenesis, oxidative stress defense, gene transcription, and longevity pathways.
• PARPs, which detect and repair DNA single- and double-strand breaks caused by metabolic stress, radiation, or inflammation.
• Membrane-bound ectoenzymes such as CD38 and CD157, which modulate calcium signaling, immune activation, and metabolic flux.

When intracellular NAD+ concentrations fall below physiological thresholds, these systems decelerate. Sirtuins lose deacetylation capacity, PARPs fail to recruit repair proteins, and the ETC leaks electrons, generating toxic levels of ROS. Restoring the cellular NAD+ pool is therefore a fundamental rate-limiting step in resolving cellular damage, reducing systemic inflammation, and restoring metabolic homeostasis (Verdin, 2015; Rajman et al., 2018).

In clinical practice, I repeatedly observe that patients who present with persistent fatigue after injury, poorly controlled metabolic markers, or slow tissue healing often show laboratory patterns consistent with mitochondrial stress and NAD+ depletion. Supporting NAD+ status while simultaneously addressing structural and inflammatory drivers produces more durable improvements than either approach alone.

Atherosclerosis and Cardiovascular Hemodynamics: Halting Plaque Progression Through Sirtuin Activation

The cardiovascular system operates under continuous high metabolic demand. Cardiomyocytes and vascular endothelial cells require uninterrupted mitochondrial ATP to maintain excitation-contraction coupling, endothelial nitric oxide (NO) synthesis, and structural compliance. Atherosclerosis is fundamentally an inflammatory, bioenergetically driven vascular pathology. During periods of shear stress, hypertension, or hyperlipidemia, circulating low-density lipoprotein (LDL) particles infiltrate the subendothelial space. Retained LDL becomes oxidized (oxLDL) by local ROS, activating endothelial adhesion molecules VCAM-1 and ICAM-1. Circulating monocytes adhere, extravasate, and differentiate into macrophages that ingest oxLDL via scavenger receptors. When overloaded, these macrophages become lipid-laden foam cells that secrete pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), recruit smooth muscle cells, and form a vulnerable necrotic lipid core beneath a fragile fibrous cap.

Modern research demonstrates that elevating the intracellular NAD+/NADH ratio through parenteral or subcutaneous NAD+ precursors directly mitigates this cascade (Zhang et al., 2016). Higher NAD+ activates endothelial and macrophage-specific SIRT1. Active SIRT1 deacetylates the p65 subunit of nuclear factor kappa B (NF-κB), suppressing transcription of pro-inflammatory cytokines, chemokines, and adhesion molecules. At the same time, SIRT1 deacetylates and activates endothelial nitric oxide synthase (eNOS), increasing local NO bioavailability, restoring vasodilation, and reducing monocyte adhesion. SIRT1 also upregulates the ATP-binding cassette transporters ABCA1 and ABCG1, promoting reverse cholesterol transport from foam cells back to high-density lipoprotein (HDL). The net result is plaque stabilization, a smaller necrotic core, and improved arterial compliance.

In our clinic, patients with elevated high-sensitivity C-reactive protein (hs-CRP), oxidized LDL, or advanced lipid particle numbers often receive coordinated care: medical clearance and pharmacotherapeutic monitoring by Dr. Cardenas, targeted NAD+ protocols, and chiropractic care to optimize autonomic tone and microcirculation. Restored parasympathetic balance and improved capillary delivery amplify the cellular effects of NAD+ repletion.

Dilated Cardiomyopathy and Heart Failure: Reversing Myocardial Bioenergetic Starvation

Dilated cardiomyopathy (DCM) and congestive heart failure have historically been viewed as progressive and largely irreversible. At its core, however, heart failure is a bioenergetic crisis. More than 90 percent of a normal cardiomyocyte’s ATP derives from mitochondrial oxidative phosphorylation. Under pathological overload, ischemia, or structural microtrauma, substrate flux through Complex I and Complex II becomes impaired. The cellular NAD+ pool depletes rapidly, mitochondrial SIRT3 becomes inactive, and Complex I subunits, along with the antioxidant enzyme superoxide dismutase 2 (SOD2), become hyperacetylated and lose activity. Cardiomyocytes uncouple oxidative phosphorylation, accumulate free radicals, experience calcium overload, and ultimately die. Chamber dilation and declining ejection fraction follow.

Landmark work published in Nature Communications demonstrated that systemic administration of NAD+ precursors can halt and reverse pathological cardiac remodeling in established dilated cardiomyopathy models (Diguet et al., 2018). Replenishing the intracellular NAD+ pool restores the bioenergetic gradient across the inner mitochondrial membrane, reactivates SIRT3, deacetylates Complex I subunits (resuming electron flux and ATP synthesis), and deacetylates SOD2 (catalyzing superoxide into hydrogen peroxide). Restored ATP also supports the sarcoplasmic reticulum calcium ATPase (SERCA2a), improving calcium clearance, diastolic relaxation, and systolic power.

In clinical observation, patients with reduced ejection fraction or significant fatigue after cardiac events or chronic overload frequently present with concurrent spinal and soft-tissue restrictions that amplify sympathetic drive and microvascular constriction. Addressing both the cellular energy deficit and the mechanical/autonomic interference produces additive benefits.

Type 2 Diabetes Mellitus: Redefining Metabolic Dysfunction as a Mitochondrial Crisis

Type 2 diabetes mellitus (T2DM) has long been framed primarily as an endocrine disorder of peripheral glucose handling. Functional medicine and molecular biochemistry reveal that hyperglycemia is largely a downstream symptom of an upstream mitochondrial bioenergetic crisis.

Chronic nutrient overload drives mitochondrial electron transport beyond capacity. Inadequate NAD+ to accept electrons at upstream junctions causes premature electron leakage from Complexes I and III onto molecular oxygen, generating high concentrations of superoxide, hydroxyl radicals, and hydrogen peroxide. These ROS act as metabolic shrapnel: they oxidize cardiolipin, damage mitochondrial DNA, and activate stress kinases (JNK, IKK, PKC). The stress kinases phosphorylate insulin receptor substrate-1 (IRS-1) on inhibitory serine residues, blocking downstream tyrosine phosphorylation of the PI3K/Akt axis. Intracellular vesicles containing GLUT4 transporters cannot translocate to the plasma membrane, trapping glucose in the vascular compartment.

In pancreatic beta cells, the same NAD+ depletion stalls glyceraldehyde-3-phosphate dehydrogenase, preventing the ATP/ADP ratio from rising enough to close ATP-sensitive potassium channels and trigger first-phase insulin secretion. Research published in Nature Communications showed that replenishing systemic NAD+ restores mitochondrial electron flux, suppresses mitochondrial ROS, eliminates inhibitory serine phosphorylation of IRS-1, and reactivates SIRT1 and AMPK, promoting mitochondrial biogenesis via PGC-1α (Yoshino et al., 2018).

At Injury Medical Clinic P, A, we routinely measure fasting insulin, HOMA-IR, HbA1c, and hs-CRP alongside biomechanical assessment. Patients frequently improve both glycemic markers and musculoskeletal function when NAD+ support, methylation cofactors, sirtuin activators, and precise chiropractic adjustments are combined under medical oversight. Improved microcirculation and reduced sympathetic tone further enhance peripheral glucose disposal.

Neurodegenerative Pathophysiology: Moving Beyond the Amyloid Fallacy in Alzheimer’s Disease

Alzheimer’s disease represents one of the most severe manifestations of bioenergetic and neuroinflammatory collapse. For decades, the amyloid cascade hypothesis dominated, yet anti-amyloid monoclonal antibodies that clear plaques have often failed to halt cognitive decline. Emerging functional neurobiology clarifies thatAlzheimer’ss is fundamentally a metabolic and mitochondrial disorder of the central nervous system—sometimes termed Type 3 diabetes. Amyloid-beta deposition is largely an end-stage, protective stress response to upstream mitochondrial exhaustion.

High basal metabolic demand leaves neurons sensitive to NAD+ depletion. Chronic oxidative DNA damage hyperactivates nuclear PARP-1, which consumes nuclear and cytoplasmic NAD+. Declining NAD+ reduces mitochondrial SIRT3 activity, leading to hyperacetylation of antioxidant defenses, electron transport uncoupling, and massive free-radical production. Unchecked ROS oxidize synaptosomal membranes, degrade synaptic junctions, and impair long-term potentiation in hippocampal CA1 networks. Severe oxidative stress and bioenergetic starvation trigger an integrated stress response that upregulates β-secretase 1 (BACE1), increasing pathological cleavage of amyloid precursor protein.

Interventional research in the Journal of Neuroscience demonstrated that exogenous NAD+ supplementation and targeted SIRT3 activation prevent neuronal death by alleviating mitochondrial oxidative stress (Cheng et al., 2018). Data published in Cell further showed that systemic NAD+ administration restores cognitive function, normalizes synaptic plasticity proteins, and prevents neurodegeneration by rescuing the mitochondrial network and stimulating mitophagy (Fang et al., 2019).

In our practice, patients with early cognitive changes often present with concurrent cervical or upper thoracic restrictions, forward head posture, and elevated inflammatory or homocysteine markers. Gentle cervical adjustments, traction to restore lordosis, and NAD+ protocols (with methylation support) address both mechanical compression of vascular and neural structures and the cellular energy deficit. Families often report improved clarity, recall, and gait stability within weeks to months.

The Common Root Cause Matrix of Degenerative Illness

Whether the clinical presentation is coronary disease, peripheral insulin resistance, neurodegeneration, osteoarthritic joint destruction, or myofascial pain, the underlying cellular dynamics converge:

• Systemic chronic inflammation driven by prolonged NF-κB, toll-like receptor, and NLRP3 inflammasome activation.
• Peripheral insulin resistance initiated by hyperinsulinemic signaling that impairs the IRS-1/PI3K/Akt axis through serine-threonine kinase phosphorylation.
• Mitochondrial bioenergetic collapse characterized by electron leakage at Complexes I and III, cardiolipin peroxidation, loss of membrane potential, and suppressed ATP synthesis.
• Systemic NAD+ exhaustion as the common denominator. Chronic inflammation activates the NAD+-consuming ectoenzyme CD38; cellular stress overactivates PARPs; mitochondrial stress depletes NADH pools.

When cellular repair goes offline, structural proteins cannot be resynthesized, lipid membranes remain peroxidized, damaged organelles cannot undergo mitophagy, and tissue progresses toward senescence and apoptotic death. Restoring NAD+ reverses this cascade across systems. Clinical observation at our clinic consistently shows that patients whose hs-CRP, fasting insulin, and subjective energy improve after combined NAD+ and structural care also report better sleep, reduced pain, and greater exercise tolerance—markers of restored metabolic flexibility.

Clinical Collaboration at Injury Medical Clinic PA: The Jimenez–Cardenas Multidisciplinary Model

Effective management of complex metabolic, cardiovascular, neurodegenerative, and post-traumatic musculoskeletal conditions requires a comprehensive, multi-modal strategy. At Injury Medical Clinic PA in El Paso, Texas, care is directed through an integrative partnership between myself—Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST—and Dr. Maria Guadalupe Cardenas, MD.

With more than 40 years of clinical experience in internal medicine, Dr. Cardenas provides essential medical oversight, diagnostic triage, laboratory clearance, and pharmacotherapeutic safety monitoring. This internal medicine foundation allows safe evaluation and co-management of complex metabolic, cardiovascular, and autoimmune profiles. I combine advanced clinical nursing credentials (APRN, FNP-BC), functional medicine certifications (CFMP, IFMCP, ATN), and chiropractic specialization (DC, CCST) to deliver evidence-based care across four primary pillars:

• Cellular bioenergetics and parenteral protocols: targeted subcutaneous and intravenous administration of NAD+ precursors, amino acid complexes, and cellular cofactors.
• Comprehensive functional diagnostics: advanced biomarker analysis including fasting insulin, HOMA-IR, hs-CRP, oxidized LDL, advanced lipid panels, homocysteine, intracellular micronutrients, and mitochondrial organic acids.
• Integrative chiropractic and neuromechanical optimization: spinal adjustments, mechanical traction, spinal decompression, and extremity realignment to correct structural subluxations, reduce mechanical nerve-root irritation, and rebalance autonomic function.
• Active rehabilitation and kinetic functional recovery: customized movement protocols, therapeutic exercise, neuromuscular re-education, and soft-tissue modalities.

This multidisciplinary approach treats structural biomechanics and cellular bioenergetics as interconnected aspects of human health. Shared records and coordinated decision-making ensure that medical contraindications are identified before advanced therapies begin and that structural progress is tracked alongside laboratory changes. Patients recovering from motor-vehicle collisions, workplace injuries, or chronic degenerative conditions receive both the medical safety net and the functional, root-cause interventions required for durable recovery.

Integrative Chiropractic Care and the Neuro-Biomechanics of Bioenergetics

Our clinical model integrates advanced chiropractic adjustments with functional cellular medicine. The nervous and metabolic systems do not operate independently; they communicate continuously through the neuro-endocrine-immune axis.

Biomechanical spinal subluxation or segmental fixation generates continuous nociceptive afferent signals to the dorsal horn. This sensory input stimulates the sympathetic nervous system, increasing sympathetic tone and triggering release of norepinephrine, epinephrine, and cortisol. Elevated catecholamines and cortisol raise vascular resistance, induce peripheral vasoconstriction, elevate blood pressure, and impair peripheral insulin sensitivity. Persistent sympathetic dominance also alters the gut microbiome, increases intestinal permeability, and accelerates inflammatory cytokine production, further depleting cellular NAD+ reserves.

Precision high-velocity, low-amplitude (HVLA) chiropractic adjustments restore normal joint mechanics and relieve pressure on compromised neural structures. The correction silences aberrant nociceptive signaling and generates a surge of mechanoreceptive and proprioceptive input through the dorsal columns to the somatosensory cortex and cerebellum. This neural reorganization reduces sympathetic drive and supports parasympathetic rebound via the vagus nerve. Vagal stimulation releases acetylcholine at peripheral postganglionic terminals; acetylcholine binds nicotinic receptors on macrophages, directly inhibiting the NF-κB pathway and reducing systemic cytokine production (Tracey, 2002). Concurrently, restored microcirculation ensures that administered bioenergetic substrates—such as parenteral NAD+—are efficiently delivered to healing tissues.

In non-surgical treatment of personal-injury and chronic musculoskeletal cases, this integration is especially powerful. Spinal decompression lowers intradiscal pressure and promotes nutrient imbibition while NAD+ support improves the cellular capacity for matrix repair. Patients frequently report faster resolution of radicular pain, improved range of motion, and concurrent gains in energy and metabolic markers when both approaches are used together under medical supervision.

Detailed Clinical Protocols: Subcutaneous and Parenteral NAD+, Diagnostics, and Rehabilitation

To translate these mechanisms into clear clinical practice, Dr. Cardenas and I utilize a step-by-step workflow at Injury Medical Clinic PA.

Stage 1: Comprehensive Medical Intake and Systemic Clearance
Dr. Cardenas performs internal medicine triage, organ-reserve assessment, and contraindication screening. I complete the functional neuromusculoskeletal and metabolic intake. We review cases together to identify patients who can safely proceed to advanced therapies.

Stage 2: Precision Laboratory and Diagnostic Mapping
Standard and advanced panels include comprehensive metabolic panel, renal and hepatic function, advanced lipids (ApoB, LDL-P, oxLDL), fasting insulin, HOMA-IR, hs-CRP, homocysteine, and HbA1c. My biomechanical diagnostics include dynamic digital radiography, postural analysis, paraspinal thermography or electromyography, and neuro-orthopedic examination.

Stage 3: Cellular Bioenergetic and Parenteral Intervention
Subcutaneous NAD+ is typically initiated at 50–100 mg per injection, two to three times weekly, for outpatient maintenance or mild-to-moderate metabolic decline. Intravenous protocols use 250–500 mg in 500 mL 0.9 percent saline, administered as a slow micro-drip over three to four hours, for more severe neuro-metabolic presentations. Every mole of NAD+ metabolized yields nicotinamide, which the enzyme nicotinamide N-methyltransferase processes using S-adenosylmethionine as a methyl donor. To protect methyl-donor pools, we concurrently provide:

• Trimethylglycine (betaine) 500–1,000 mg daily
• L-5-methyltetrahydrofolate 1,000 mcg daily
• Methylcobalamin 1,000 mcg daily
• Pyridoxal-5-phosphate 50 mg daily

Oral sirtuin activators commonly include trans-resveratrol 500 mg daily (allosteric SIRT1 activator) and quercetin phytosome 500 mg daily (natural CD38 inhibitor). We add additional mitochondrial cofactors, such as CoQ10 and alpha-lipoic acid, based on individual organic-acid or nutrient testing.

Stage 4: Integrative Chiropractic and Neuromusculoskeletal Restoration
Segment-specific HVLA adjustments normalize joint mechanics and down-regulate dorsal-horn nociception. Flexion-distraction and computerized spinal decompression lower intradiscal pressures and relieve neural compression. Soft-tissue decompression and myofascial active-release techniques address chronic hypertonicity. Extremity mobilization restores kinetic-chain mechanics.

Stage 5: Functional Rehabilitation, Movement Re-education, and Outcome Retesting
Core dynamic stabilization, scapular stabilization, postural correction, and gait training retrain motor pathways. Sixty-to-ninety-day laboratory and biomechanical retesting quantifies systemic and structural resolution.

These protocols are individualized. Dr. Cardenas adjusts dosing, frequency, and adjunctive nutraceuticals based on serial laboratory results, clinical response, and ongoing medical oversight. The rationale for each element is straightforward: restore the rate-limiting coenzyme, protect related metabolic pathways (methylation), inhibit excessive NAD+ consumption, activate downstream sirtuin signaling, and remove mechanical and autonomic barriers to delivery and repair.

Patient Case Studies: Clinical Applications from El Paso, Texas

Case Study 1: Reversing Severe Metabolic Dysfunction and Post-Traumatic Disc Herniation
A 54-year-old male contractor presented after a motor-vehicle collision with severe low-back pain, left L5–S1 sciatica, and profound fatigue. Medical evaluation by Dr. Cardenas identified long-standing, poorly controlled Type 2 diabetes on metformin. Biomechanical examination revealed antalgic posture, restricted lumbar motion, paraspinal spasm, and MRI confirmation of a 6 mm posterolateral disc protrusion at L5–S1 compressing the traversing S1 root. Baseline markers: fasting glucose 184 mg/dL, HbA1c 8.9 percent, HOMA-IR 6.8, hs-CRP 5.4 mg/L.

Treatment included medical co-management; subcutaneous NAD+ 100 mg three times weekly for 12 weeks with methylation support and quercetin; computerized non-surgical spinal decompression at L5–S1; gentle sacroiliac and lumbar adjustments; soft-tissue release; and progressive core rehabilitation. At 12 weeks, fasting glucose normalized to 98 mg/dL (metformin dose unchanged), HbA1c fell to 5.5 percent, HOMA-IR dropped to 1.4, and hs-CRP declined to 0.8 mg/L. Sciatic pain resolved completely, lumbar range of motion returned to normal, and the patient resumed full physical work.

Case Study 2: Neuro-Metabolic Recovery and Spinal Rehabilitation in Early Cognitive Decline
A 68-year-old retired educator presented with progressive memory decline, word-finding difficulty, brain fog, and severe cervicothoracic pain with tension headaches. Initial Montreal Cognitive Assessment score was 21/30. Examination showed 42 mm forward head posture, loss of cervical lordosis, C1–C2 fixation, and upper-trapezius/levator hypertonicity. Baseline: fasting insulin 18.2 µIU/mL, homocysteine 16.4 µmol/L, hs-CRP 3.8 mg/L.

After medical clearance, the patient received subcutaneous NAD+ 75 mg three times weekly for eight weeks, CoQ10, alpha-lipoic acid, trans-resveratrol, and high-dose active B-complex vitamins, plus gentle cervical manipulation, lordosis traction, and targeted myofascial release. At 10 weeks, the MoCA score improved to 28/30, homocysteine normalized to 8.2 µmol/L, hs-CRP fell to 0.6 mg/L, headaches resolved, and radiographs demonstrated a 15-degree improvement in cervical lordosis. The patient reported restored executive memory and pain-free gait.

These cases illustrate the practical synergy of medical oversight, cellular bioenergetic restoration, and precise structural correction. Similar patterns appear regularly in our personal-injury and chronic-disease caseload. When we address the cellular energy deficit and mechanical interference together, both laboratory markers and functional capacity improve more rapidly and more completely.

The Future of Bioenergetics, Metabolic Health, and Multidisciplinary Clinical Care

Managing complex chronic disease requires moving past fragmented, single-system models. Metabolic function, cellular energy production, and physical biomechanics are interconnected. When cellular bioenergetics fail—when NAD+ is depleted—mitochondrial electron transport stalls, ROS accumulate, cell signaling desensitizes, and tissues sustain structural damage. Whether the presentation is atherosclerotic change, myocardial dysfunction, insulin resistance, neurodegeneration, or chronic musculoskeletal pain, cellular energy failure sits near the center of the process.

By combining the medical diagnostic expertise of Dr. Maria Guadalupe Cardenas, MD, with the chiropractic, nursing, and functional-medicine approach I bring to the clinic, the team at Injury Medical Clinic PA delivers a comprehensive, root-cause clinical model. Restoring the cellular NAD+ pool, clearing structural nervous-system interference, reducing systemic inflammation, and supporting the body’s innate repair mechanisms creates a clear pathway to long-term health, structural stability, and metabolic vitality.

Ongoing clinical observations at wellnessdoctorrx.com continue to refine these protocols. In our experience, patients who receive coordinated care consistently show improvements in inflammatory markers, insulin sensitivity, pain scores, and quality-of-life measures that neither isolated pharmacotherapy nor isolated structural care has matched. Integrating evidence-based cellular medicine with non-surgical biomechanical rehabilitation under proper medical direction offers a practical, scalable model for addressing the shared roots of modern chronic disease.

References

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• Diguet, N., Trammell, S. A. J., Tannous, C., Deloux, R., Piquereau, J., Mougenot, N., Gouge, A., Gressette, M., Manoury, B., Blanc, J., Breton, M., Decaux, J. F., Garnier, A., Brenner, C., & Mericskay, M. (2018). Nicotinamide riboside preserves cardiac function in a mouse model of dilated cardiomyopathy. Nature Communications, 9(1), 2756. https://doi.org/10.1038/s41467-018-05390-3
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• Gomes, A. P., Price, N. L., Ling, A. J., Moslehi, J. J., Montgomery, M. K., Rajman, L., White, J. P., Teodoro, J. S., Wrann, C. D., Hubbard, B. P., Mercken, E. M., Palmeira, C. M., de Cabo, R., Rolo, A. P., Turner, N., Bell, E. L., & Sinclair, D. A. (2013). Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 155(7), 1624–1638. https://doi.org/10.1016/j.cell.2013.11.037
• Rajman, L., Chwalek, K., & Sinclair, D. A. (2018). Therapeutic potential of NAD-boosting molecules: The in vivo evidence. Cell Metabolism, 27(3), 529–547. https://doi.org/10.1016/j.cmet.2018.02.011
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• Clinical observations and additional educational resources are available at wellnessdoctorrx.com and through the professional network of Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST.

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