Unlock the secrets of chiropractic restoration and metabolic health for a balanced body and improved wellness.

Abstract

Chronic conditions such as atherosclerosis, dilated cardiomyopathy, type 2 diabetes, and Alzheimer’s disease often share a common cellular origin: progressive depletion of nicotinamide adenine dinucleotide (NAD+), mitochondrial decay, and the resulting cascade of oxidative stress and inflammation. This educational post, written from the clinical perspective of Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, explores NAD+ biochemistry as both a redox cofactor and a cosubstrate for sirtuins, PARPs, and CD38. Drawing on modern research, it traces how NAD+ decline impairs oxidative phosphorylation, disrupts mitochondrial quality control, and amplifies disease across vascular, cardiac, metabolic, and neurological systems. The post then details the multidisciplinary protocols used at Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas. There, 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, serves as Medical Director and Collaborative Physician. Working alongside Dr. Jimenez, the team integrates medical oversight, functional diagnostics, targeted NAD+ restoration, and non-surgical chiropractic care to address both systemic bioenergetic failure and biomechanical stressors that perpetuate sympathetic overactivity, tissue hypoxia, and impaired nutrient delivery. Clinical observations from Dr. Jimenez’s practice, documented at chiropracticscientist.com, illustrate how this combined approach supports recovery in personal injury, cardiometabolic, and chronic degenerative presentations.

Understanding the Multidisciplinary Model at Injury Medical Clinic PA

At Injury Medical Clinic PA in El Paso, Texas, care begins with the recognition that many patients arrive with overlapping structural, metabolic, and inflammatory problems. Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, evaluates biomechanical alignment, neuromuscular function, and functional medicine markers. Dr. Maria Guadalupe Cardenas, MD, provides medical direction. With more than four decades as a board-certified internist, she oversees diagnostic workups, laboratory interpretation, cardiovascular and metabolic risk stratification, and any indicated pharmacotherapy. This collaborative structure is common in integrative injury clinics: the physician supplies medical oversight and systemic management while the chiropractor addresses spinal mechanics, afferent signaling, and rehabilitation.

The team’s approach rests on a practical observation drawn from years of clinical work. Patients with unresolved chronic pain, vascular stiffness, or neurocognitive fatigue frequently show laboratory or clinical signs of impaired cellular energy production. When NAD+ pools are low, tissues cannot repair efficiently, clear inflammation, or maintain normal autonomic tone. Chiropractic adjustments and decompression are used not as isolated mechanical corrections but as interventions that reduce persistent nociceptive drive, lower sympathetic hyperactivity, and improve local microvascular perfusion. Better perfusion supports the delivery of oxygen, substrates, and any systemic NAD+ precursors or therapies. Functional medicine testing—organic acids, inflammatory markers, and autonomic assessments—helps both clinicians track progress. This integrated model is applied to personal injury cases, post-trauma rehabilitation, and chronic cardiometabolic conditions.

The Fundamental Biochemical Architecture of NAD+ and Cellular Respiration

Every human cell must continuously generate and manage energy. NAD+ sits at the center of this process. It exists in two primary states: the oxidized form, NAD+, and the reduced form, NADH. In the cytosol, glycolysis converts one molecule of glucose into two molecules of pyruvate while reducing two molecules of NAD+ to NADH. Pyruvate then enters the mitochondrial matrix, where the tricarboxylic acid cycle generates additional NADH and FADH2. These reduced carriers donate electrons to the electron transport chain embedded in the inner mitochondrial membrane.

At Complex I, NADH is reoxidized to NAD+, and the released electrons flow through iron-sulfur clusters to ubiquinone. This energy transfer pumps protons into the intermembrane space, creating an electrochemical gradient. Complex V (ATP synthase) uses the return of those protons to convert ADP and inorganic phosphate into ATP. This process, oxidative phosphorylation, supplies most cellular ATP. When the total NAD+ pool is adequate, and the NAD+/NADH ratio remains favorable, electron flow stays efficient, reactive oxygen species generation remains low, and ATP production supports ion homeostasis, protein synthesis, and membrane repair.

NAD+ also serves as an irreversible cosubstrate for three major enzyme families. Sirtuins (SIRT1–SIRT7) use NAD+ to remove acetyl and acyl groups from proteins, thereby regulating gene expression, mitochondrial biogenesis, and stress resistance. Poly(ADP-ribose) polymerases (PARPs) consume NAD+ to attach poly(ADP-ribose) chains to nuclear proteins during DNA repair. CD38 and CD157 are glycohydrolases that degrade NAD+ while generating cyclic ADP-ribose. Because these reactions consume NAD+ rather than merely cycling it, the cell must continuously resynthesize the nucleotide through the salvage pathway, whose rate-limiting enzyme is nicotinamide phosphoribosyltransferase (NAMPT).

Clinical observations at the clinic frequently show that patients with long-standing pain or metabolic syndrome exhibit signs consistent with compromised NAD+ availability. Organic acid profiles may reveal elevated markers of incomplete beta-oxidation or Krebs-cycle intermediates, while inflammatory panels show elevated high-sensitivity C-reactive protein. These findings guided decisions to support NAD+ restoration while also addressing mechanical contributors to sympathetic drive.

How NAD+ Depletion Creates the Vicious Cycle of Mitochondrial Dysfunction

With age, chronic inflammation, trauma, and metabolic overload, intracellular NAD+ levels decline. Two processes accelerate the loss. First, NAMPT expression falls under inflammatory and circadian stress, slowing resynthesis. Second, consumption rises sharply. DNA damage activates PARP1, which can deplete the NAD+ pool within minutes. CD38, upregulated on inflammatory macrophages, hydrolyzes large quantities of NAD+ for every molecule of cyclic ADP-ribose produced. The resulting drop in NAD+ inactivates sirtuins. Mitochondrial SIRT3 normally deacetylates and activates superoxide dismutase 2 (SOD2) and subunits of the electron transport chain. When SIRT3 activity falls, SOD2 remains hyperacetylated and inactive, superoxide accumulates, and electron transport components become less efficient. Electron leakage at Complexes I and III generates additional reactive oxygen species that damage mitochondrial DNA, lipids, and proteins.

Damaged mitochondria lose membrane potential, open the permeability transition pore, and release cytochrome c and mitochondrial DNA fragments. These molecules activate the NLRP3 inflammasome and the cGAS-STING pathway, driving production of interleukin-1 beta, interleukin-18, and interleukin-6. The inflammatory cytokines further upregulate CD38 and PARP1, consuming still more NAD+. The cycle becomes self-reinforcing. In clinical practice, this pattern appears in patients whose pain or fatigue does not resolve with local treatment alone. Therefore, supporting NAD+ repletion while reducing the mechanical and inflammatory drivers that elevate CD38 and PARP activity is a core strategy.

NAD+ Restoration and Atherosclerotic Stabilization

Atherosclerosis is a chronic inflammatory disease of the arterial wall. In regions of disturbed flow, endothelial cells become activated, express adhesion molecules, and recruit monocytes. Oxidized lipoproteins further impair endothelial nitric oxide synthase (eNOS). When intracellular NAD+ is low, SIRT1 activity declines, eNOS remains hyperacetylated at key lysine residues, and the enzyme uncouples, producing superoxide instead of nitric oxide. Research has shown that restoring NAD+ reactivates SIRT1, which deacetylates eNOS and restores nitric oxide production. At the same time, SIRT1 deacetylates the p65 subunit of nuclear factor kappa B, limiting transcription of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and monocyte chemoattractant protein-1. Monocyte recruitment therefore decreases.

Within the vessel wall, macrophages that ingest oxidized lipids develop defective autophagy and become foam cells. NAD+ repletion re-establishes autophagic flux through AMPK-SIRT1-TFEB signaling, promoting cholesterol efflux via ABCA1 and ABCG1. Improved efferocytosis clears apoptotic debris and shrinks the necrotic core. Matrix metalloproteinase activity declines, preserving the fibrous cap. Landmark experimental work demonstrated that systemic or subcutaneous NAD+ repletion reduced plaque size and inflammatory content. In the clinic, Dr. Cardenas evaluates patients with elevated cardiovascular risk markers for lipid particle number, blood pressure, and inflammatory status. Concurrent chiropractic care addresses thoracic and cervical mechanics that can elevate sympathetic tone and impair vascular regulation. Together, they support both the endothelial environment and the mechanical factors that influence local perfusion.

Reversing Cardiac Metabolic Failure in Dilated Cardiomyopathy

The myocardium consumes large amounts of ATP daily. Under healthy conditions, beta-oxidation of long-chain fatty acids generates most of that ATP. In dilated cardiomyopathy, mitochondrial dysfunction shifts metabolism toward glycolysis, reducing ATP yield by more than 80%. The resulting energy deficit impairs the sarcoplasmic reticulum calcium ATPase (SERCA2a). Cytosolic calcium remains elevated during diastole, elevating filling pressures and activating pro-fibrotic signaling.

NAD+ repletion restores SIRT3 activity within the mitochondrial matrix. SIRT3 deacetylates fatty-acid oxidation enzymes and subunits of the electron transport chain and ATP synthase, restoring efficient oxidative phosphorylation. Increased ATP availability re-energizes SERCA2a, improving diastolic calcium reuptake, chamber filling, and systolic force. Experimental studies published in 2018 and 2019 showed that nicotinamide riboside or related NAD+ strategies preserved or improved cardiac function and chamber dimensions in models of dilated cardiomyopathy. At Injury Medical Clinic PA, we provide coordinated evaluation for patients with cardiometabolic presentations. Dr. Cardenas monitors ejection fraction, wall stress indicators, and metabolic labs. Chiropractic protocols focus on thoracic mobility and autonomic balance because chronic sympathetic drive increases myocardial oxygen demand while reducing coronary microvascular perfusion. Restoring parasympathetic tone through reduced nociceptive input supports the energetic environment created by NAD+ support.

Type 2 Diabetes as a Mitochondrial and Bioenergetic Disorder

Type 2 diabetes is frequently approached as a problem of elevated glucose. In functional practice, it is viewed as impaired substrate oxidation and progressive NAD+ depletion. Excess nutrients saturate mitochondrial capacity, generating diacylglycerols and ceramides that activate serine kinases. These kinases phosphorylate insulin receptor substrate-1 on inhibitory serine residues, blocking downstream PI3K-Akt signaling and GLUT4 translocation. Concurrently, uncoupled mitochondria produce superoxide that damages DNA and further activates PARP1, consuming NAD+.

NAD+ repletion upregulates SIRT1 and AMPK. SIRT1 deacetylates and activates insulin receptor substrate-1 on tyrosine residues while suppressing the inhibitory serine kinases. Improved beta-oxidation clears the toxic lipid intermediates. In pancreatic beta cells, restored mitochondrial coupling re-establishes the ATP/ADP rise that closes ATP-sensitive potassium channels, allowing normal glucose-stimulated insulin secretion. Research published in 2019 and 2021 showed that administering NAD+ precursors improved insulin sensitivity and reduced metabolic inflammation in human subjects. Clinical observations from Dr. Jimenez’s practice, available at chiropracticscientist.com, include patients whose HOMA-IR and HbA1c improved when metabolic support was combined with interventions that reduced sympathetic overactivity and improved movement capacity. Graded rehabilitation and chiropractic care enable patients to increase daily activity once pain and autonomic imbalance are addressed, further supporting insulin sensitivity.

Alzheimer’s Disease as Type 3 Diabetes and Primary Mitochondrial Collapse

Conventional models have emphasized extracellular amyloid plaques and intracellular tau tangles. Repeated trial failures targeting amyloid clearance have prompted re-examination of upstream drivers. Neuronal NAD+ depletion produces mitochondrial depolarization, electron leakage, and massive superoxide and peroxynitrite generation. Oxidative damage to synaptic membranes activates the integrated stress response, phosphorylating eIF2-alpha and selectively increasing translation of beta-site APP cleaving enzyme 1. Amyloid precursor protein is therefore processed toward amyloid-beta. Amyloid accumulation can be understood as a downstream marker of energetic failure rather than the sole initiating event.

NAD+ repletion crosses the blood-brain barrier, restores neuronal pools, and activates mitochondrial SIRT3. SIRT3 deacetylates SOD2 and glutathione peroxidase, reducing oxidative stress. At the same time, SIRT1 stimulates PGC-1alpha-mediated mitochondrial biogenesis and normalizes PINK1/Parkin-mediated mitophagy, clearing damaged organelles. Studies in the Journal of Neuroscience (2018) and related work in 2019 and 2020 showed that these changes preserved long-term potentiation, reduced pathology, and improved cognitive measures in experimental models. In the clinic, patients with cognitive concerns or post-traumatic brain injury receive coordinated assessment. Dr. Cardenas’s medical evaluation includes metabolic and vascular risk factors. Chiropractic and rehabilitation protocols address cervical mechanics and autonomic regulation, because chronic neck pain and sympathetic hyperactivity can further impair cerebral perfusion and exacerbate neuroinflammation. An integrated strategy supports cellular energetics while optimizing mechanical and autonomic factors.

The Triad of Chronic Disease: Mitochondrial Dysfunction, Insulin Resistance, and Systemic Inflammation

Mitochondrial dysfunction, insulin resistance, and systemic inflammation reinforce one another. Impaired oxidative phosphorylation increases reactive oxygen species and releases damage-associated molecular patterns that activate NF-?B and the NLRP3 inflammasome. The resulting cytokines promote further insulin resistance and CD38 upregulation. Insulin resistance itself increases ectopic lipid accumulation, which further stresses mitochondria. NAD+ depletion sits at the center of this triad because it simultaneously turns off antioxidant defenses, impairs metabolic flexibility, and fails to restrain inflammatory transcription. Breaking the cycle requires simultaneous attention to cellular fuel supply, inflammatory drivers, and the mechanical factors that sustain sympathetic tone and local hypoxia.

Integrative Chiropractic Care Within Non-Surgical Treatment Protocols

Spinal subluxation complexes and kinetic-chain imbalances generate continuous nociceptive afferent input. This input drives segmental and supraspinal sympathetic hyperactivity, producing peripheral vasoconstriction, elevated cortisol and catecholamines, and local tissue hypoxia. Hypoxic cells shift toward anaerobic metabolism, depleting cytosolic NAD+ and increasing oxidative stress. High-velocity, low-amplitude adjustments stimulate high-threshold mechanoreceptors, activating inhibitory interneurons in the dorsal horn and gating nociceptive transmission. Reduced nociceptive drive lowers sympathetic outflow and increases vagal activity. Vagal acetylcholine binds alpha-7 nicotinic receptors on macrophages, suppressing NF-kappa B and cytokine production. Restored microvascular perfusion improves delivery of oxygen, glucose, and any circulating NAD+ precursors or therapeutics.

Motorized spinal decompression rehydrates intervertebral discs and reduces mechanical irritation of adjacent neural structures, further decreasing afferent drive. In personal injury cases, these interventions are combined with graded neuromuscular rehabilitation to restore motor firing patterns. Clinical observations documented by Dr. Jimenez indicate that patients who receive concurrent chiropractic care alongside metabolic or NAD+-focused support often report faster resolution of pain and improved exercise tolerance. The structural intervention does not replace medical or nutritional care; it creates a physiological environment in which those interventions can be more effective by reducing the constant sympathetic and inflammatory load.

Clinical Case Protocols for Post-Trauma and Cardiometabolic Care

Post-trauma protocols begin with dual evaluation. Dr. Cardenas assesses soft-tissue inflammation, cardiovascular stability, and systemic labs. Dr. Jimenez performs biomechanical and motion analysis. Intervention combines targeted adjustments, decompression, and kinetic-chain rehabilitation with subcutaneous or systemic NAD+ repletion, oral nicotinamide riboside or nicotinamide mononucleotide support, and targeted mitochondrial micronutrients. We track outcomes using range of motion, visual analog scale scores, and inflammatory markers.

Cardiometabolic protocols include advanced lipid particle testing, fasting insulin, HbA1c, and organic acid profiling. Medical management addresses risk stratification and indicated pharmacotherapy. Functional interventions emphasize NAD+ restoration, time-restricted or lower-glycemic nutrition, and autonomic-focused adjustments. Long-term goals include improved HOMA-IR, reduced visceral adiposity, and sustained bioenergetic capacity. Cases summarized on chiropracticscientist.com illustrate measurable improvements in weight, metabolic markers, and functional capacity when these elements are coordinated.

Actionable Takeaways

NAD+ functions as both an essential redox carrier and a regulatory cosubstrate; its progressive depletion drives mitochondrial decay and multi-system failure. Atherosclerosis, dilated cardiomyopathy, type 2 diabetes, and Alzheimer’s disease share upstream bioenergetic and oxidative pathology. Combining Dr. Cardenas’s medical oversight with functional medicine and non-surgical chiropractic care from Dr. Jimenez addresses both cellular metabolism and the biomechanical drivers of sympathetic overactivity and impaired perfusion. Restoring alignment and autonomic balance enhances the delivery and effectiveness of cellular support strategies.

References

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