Stem Cells and Inflammation: The Two-Way Relationship That Determines Your Recovery Capacity

The relationship between stem cells and inflammation is a complex feedback loop that determines how effectively your body maintains and repairs tissue. Acute inflammation generates repair signals that recruit stem cells to damaged areas, whereas persistent low-grade chronic inflammation impairs stem cells' function and navigation.

Understanding this bidirectional relationship reveals why some people recover quickly from injury while others experience prolonged healing times, why tissue repair capacity declines with age, and why reducing chronic inflammation represents one of the most impactful interventions for supporting optimal stem cell function.

This article discusses how inflammation affects stem cell mobilization, circulation, and homing, how stem cells themselves modulate inflammatory responses, and evidence-based approaches - both lifestyle and targeted supplementation - that optimize this critical relationship for effective tissue repair and maintenance.

Acute vs. Chronic Inflammation: A Critical Distinction

The relationship between stem cells and inflammation differs dramatically depending on whether inflammation is acute or chronic. These two forms of inflammation have opposite effects on tissue repair.

Acute Inflammation: The Beneficial Signal

Acute inflammation following an injury or infection is essential for tissue repair. When tissues are damaged, resident immune cells and damaged cells themselves release inflammatory mediators, including cytokines (IL-1, IL-6, TNF-alpha), chemokines (particularly CXCL12/SDF-1), and damage-associated molecular patterns (DAMPs), along with mediators of stem cell mobilization (G-SCF, GM-CSF, IL-8, S1P). This physiological response creates a localized inflammatory mechanism that:

• Signals stem cells stored in the bone marrow to mobilize into circulation
• Creates chemokine gradients that guide circulating stem cells to the injury site
• Upregulates adhesion molecules on endothelial cells, allowing stem cells to exit circulation and enter tissue
• Provides signals that influence stem cell differentiation into specialized cells
• Recruits immune cells that clear debris and prepare tissue for regeneration

Research published in Nature Immunology demonstrates that acute inflammatory signals are necessary for effective stem cell recruitment and tissue repair. When these signals are partially or completely blocked, healing is actually impaired.

Chronic Inflammation: The Destructive Noise

Chronic low-grade inflammation represents a fundamentally different internal environment. Instead of a targeted, time-limited response to injury, chronic inflammation involves sustained elevation of inflammatory markers in the systemic circulation and throughout the body. This creates what researchers call "inflammaging" - the increase in serum baseline inflammatory cytokines that contributes to multiple chronic conditions.

Chronic inflammation disrupts stem cell function through several mechanisms:

• Signal interference: Elevated inflammatory cytokines in the circulatory system create "background noise" that masks repair signals from specific damaged tissue
• Impaired mobilization: Chronic inflammation can suppress bone marrow function and alter stem cell release patterns
• Reduced homing accuracy: When inflammatory signals are elevated in the system, stem cells lose the ability to clearly distinguish real injury sites from diffused general inflammation
• Oxidative damage: Chronic inflammation produces reactive oxygen species that damage stem cells and the receptors they use for navigation
• Premature senescence: Prolonged inflammatory exposure can push stem cells into a senescence state, permanently removing them from the functional pool

Essentially, systemic inflammation impairs stem cell homing through elevated circulating SDF-1 and inflammatory signaling that reduce the tissue-to-blood chemokine gradient and may prematurely activate migration machinery in circulating stem cells. When stem cells reach the damaged tissue, they have lost their ability to migrate in that tissue. Together, these mechanisms reduce the ability of stem cells to respond appropriately to SDF-1 signals emitted by damaged tissues.

Studies show that individuals with elevated markers of chronic inflammation (high-sensitivity CRP >3.0 mg/L, IL-6 >5 pg/mL) demonstrate impaired wound healing, slower post-surgical recovery, and reduced tissue regeneration capacity despite normal stem cell counts in circulation.

How Inflammation Affects the Three Pathways of Stem Cell Function

The stem cell-based tissue repair system operates through three essential pathways - release, microcirculation, and signaling. Inflammation impacts each pathway differently, with effects that differ markedly between acute and chronic.

Pathway 1: Endogenous Stem Cell Release

Acute inflammation triggers stem cell mobilization from bone marrow through several mechanisms. Inflammatory cytokines modulate what is referred to as the CXCR4/SDF-1 axis (the primary mechanism to release or retain stem cells in bone marrow niches), through the upregulation of enzymes like matrix metalloproteinases that help stem cells exit bone marrow spaces. This indicates a physiologically appropriate response to tissue demand. In this process, stem cells essentially follow the concentration gradient of SDF-1, which is modulated by the action of various cytokines.

Chronic inflammation, however, can disrupt the normal regulation of stem cell maintenance and function. Persistent inflammatory signaling alters the bone marrow microenvironment, affecting the interactions between stem cells and their supporting niche. As reported, these changes can impair stem cell self-renewal, differentiation, and responsiveness to physiological signals that regulate mobilization and repair. Chronic inflammation primarily reduces the functional capacity of the stem cell compartment and alters the regulatory environment that controls mobilization and tissue repair.

Data demonstrates that individuals with chronic inflammatory conditions show altered stem cell mobilization patterns compared to healthy controls, with implications for both tissue repair capacity and cardiovascular risk.

Pathway 2: Microcirculation and Physical Delivery

Acute inflammation at injury sites increases local blood flow and upregulates adhesion molecules (VCAM-1, ICAM-1) on endothelial cells, facilitating stem cell extravasation from circulation into tissue. This is beneficial and necessary for repair.

Chronic inflammation impairs microcirculation through multiple mechanisms:

• Endothelial dysfunction: Sustained inflammation damages the endothelial glycocalyx - the protective layer on blood vessel surfaces that presents chemokines and supports stem cell rolling and adhesion
• Increased blood viscosity: Chronic inflammation elevates fibrinogen and other acute-phase proteins, making blood more viscous and impeding flow through capillaries
• Capillary rarefaction: Long-term inflammation contributes to loss of capillary density in tissue, reducing the physical pathways for stem cell delivery
• Oxidative damage: Inflammation-generated reactive oxygen species damage blood vessel walls and impair vasodilation

Studies using contrast-enhanced ultrasound and other imaging techniques show that chronic inflammatory conditions correlate with reduced microvascular density and impaired tissue perfusion, creating physical barriers to stem cell delivery regardless of the number of circulating stem cells.

Pathway 3: Signaling and Navigation

This pathway shows the most dynamic difference between acute and chronic inflammation. Acute inflammation at an injury site creates a clear gradient of chemokines and cytokines - high concentrations at the damage location, progressively lower concentrations farther away. Stem cells follow this gradient "uphill" to reach the precise location requiring repair.

Chronic inflammation destroys this gradient clarity. When inflammatory markers are elevated throughout the body, especially SDF-1, stem cells see high concentrations of cytokines everywhere in the body, making it difficult to localize the true source of injury and accurately home to sites of damage. Stem cells can also be activated for migration outside the microvasculature, reducing their capacity to migrate when they reach the damaged tissue.

The signal-to-noise ratio largely determines stem cell homing effectiveness. Experimental studies show that inflammatory cytokines such as IL-6 and TNF-alpha can alter stem cell function and responsiveness to chemokine gradients. Because stem cell homing depends largely on the SDF-1/CXCR4 signaling axis, inflammatory environments that disrupt this signaling can impair the migration of stem cells to sites of tissue injury even when stem cell numbers and injury signals are present. Studies quantifying this ratio show that individuals with chronic inflammation (elevated baseline IL-6, TNF-alpha, CRP) demonstrate significantly impaired stem cell homing to injury sites in experimental models, even when stem cell numbers and injury signals are equivalent to those of healthy controls.

How Stem Cells Modulate Inflammation

The relationship between stem cells and inflammation is bidirectional - not only does inflammation affect stem cell function, but stem cells themselves influence inflammatory responses. This explains why supporting optimal stem cell function may help regulate inflammation.

Paracrine Anti-Inflammatory Effects

When stem cells successfully penetrate damaged tissue, they secrete factors that modulate local inflammation by releasing anti-inflammatory cytokines. Research has demonstrated that stem cells release anti-inflammatory cytokines, including IL-10 and TGF-beta, growth factors that support tissue repair, and extracellular vesicles containing microRNAs that alter gene expression in immune cells.

Together, these paracrine signals help shift the local environment from a pro-inflammatory phase (dominated by M1 macrophages and inflammatory cytokines) to a repair phase (with M2 macrophages and regenerative factors). This coordinated transition from inflammation to repair is essential for effective healing; healing cannot take place in the presence of sustained inflammation.

Studies show that the secretome (collection of secreted factors) from stem cells can reduce inflammatory markers and support tissue repair even in the absence of stem cell engraftment or differentiation, suggesting that stem cells have therapeutic benefit beyond actual renewal of tissue.

Immune Cell Interaction

Stem cells interact directly with immune cells, influencing their behavior. Stem cells can:

• Suppress excessive T cell proliferation and activity
• Promote regulatory T cells (Tregs) that dampen inflammatory responses
• Modulate macrophage polarization from pro-inflammatory M1 toward tissue-remodeling M2 phenotype
• Influence neutrophil recruitment and apoptosis, affecting the resolution of acute inflammation

These immunomodulatory properties are the reason endogenous stem cell mobilization can potentially be beneficial not only in tissue repair but also in autoimmune and chronic inflammatory conditions.

Mitochondrial Transfer

Emerging research reveals that stem cells can transfer healthy mitochondria to damaged cells through mechanisms including direct cell-cell communication and extracellular vesicles. Since damaged mitochondria produce excessive reactive oxygen species that perpetuate inflammation, this mitochondrial transfer may help break inflammatory cycles.

Studies in models of acute lung injury and other conditions show that stem cell-mediated mitochondrial transfer correlates with reduced oxidative stress and improved outcomes, suggesting this as one mechanism by which stem cells help resolve inflammation in the body.

The Inflammaging Phenomenon - Why Recovery Declines With Age

One of the most consistent findings in aging research is the progressive increase in baseline inflammatory markers - a phenomenon termed "inflammaging." This provides a physiological basis for the age-related decline in tissue repair capacity.

Sources of Age-Related Inflammation

Multiple factors contribute to increased inflammation with aging:

• Senescent cell accumulation: Senescent cells produce high levels of inflammatory cytokines (the senescence-associated secretory phenotype or SASP), contributing significantly to background inflammatory noise
• Immunosenescence: Age-related changes in immune cell function lead to chronic activation and inflammatory cytokine production
• Mitochondrial dysfunction: Damaged mitochondria accumulate with age, producing reactive oxygen species that trigger inflammatory pathways
• Gut dysbiosis: Age-related changes in gut microbiome composition increase production of inflammatory metabolites and reduce anti-inflammatory compounds
• Visceral fat accumulation: Adipose tissue, particularly visceral fat, produces inflammatory adipokines
• Chronic antigenic exposure: Lifelong exposure to infections (particularly persistent viruses like CMV) creates ongoing immune activation

Data from the Baltimore Longitudinal Study of Aging and other large cohorts show progressive increases in IL-6 (approximately 2-4% per year after age 60), TNF-alpha, and CRP levels even in individuals who remain relatively healthy. This baseline elevation impairs stem cell signaling regardless of the individual's circulating stem cell numbers.

The Vicious Cycle

Inflammaging creates a self-reinforcing cycle. Chronic inflammation impairs stem cell function, reducing tissue maintenance and repair capacity. This leads to the accumulation of damaged tissue and cells, which produce more inflammatory signals, further elevating background noise. The result is accelerated tissue aging and reduced regenerative capacity.

Research in Nature Medicine demonstrates that interventions reducing chronic inflammation in aged animals partially restore stem cell homing and tissue repair capacity, suggesting that a significant portion of the age-related decline in regenerative capacity stems from the chronic inflammatory environment.

Measuring Your Inflammatory Load

Understanding your personal inflammatory status provides insight into how to support your stem cells' function. Several accessible biomarkers can indicate an inflammatory condition:

High-Sensitivity C-Reactive Protein (hs-CRP)

CRP is produced by the liver in response to inflammatory cytokines. High-sensitivity testing allows detection of low-grade chronic inflammation:

• Optimal: below 1.0 mg/L (minimal background noise)
• Moderate: 1.0-3.0 mg/L (some interference with signaling)
• High: above 3.0 mg/L (significant signal-to-noise impairment)

Research has shown that hs-CRP above 3.0 mg/L correlates with measurably impaired tissue repair, slower wound healing, and increased cardiovascular risk. This marker can provide a practical indicator of whether chronic inflammation is likely interfering with stem cell function.

Interleukin-6 (IL-6)

IL-6 serves as both a pro-inflammatory cytokine and a marker of systemic inflammation. Normal levels are typically below 5 pg/mL, with lower being better. Elevated IL-6 directly interferes with stem cell signaling pathways and correlates with impaired homing efficiency.

TNF-alpha

Tumor necrosis factor-alpha represents another key inflammatory cytokine. Chronic elevation indicates ongoing inflammatory activation that contributes to background noise. Normal ranges vary by laboratory, but lower values consistently associate with better tissue repair capacity.

Functional Assessment

Beyond laboratory markers, functional indicators provide a practical assessment of inflammatory burden, which also indicate reduced stem cell function:

• Recovery time: How quickly you recover from exercise, minor injuries, or minor illness
• Sleep quality: Poor sleep both causes and results from inflammation
• Energy levels: Chronic inflammation contributes to fatigue
• Joint comfort: Morning stiffness or persistent discomfort suggests inflammation
• Skin health: Chronic inflammation manifests in skin aging and slows wound healing

Natural Anti-Inflammatory Approaches - Dietary Interventions

Multiple dietary strategies offer measurable effects on inflammatory markers, improving the internal environment for stem cell activity.

Omega-3 Fatty Acids

EPA and DHA from marine sources reduce inflammatory eicosanoid production and promote specialized pro-resolving mediators (SPMs) that actively resolve inflammation. Meta-analyses of clinical trials show that 3-4 grams of combined EPA/DHA daily reduces CRP, IL-6, and TNF-alpha.

The mechanism involves displacement of arachidonic acid from cell membranes, reducing substrate availability for pro-inflammatory prostaglandin and leukotriene synthesis. Additionally, EPA and DHA-derived resolvins, protectins, and maresins actively promote the transition from inflammation to resolution.

Food sources providing meaningful omega-3 doses include wild-caught fatty fish (salmon, mackerel, sardines, anchovies). Most people consume insufficient amounts from diet alone, making supplementation with fish oil or algae-based omega-3s a practical option.

Polyphenol-Rich Foods

Polyphenols from colorful plant foods have anti-inflammatory and antioxidant properties, and the effects are shown through multiple mechanisms, including Nrf2 pathway activation, direct free radical scavenging, and modulation of inflammatory gene expression.

Particularly beneficial sources include:

• Berries: Anthocyanins reduce oxidative stress and inflammatory markers
• Green tea: EGCG inhibits inflammatory pathways and supports endothelial health
• Extra virgin olive oil: Oleocanthal inhibits COX enzyme
• Dark chocolate: Cocoa flavanols improve endothelial function and reduce inflammation (choose 70%+ cacao)
• Pomegranate: Punicalagins support vascular health and reduce oxidative stress

Studies show that diets rich in diverse polyphenols (consuming 500-1000mg daily from varied sources) significantly reduce inflammatory markers over 8-12 weeks.

Cruciferous Vegetables

Sulforaphane from cruciferous vegetables activates Nrf2, triggering production of endogenous antioxidant enzymes. This creates lasting protection against oxidative stress and inflammatory damage. Broccoli sprouts contain particularly high concentrations of glucoraphanin (the sulforaphane precursor), providing potent Nrf2 activation.

Reducing Pro-Inflammatory Foods

Eliminating or minimizing foods that actively promote inflammation is as important as adding anti-inflammatory foods:

• Refined sugars and high-glycemic carbohydrates: Trigger inflammatory cytokine production and oxidative stress
• Refined vegetable oils high in omega-6: Excessive omega-6 (from soybean, corn, safflower oils) promotes inflammatory eicosanoid production
• Trans fats: Directly promote inflammation and endothelial dysfunction
• Excessive alcohol: Increases gut permeability and inflammatory markers
• Processed meats: Advanced glycation end products (AGEs) and other compounds promote inflammation

Natural Anti-Inflammatory Approaches - Lifestyle Interventions

Exercise - Balancing Acute and Chronic Effects

Exercise creates an acute inflammatory response during and immediately after activity (elevated IL-6, cortisol, and other markers). However, regular exercise training produces chronic anti-inflammatory effects, reducing baseline inflammatory markers and improving tissue repair capacity.

Regular moderate exercise (150 minutes weekly) reduces hs-CRP, IL-6, and TNF-alpha over time. High-intensity interval training (HIIT) provides additional benefits by increasing stem cell mobilization and improving microcirculatory function.

The key is to allow adequate recovery between sessions. Excessive training without recovery creates chronic elevation of inflammatory markers and impaired tissue repair - the overtraining syndrome. Rest days and sleep are important for allowing the anti-inflammatory adaptations to manifest.

Sleep - The Anti-Inflammatory Reset

Sleep deprivation rapidly increases inflammatory markers. Studies show that even partial sleep restriction (4-5 hours nightly for one week) significantly elevates IL-6, TNF-alpha, and CRP. Consistently obtaining 7-9 hours of quality sleep helps maintain lower baseline inflammation.

The mechanisms involve multiple pathways. Sleep allows clearance of metabolic waste from the brain via the glymphatic system, reduces sympathetic nervous system activation, and permits proper immune system regulation. Chronic sleep deprivation creates a pro-inflammatory state that impairs stem cell signaling.

Practical sleep optimization includes consistent sleep-wake timing, cool dark bedrooms, limiting blue light exposure in evenings, and managing stress.

Stress Management - Cortisol and Inflammation

Chronic psychological stress elevates cortisol, which paradoxically increases inflammatory cytokine production despite cortisol's intended anti-inflammatory effects. This occurs through glucocorticoid receptor resistance - tissues become less responsive to cortisol's signals, allowing inflammatory pathways to activate despite high cortisol levels.

Stress reduction practices, including meditation, breathwork, yoga, and nature exposure, measurably reduce inflammatory markers. An 8-week mindfulness meditation program can potentially show significant reductions in IL-6 and CRP.

Intermittent Fasting - Cellular Stress Response

Time-restricted eating and intermittent fasting trigger cellular stress responses that can reduce inflammation. During fasting periods, cells upregulate autophagy (cellular cleanup processes), reduce oxidative stress, and shift toward anti-inflammatory metabolic states.

Time-restricted eating (16:8 pattern - eating within an 8-hour window daily) can reduce inflammatory markers in some individuals, though effects vary. Extended fasts (48-72 hours) show more robust anti-inflammatory effects and stem cell mobilization, though these may be impractical for most people to perform regularly.

The anti-inflammatory benefits of fasting are related to reduced oxidative stress, improved mitochondrial function, and activation of cellular stress response pathways, including Nrf2 and sirtuins.

Targeted Supplementation - Addressing the Signal-to-Noise Ratio

While diet and lifestyle create the foundation for managing inflammation, targeted supplementation with specific biological compounds can provide advanced support for optimizing the signal-to-noise ratio that determines stem cell homing effectiveness.

Curcumin - COX-2 Inhibition

Curcumin from turmeric inhibits cyclooxygenase-2 (COX-2) enzyme activity, reducing production of pro-inflammatory prostaglandins. Multiple clinical trials demonstrate that bioavailability-enhanced curcumin formulations (with piperine or other absorption enhancers) significantly reduce CRP, IL-6, and TNF-alpha.

Curcumin has poor absorption but rapid metabolism. While dietary turmeric provides some benefits, achieving therapeutic doses requires either consuming impractical amounts or using enhanced supplement formulations.

Phycocyanin from Spirulina - Multi-Pathway Anti-Inflammatory

Phycocyanin, the blue pigment in spirulina, has potent anti-inflammatory effects through COX-2 inhibition, Nrf2 activation, and direct antioxidant activity. Research shows that phycocyanin reduces the production of inflammatory prostaglandins, cytokines, and reactive oxygen species.

The critical factor is phycocyanin concentration. Most spirulina products contain 5-15% phycocyanin that provide modest benefits. Research that shows significant anti-inflammatory effects uses spirulina extracts standardized to 30-40% phycocyanin content.

Bromelain - Proteolytic Enzyme

Bromelain, derived from pineapple stems, is a proteolytic enzyme that demonstrates anti-inflammatory effects through multiple mechanisms, including breakdown of inflammatory mediators, modulation of immune cell activity, and reduction of edema. Its proteolytic action can cleave proteins that drive swelling, leukocyte recruitment, and inflammatory signaling.

Astaxanthin - Lipid-Soluble Antioxidant

Astaxanthin from the microalgae Haematococcus pluvialis provides powerful antioxidant protection, particularly in lipid-rich environments like cell membranes. By reducing oxidative stress, astaxanthin indirectly reduces inflammatory pathway activation. Its lipid-soluble nature allows it to protect cell membrane structures critical for stem cell signaling.

STEMREGEN® Signal™ - Addressing Background Noise

STEMREGEN® Signal™ specifically addresses inflammatory background noise through a synergistic combination of compounds targeting different inflammatory pathways. The formulation includes:

• Spirulina extract standardized to 30% phycocyanin: Provides concentrated phycocyanin at levels shown effective in research
• Bromelain: Proteolytic enzyme reducing inflammatory mediators
• Curcumin: COX-2 inhibition and inflammatory cytokine reduction
• Astaxanthin from Haematococcus pluvialis: Lipid-soluble antioxidant protecting cell membranes
• Piperine from black pepper extract: Enhances bioavailability of curcumin and other compounds

This combination of plant extracts helps stabilize the signal-to-noise ratio by reducing the production of inflammatory cytokines (IL-6, TNF-alpha) that create background noise, thereby improving the clarity of repair signals released from damaged tissue. By targeting COX-2, Nrf2 pathways, and oxidative stress simultaneously, Signal™ provides excellent support for optimizing stem cell signaling.

The Complete STEMREGEN® Protocol - Addressing All Three Pathways

Reducing inflammatory noise through Signal™ is one component of optimal stem cell function. The complete STEMREGEN® protocol addresses all three essential pathways that enable stem cells to effectively contribute to the entire tissue repair process.

Pathway 1: Release (STEMREGEN® SPORT™ or Release™)

Triggers Endogenous Stem Cell Mobilization (ESCM) from bone marrow through clinically-tested botanical compounds. The formulation includes SeaStem® from Tibetan Plateau sea buckthorn (not generic sea buckthorn - the harsh climate creates unique phytochemical profiles), StemAloe™ (a unique aloe extract), and AFA from Klamath Lake that specifically modulates the SDF-1/CXCR4 axis.

Additional ingredients, including Panax notoginseng, Pterocarpus marsupium (98% pterostilbene) in SPORT™ only, Fucus vesiculosus extract (20% phlorotannins, containing fucoidan), and beta-glucans (85%, 1→3 bonds) support comprehensive stem cell mobilization and homing receptor expression. This product ensures plenty of stem cells are available in circulation to respond to tissue signaling for repair.

Pathway 2: Microcirculation (STEMREGEN® Mobilize™)

Supports the delivery of stem cells through the microvasculature to reach tissue. The formulation improves blood viscosity for effective cellular entrainment (nattokinase), endothelial glycocalyx health (fucoidan from Ascophyllum nodosum), capillary integrity (rutin, hesperidin, quercetin from Sophora japonica, gotu kola extract with 90% triterpenoids, pomegranate extract with 40% ellagic acid), and nitric oxide production for vasodilation (L-citrulline, beetroot extract with 10% nitrate). This product ensures that released stem cells travel through the fine capillaries smoothly to reach tissue and are not blocked by impaired microcirculation.

Pathway 3: Signaling (STEMREGEN® Signal™)

Optimizes signal-to-noise ratio by reducing inflammatory background noise that obscures tissue repair signals. By lowering baseline inflammatory markers through multiple mechanisms (COX-2 inhibition, Nrf2 activation, antioxidant protection), Signal™ allows stem cells to distinguish genuine repair signals from generalized diffused inflammation.

This comprehensive three-pathway approach supports the entire stem cell-based tissue repair process that requires coordination across Endogenous Stem Cell Mobilization (ESCM), stem cell delivery, and accurate homing for optimal health outcomes over the long term.

Managing Inflammation to Support Stem Cell Function

With aging, rising baseline inflammation markers contribute to reduced repair capacity - but this is not an inevitable process. Reducing inflammatory background noise through diet, lifestyle, and targeted supplementation can improve the clarity of repair signals, allowing circulating stem cells to navigate effectively to tissues requiring repair and renewal. STEMREGEN® Signal™ is specifically formulated to reduce background noise and create clearer pathways for stem cells to navigate toward damaged tissues.

Including the STEMREGEN® protocol in your daily routine can support stem cell function from start to end by strengthening all three pathways: release (SPORT™ or Release™), microcirculation (Mobilize™), and signal clarity (Signal™), alongside lifestyle measures that reduce chronic systemic inflammation.