Macrophage Polarization Peptides in Canada: A Research Guide to M1/M2 States, Inflammation Resolution, Repair Signalling, and RUO Sourcing

Why macrophage polarization deserves its own recovery peptide guide#

Northern Compound already covers inflammation-resolution peptides, wound-healing peptide research, fibrosis and scar-tissue models, angiogenesis peptides, muscle injury research, and compound-level guides for BPC-157, KPV, TB-500, and thymosin alpha-1. What was still missing was a macrophage-first guide: how should Canadian readers evaluate peptide claims when the main research question is whether immune-cell phenotype, inflammatory timing, efferocytosis, and repair quality change in a tissue model?

That gap matters because macrophage language is easy to flatten. A supplier page, abstract, or review may say a compound “reduces inflammation” or “promotes M2 macrophages.” Those phrases sound precise, but they often hide the most important details: tissue type, injury stage, microbial context, species, assay timing, marker panel, vehicle control, contamination control, and whether the downstream tissue outcome improved or merely changed.

Macrophages do not exist to fit a marketing binary. They clear debris, recognise danger signals, coordinate innate and adaptive immune responses, release inflammatory mediators, support angiogenesis, remodel extracellular matrix, promote or restrain fibrosis, phagocytose microbes, perform efferocytosis of dying cells, and help decide whether a wound transitions from inflammation to repair. The same macrophage-associated marker can mean different things in skin, tendon, skeletal muscle, gut, nerve, lung, myocardium, or a cell-culture dish.

This article is written for non-clinical research-use-only evaluation. It does not provide medical advice, infection guidance, immune-therapy recommendations, wound-management instructions, dosing, route selection, compounding instructions, or personal-use suggestions. Disease terms appear only because the experimental literature uses them to describe model systems.

The short answer: define the macrophage question before choosing the peptide#

A defensible macrophage-polarization project starts with a specific question. Is the model testing suppression of an early inflammatory burst? Resolution after the inflammatory phase has done its job? Efferocytosis of apoptotic cells? Fibrosis restraint after repair begins? Host defence against a microbial challenge? Angiogenesis and granulation tissue? Matrix organisation in tendon or muscle? Those are related, but not interchangeable.

For the current Northern Compound product map, BPC-157 is the most coherent live reference when the research question combines tissue repair, angiogenesis, gut-derived injury models, or vascular response with immune timing. KPV is more coherent when the question centres on inflammatory signalling and epithelial or innate-immune tone. TB-500 fits migration, actin, wound-bed, and repair-context models where macrophage infiltration may be one layer among several. LL-37 belongs when host-defence peptide biology, antimicrobial challenge, or biofilm-macrophage interaction is central. Thymosin Alpha-1 is a better fit for immune-regulation and antigen-presentation context than for simple tissue-repair marketing. GHK-Cu belongs when matrix remodelling, wound quality, or copper-associated repair signalling is part of the endpoint panel.

The peptide should follow the hypothesis. A product link is a route to inspect current RUO supplier documentation, not evidence that a material improves human recovery.

Macrophage polarization is a spectrum, not a switch#

The older M1/M2 shorthand remains useful as a teaching tool, but it is too blunt for serious peptide evaluation. M1-like macrophages are often associated with inflammatory, microbicidal, glycolytic, nitric-oxide-producing states induced by signals such as LPS and interferon-gamma. M2-like macrophages are often associated with tissue repair, IL-4/IL-13 signalling, efferocytosis, matrix remodelling, and anti-inflammatory mediators. Real tissues rarely follow that clean two-box model.

Modern reviews emphasize macrophage plasticity and context-specific activation states rather than fixed identities (PMID: 25319329; PMID: 26982353). A macrophage in a sterile muscle injury is not the same as a macrophage in a contaminated wound, an inflamed gut barrier, a fibrotic tendon, or an ischaemic tissue. Even within one wound, the macrophage population changes over time as neutrophils arrive, microbes or debris are cleared, apoptotic cells are removed, endothelial cells sprout, fibroblasts deposit matrix, and collagen matures.

That time dimension is central. Early inflammatory macrophage activity can be necessary for clearing damaged tissue. Blocking it too strongly or too early may impair repair. Later, persistent inflammatory signalling can delay healing or contribute to tissue damage. A reparative macrophage shift can support matrix rebuilding, but a persistent pro-fibrotic repair signal can produce excessive scar. Therefore, the best question is rarely “does this peptide make macrophages M2?” The better question is “does this peptide change the right macrophage functions at the right time, and does the tissue outcome improve without hidden trade-offs?”

BPC-157: repair context, vascular signalling, and immune timing#

BPC-157 is often discussed across gastric, tendon, ligament, muscle, vascular, and wound-repair models. In a macrophage-polarization guide, the most useful framing is not that BPC-157 is an “anti-inflammatory peptide.” That is too broad. The useful question is whether BPC-157 changes the timing and coordination of inflammation, vascular repair, fibroblast activity, and tissue organisation in a model where macrophages are measured directly.

A strong BPC-157 macrophage study would not rely on one cytokine. It would include a time course: early inflammatory markers, neutrophil activity, macrophage infiltration, phagocytic or efferocytic function, angiogenesis markers, fibroblast and matrix endpoints, histology, and functional recovery appropriate to the tissue. If the model is tendon, ligament, or muscle, mechanical properties matter. If the model is gut or barrier injury, permeability and epithelial continuity matter. If the model is vascular injury, endothelial repair and perfusion matter.

The macrophage question is especially important because tissue repair can look better for several reasons. A compound may reduce excessive inflammation, improve microvascular flow, alter fibroblast migration, protect endothelial cells, reduce oxidative stress, or change macrophage phenotype. Those mechanisms are not mutually exclusive, but the article or protocol should not pretend they are proven when only one layer was measured.

Canadian RUO evaluation should treat BPC-157 documentation as part of the method. A macrophage assay is sensitive to endotoxin and microbial contamination. A tissue-repair model is sensitive to peptide degradation, fill error, vehicle effects, and storage history. Lot-specific HPLC purity, mass confirmation, batch number, fill amount, storage conditions, and research-use-only labelling should be checked before interpreting subtle immune or repair endpoints.

KPV: inflammatory tone without erasing host defence#

KPV is a tripeptide sequence associated with alpha-MSH-derived anti-inflammatory signalling. It often appears in discussions of NF-kB, cytokines, epithelial inflammation, and barrier models. In macrophage research, KPV is most coherent when the question is inflammatory tone: does a defined macrophage or epithelial-immune model produce less inflammatory signal under controlled conditions?

That does not mean KPV should be described as a universal macrophage polarizer. A reduced TNF-alpha or IL-6 signal can be useful evidence, but it is incomplete. If the model includes microbes, the protocol should also measure microbial burden and phagocytic function. If the model includes sterile injury, it should measure debris clearance and tissue repair. If the model claims resolution, it should measure time course and efferocytosis rather than one cytokine at one time point.

This distinction protects the science and the compliance posture. Lower inflammation is not always better. In early injury or infection models, inflammatory activation may be necessary. In chronic or sterile inflammatory models, persistent activation may be harmful. KPV may be most useful as a research tool for separating inflammatory signalling from tissue damage, but the design must prove the separation.

For sourcing, KPV should still be treated as a contamination-sensitive immune research material. Small peptides can be mischaracterised by sloppy documentation. A macrophage assay with endotoxin contamination can generate a false inflammatory baseline; a vehicle or pH issue can alter cell viability; a fill mismatch can distort a concentration-response curve. The COA is not administrative paperwork. It is part of experimental validity.

TB-500 and thymosin beta-4 context: migration, wound-bed organisation, and immune-cell movement#

TB-500 is commonly described as a synthetic fragment related to thymosin beta-4 research. The thymosin beta-4 literature includes cell migration, actin dynamics, angiogenesis-adjacent effects, wound repair, and inflammatory context. In macrophage-polarization language, TB-500 should be framed cautiously: it may be relevant to how cells move and organise within a repair environment, but that is not the same as proving a clean M1-to-M2 switch.

A well-designed TB-500 macrophage-adjacent study would ask where macrophages are, what they are doing, and how that relates to tissue architecture. Are macrophages recruited earlier or later? Do they clear debris more efficiently? Does the wound bed form better granulation tissue? Are endothelial and fibroblast responses coordinated? Does the tissue show better organisation rather than simply faster closure? Are inflammatory cytokines lower because repair is resolving, or because immune recruitment was impaired?

The answer requires paired endpoints. Immunostaining for macrophage markers can show localization. Flow cytometry can show phenotype distribution. Cytokines can show inflammatory state. Histology and mechanical testing can show repair quality. Angiogenesis markers can show vascular context. Without those layers, a broad “recovery” claim overextends the evidence.

Canadian readers should also distinguish live product references from literature terms. TB-500 is a supplier product name; thymosin beta-4 is a broader biological molecule with its own literature. The exact material, sequence, purity, and documentation matter before drawing comparisons.

LL-37: host defence and macrophage activation are context-dependent#

LL-37 is the active human cathelicidin peptide and a central host-defence molecule. It can be antimicrobial, chemotactic, immunomodulatory, wound-associated, and inflammatory depending on context. That makes it important for macrophage research, but also easy to misuse.

In a microbial challenge, LL-37 may alter macrophage interpretation in several ways. It may affect the microbe directly, change microbial products available to macrophages, influence chemotaxis, form complexes with nucleic acids, alter cytokine signalling, or interact with epithelial and neutrophil responses. If a model measures macrophage cytokines after LL-37 exposure but does not measure microbial burden, cytotoxicity, and peptide stability, the result is hard to interpret.

Reviews of cathelicidin biology describe LL-37 as both antimicrobial and immunomodulatory, with effects shaped by matrix, concentration, proteases, salts, serum proteins, and tissue state (PMC3699762). That context matters for recovery research. In a clean wound model, LL-37 may be discussed around host defence and repair. In an inflammatory skin model, excessive cathelicidin signalling can be part of pathology-like mechanisms. In a biofilm model, it may affect microbes and host cells at the same time.

A strong LL-37 macrophage protocol should include microbial burden when microbes are present, cell viability when host cells are exposed, cytokine panels, phagocytosis or efferocytosis where relevant, and peptide recovery from the matrix. Without those controls, “LL-37 modulates macrophages” is too vague.

Thymosin alpha-1: immune regulation rather than simple repair acceleration#

Thymosin Alpha-1 is studied around immune regulation, antigen presentation, T-cell context, dendritic cells, innate immune signalling, and host-defence models. It can intersect with macrophage biology because macrophages are antigen-presenting and cytokine-producing cells, but it should not be reduced to a generic recovery peptide.

In macrophage research, thymosin alpha-1 is most coherent when the model includes immune competence, pathogen-associated stimulation, antigen-presentation context, TLR signalling, or interaction with adaptive immune cells. Endpoints might include cytokines, phagocytosis, MHC or costimulatory markers, interferon-associated pathways, T-cell activation context, and microbial or viral challenge outcomes. If the model is a sterile tendon injury with no immune-regulatory endpoint, thymosin alpha-1 may be less direct than BPC-157, TB-500, KPV, or GHK-Cu.

The key caution is balance. Immune regulation is not simply suppression. A protocol may show lower damaging inflammation, stronger pathogen clearance, improved antigen presentation, or altered cytokine timing. Those are different outcomes. The article, protocol, and supplier pathway should avoid implying broad immune benefit without specifying the model.

GHK-Cu: matrix remodelling, copper context, and macrophage-fibroblast crosstalk#

GHK-Cu is usually discussed around copper-binding, extracellular matrix, collagen remodelling, wound repair, angiogenesis-adjacent signals, and skin or tissue quality endpoints. Macrophages matter here because they communicate with fibroblasts and endothelial cells during the transition from inflammation to repair. But GHK-Cu should not be described as a macrophage peptide unless the macrophage layer is measured.

A useful GHK-Cu macrophage-adjacent protocol might ask whether macrophage-conditioned media changes fibroblast collagen output after peptide exposure, whether wound macrophage markers align with improved collagen architecture, or whether inflammatory resolution precedes better matrix organisation. It should also watch for fibrosis. A repair-oriented macrophage state may support matrix deposition, but excessive TGF-beta, myofibroblast activation, or collagen accumulation can produce stiff scar.

Copper context deserves special attention. Copper can influence redox chemistry, enzyme function, microbial growth, and cell behaviour. The protocol should separate GHK-Cu effects from vehicle, copper state, pH, and matrix interactions. Supplier documentation should identify the material clearly rather than relying on cosmetic-grade language or generic topical claims.

What endpoints separate real polarization evidence from marker shopping?#

Macrophage polarization evidence is strongest when it combines phenotype, function, timing, and tissue outcome. A single marker is not enough. CD86 without cytokines, CD206 without function, arginase-1 without fibrosis context, or IL-10 without efferocytosis can all mislead.

A practical endpoint panel can include:

1. Phenotype markers: iNOS, CD86, MHC-II, TNF-alpha, IL-1 beta, IL-6, arginase-1, CD206, CD163, IL-10, TGF-beta, and tissue-specific markers where validated.
2. Cell identity and localization: flow cytometry, immunohistochemistry, immunofluorescence, spatial profiling, single-cell RNA sequencing, or lineage-tracing in appropriate models.
3. Function: phagocytosis, efferocytosis, ROS generation, nitric oxide, antigen presentation, chemotaxis, microbial killing, and secretion profile.
4. Time course: early inflammatory phase, transition phase, repair phase, and remodelling phase rather than one convenient endpoint.
5. Tissue outcome: wound closure quality, tensile strength, histology, collagen organisation, angiogenesis, perfusion, oedema, fibrosis, and functional recovery.
6. Material controls: vehicle, peptide stability, lot identity, endotoxin awareness, sterility or microbial context, and blinded analysis where feasible.

Marker shopping happens when a study picks the one marker that supports the desired story and ignores contradictory layers. For example, increased CD206 might sound reparative, but if collagen is disorganised and alpha-SMA is high, the tissue may be shifting toward fibrosis. Lower TNF-alpha might sound anti-inflammatory, but if microbial burden rises, host defence may be impaired. A peptide article should make those trade-offs visible.

Model selection: cell culture, organoids, animal injury, and ex vivo tissue#

Cell culture allows clean stimulation and measurement, but macrophages in a dish do not recreate tissue architecture. Bone-marrow-derived macrophages, THP-1-derived macrophage-like cells, primary human monocyte-derived macrophages, and tissue-resident macrophages can behave differently. LPS, interferon-gamma, IL-4, IL-13, immune complexes, apoptotic cells, and microbial products all create different activation states. A peptide result in one system should not be generalized to all macrophages.

Co-culture models add realism. Macrophages with fibroblasts, endothelial cells, keratinocytes, myoblasts, tenocytes, chondrocytes, epithelial cells, or neurons can reveal crosstalk that single-cell assays miss. They also add complexity: a cytokine change may originate from either cell type, and peptide stability can differ in conditioned media.

Animal injury models add immune recruitment, vasculature, matrix, nerves, and mechanical loading. They are stronger for tissue-repair claims but harder to interpret mechanistically. Wound size, microbial status, strain, age, sex, housing, analgesia, anaesthesia, dressing, loading, and sampling time can all affect macrophage dynamics.

Ex vivo tissue models can preserve architecture while allowing controlled exposure. They may be useful for skin, gut, tendon, or muscle questions, but viability windows and diffusion limits matter. A peptide that looks active at the tissue surface may not reach deeper macrophage populations.

The model should match the claim. A THP-1 cytokine assay can support an inflammatory-signalling hypothesis. It cannot prove tendon recovery. A mouse wound study can support tissue repair in that model. It cannot prove human use. This distinction is essential for Northern Compound’s research-use-only editorial posture.

COA and contamination checklist for Canadian RUO macrophage studies#

Macrophage assays are unusually vulnerable to material artefacts. Endotoxin can activate TLR4 and produce inflammatory cytokines. Microbial contamination can change baseline activation. Peptide degradation can create inactive or differently active fragments. Incorrect fill can distort concentration-response curves. Storage drift can make one lot behave differently from another. Vehicle composition can alter pH, osmolarity, cell viability, or microbial growth.

Before interpreting a macrophage peptide experiment, Canadian readers should look for:

• lot-specific HPLC purity rather than generic purity language;
• mass confirmation or another identity method appropriate to the peptide;
• fill amount, batch number, and vial label matching the COA;
• storage conditions and cold-chain expectations;
• endotoxin or microbial context when immune, cytokine, endothelial, barrier, or host-defence endpoints are central;
• clear research-use-only labelling and no treatment, dosing, or human-use positioning;
• compatibility between the material, vehicle, and the planned cell or tissue model;
• current product destinations that avoid 404s and preserve attribution when reached from Northern Compound.

BPC-157, KPV, TB-500, LL-37, Thymosin Alpha-1, and GHK-Cu should be assessed through that documentation lens. The link is not a recommendation for personal use; it is a way to inspect current supplier information for research-use-only materials.

How macrophage claims go wrong#

Several recurring mistakes show up in macrophage-polarization content.

First, the M1/M2 binary is overused. If an article says “M2 macrophages heal tissue,” ask which M2-like state, at what time, in which tissue, and with what fibrosis endpoint. Reparative does not always mean optimal.

Second, anti-inflammatory language hides host-defence trade-offs. A cytokine reduction may be useful in sterile chronic inflammation. It may be harmful in a microbial challenge if clearance is impaired. LL-37 and thymosin alpha-1 discussions especially need microbial or host-defence endpoints when infection-like models are involved.

Third, macrophage markers are treated as tissue outcomes. A marker shift is not a healed tendon, a stronger wound, a better muscle, or a less fibrotic scar. Tissue structure and function must be measured.

Fourth, supplier documentation is separated from experimental validity. In immune-cell work, COA quality is not just a purchasing issue. It determines whether cytokines, phenotype markers, and repair readouts can be trusted.

Fifth, peptide categories are confused. BPC-157, KPV, TB-500, LL-37, thymosin alpha-1, and GHK-Cu are not interchangeable “recovery peptides.” Each has a different best-fit research question. A good protocol begins with biology, then chooses the material.

Practical review checklist before accepting a macrophage-polarization claim#

Before relying on a macrophage-related peptide claim, ask:

1. What tissue, species, cell source, and injury or stimulation model was used?
2. Was the question early inflammation, resolution, efferocytosis, host defence, angiogenesis, fibrosis, or repair quality?
3. Were macrophages measured directly, or inferred from bulk cytokines?
4. Did the study use multiple markers rather than one M1 or M2 label?
5. Was the time course appropriate for macrophage transition?
6. Were functional endpoints such as phagocytosis, efferocytosis, microbial burden, or tissue strength included?
7. Were fibrosis and matrix quality measured when reparative markers increased?
8. Were vehicle, viability, endotoxin, sterility, and peptide identity controlled?
9. Does the article separate literature context from current supplier claims?
10. Does the language remain research-use-only, without dosing, route, treatment, or personal-use advice?

If the answer to several questions is no, the claim may still be interesting, but it should be treated as preliminary. Macrophage biology is too dynamic for one-marker certainty.

Tissue-specific interpretation: why macrophage endpoints shift by recovery model#

A macrophage marker panel should be adapted to the tissue rather than copied from a generic inflammation paper. The recovery category spans skin, tendon, ligament, muscle, gut barrier, nerve, vascular injury, and scar biology. Each tissue gives macrophages different instructions through extracellular matrix, resident stromal cells, oxygen tension, mechanical load, microbial exposure, and local growth factors.

In skin wounds, macrophage interpretation should include microbial burden, keratinocyte migration, angiogenesis, granulation tissue, collagen deposition, and closure quality. A reduction in inflammatory cytokines may be encouraging if bacterial burden is controlled and re-epithelialisation improves. It is less convincing if the wound closes faster but leaves disorganised collagen, persistent biofilm, or poor barrier quality. This is where wound-healing peptide research, skin microbiome peptides, and LL-37 versus KPV become relevant internal context.

In tendon and ligament models, macrophage timing should be linked to tenocyte behaviour, collagen alignment, crosslinking, mechanical strength, and adhesions. A pro-repair macrophage signal can be useful early if it helps transition from inflammation to matrix organisation. It can be counterproductive if it supports excess scar or disorganised collagen. For BPC-157 or TB-500 discussions, the strongest evidence would pair immune markers with histology and tensile testing rather than relying on cytokines alone.

In muscle injury models, macrophage phenotypes are often discussed as a sequence: inflammatory cells clear necrotic debris, then reparative cells support satellite-cell activity and tissue rebuilding. But the sequence is not automatic. If a peptide appears to speed a reparative marker without adequate clearance of damaged fibres, later regeneration may suffer. If inflammatory activity persists, fibrosis can replace functional muscle. A careful article should connect macrophage data to myofibre cross-sectional area, central nucleation, satellite-cell markers, fibrosis, vascularisation, and force output where available.

In gut and epithelial-barrier models, macrophage claims need epithelial integrity and microbial context. KPV, BPC-157, LL-37, and larazotide-adjacent literature can all touch barrier questions, but macrophage interpretation depends on permeability, tight junctions, microbial products, epithelial viability, and cytokine gradients. Lower macrophage activation may look beneficial in sterile barrier irritation. In a microbial challenge, it must be balanced against pathogen handling and epithelial defence.

In nerve and neuroinflammatory recovery models, macrophage and microglia terminology can blur. Peripheral nerve repair involves infiltrating macrophages, Schwann cells, axon debris clearance, angiogenesis, and remyelination. Central nervous system models involve microglia and border-associated macrophages with different biology. A peptide article should not transfer a peripheral macrophage result directly to brain repair without measuring the relevant cell population and barrier context.

This tissue-specific view prevents a common SEO error: turning “macrophage modulation” into a universal recovery phrase. The more precise the tissue and endpoint, the more useful the peptide discussion becomes.

Product-map summary for macrophage-polarization research#

The live product map is intentionally narrower than the literature map. Some compounds may appear in older studies, foreign clinical contexts, or unavailable store categories. Northern Compound should still discuss literature when useful, but ProductLink references should remain current, attribution-preserving, and clear about research-use-only status.

How to cite macrophage peptide evidence responsibly#

Responsible citation means matching the claim to the evidence level. A review article can define macrophage plasticity, but it cannot prove a specific peptide effect. A cell study can support a mechanism, but it cannot prove tissue recovery. An animal wound model can show tissue-level plausibility, but it cannot become human guidance. A supplier COA can support material identity, but it cannot substitute for biological evidence.

A cautious Northern Compound phrasing pattern is: “In non-clinical models, this peptide is relevant to macrophage-adjacent questions when the protocol measures X, Y, and Z.” A weaker phrasing pattern is: “This peptide promotes healing by turning M1 macrophages into M2 macrophages.” The first sentence leaves room for uncertainty, model specificity, and endpoint quality. The second overstates mechanism and invites personal-use interpretation.

When citing macrophage research, readers should prefer papers that specify cell source, stimulation condition, peptide identity, concentration verification, vehicle, endotoxin context, marker panel, time course, and tissue outcome. If the article is a review, it should be used to frame biology rather than to rank products. If the paper uses disease models, the article should describe them as experimental contexts, not as treatment indications.

Where this guide fits in the Northern Compound recovery library#

This macrophage guide is not a replacement for the existing recovery articles. It is a connective layer. The inflammation-resolution guide explains why ending inflammation is an active process rather than passive suppression. The fibrosis and scar-tissue guide explains why repair can overshoot into stiff matrix. The angiogenesis guide covers vascular repair signals that macrophages can influence. The muscle injury, tendon and ligament, and wound-healing guides provide tissue-specific contexts.

The macrophage lens helps readers compare those topics without collapsing them. If a peptide is being discussed for tendon, ask about macrophage timing and collagen alignment. If it is being discussed for wounds, ask about microbes, keratinocytes, angiogenesis, and closure quality. If it is being discussed for fibrosis, ask whether reparative macrophage signals became excessive. If it is being discussed for inflammation resolution, ask whether efferocytosis and tissue function were measured.

That is the editorial value of the topic gap: it gives Canadian readers a practical immunology filter for recovery-peptide claims while preserving RUO boundaries and supplier-documentation discipline.

FAQ#

Bottom line for Canadian researchers#

Macrophage polarization is one of the most useful lenses for recovery peptide research because it connects inflammation, debris clearance, host defence, angiogenesis, matrix remodelling, and tissue outcome. It is also one of the easiest lenses to misuse. The M1/M2 shorthand can introduce a topic, but it cannot carry a serious claim.

A stronger Canadian RUO review asks whether the peptide changes a defined macrophage function at a defined time in a defined model, and whether that change improves tissue outcome without increasing infection risk, fibrosis, cytotoxicity, or interpretive noise. It checks the material before trusting the biology. It treats product links as documentation checkpoints, not clinical recommendations.

For current Northern Compound coverage, this macrophage-first guide sits between inflammation resolution, wound healing, fibrosis, angiogenesis, muscle injury, tendon repair, and compound-level research profiles. It helps answer a question those guides touch but do not centre: when recovery content says “modulates inflammation,” what exactly should a careful reader demand before believing it?