The Framework

01 — Scope

What this site is

Mechanica Natura is an educational reference. It organises and presents published scientific research on nutraceuticals in oncology-adjacent contexts. It does not conduct original research, does not issue clinical recommendations, and does not replace the judgment of a qualified healthcare professional.

The site was built from direct, personal experience navigating cancer — the frustration of finding information that was either superficial, commercially motivated, or technically inaccessible to people without a research background. What was missing was structure: a way to move from a compound name to its biological rationale, from a research finding to the evidence tier it actually belongs to, and from a pathway to the compounds studied in relation to it. That structure is what this site provides.

Whether you are navigating an active diagnosis, supporting someone who is, or simply looking for well-structured information on compounds you have encountered in an oncology context — this site is built for you. No prior scientific background is required. Where technical terms appear, they are explained.

Every compound profile can be read at two depths. The Summary view — the default — presents the same findings in plain language, calibrated for readers without a scientific background. The Research view exposes the same underlying evidence in fuller technical detail, including mechanistic language and pathway-level specificity, for readers who want it. A toggle at the top of every profile switches between them. Switching depth does not change the underlying cited evidence or its assigned tier; it changes the level of explanation shown.

02 — Classification

The Functional Framework

Every compound profiled on this site is classified using the Functional Framework — a two-level classification system that organises nutraceuticals by the type of biological mechanism they have been studied in relation to in peer-reviewed research.

The framework has two levels. The five Level 1 (L1) roles — Contain, Starve, Weaken, Attack, and Protect — are the top-level categories, each representing a broad strategic orientation drawn from cancer biology. Each L1 role is subdivided into Level 2 (L2) roles that describe more precisely how a compound contributes to that objective. On individual compound profiles, pathways are grouped by their L2 role, with the parent L1 shown alongside as a contextual label.

A compound may carry one role, several, or all five, depending on what the evidence supports. Roles are assigned only when backed by pathway-level evidence. Where a role is absent, that absence is itself informative — within the literature reviewed and the site’s stated inclusion criteria, the available evidence does not support that classification for this compound.

Level 1 (L1) roles and their Level 2 (L2) subdivisions

03 — Evidence

Evidence hierarchy

All evidence on this site is classified into one of three tiers, presented on each compound profile in fixed order from highest to lowest clinical relevance. This order is never reversed and the tier is never omitted. Understanding what each tier can and cannot tell you is essential to reading this site correctly.

The translation problem

Moving from in vitro signal to animal model to human outcome is not a straight line — it is a series of increasingly difficult translations, each of which can fail. A compound that affects cancer cells in a laboratory setting does not necessarily do so in a living organism. A compound that reduces tumour growth in animal models does not necessarily do so in humans. A compound that produces a measurable biomarker change in humans does not necessarily change clinical outcomes.

Each tier of evidence is presented on its own terms, without implying translation between them. When a compound is described in the in vitro context, the language reflects that context. The distinction is maintained throughout — not because it is a legal formality, but because it is scientifically accurate and practically important.

04 — Pathways

The Pathway lens

A biological pathway is a defined sequence of molecular events within or between cells — a signalling cascade, metabolic process, or regulatory circuit that produces a measurable biological outcome. Cancer cells depend on, alter, or hijack many of these pathways to survive, proliferate, and evade treatment. Understanding which pathways are involved is a prerequisite for understanding why a compound is discussed in an oncology context at all.

We currently reference 70+ cancer-related pathways — a fraction of known biological pathways in the human body and certainly not all known cancer-related pathways. These pathways represent some of the more frequently referenced pathways spanning core metabolism, lipid biology, amino acid systems, cell death programmes, immune modulation, and signalling cascades. We will continue to add more pathways as new research brings greater understanding of them and identifies additional nutraceutical–pathway relationships for evaluation.

Every pathway has a canonical identifier used internally to maintain consistency across all compound profiles.

Key pathways vs expanded pathways

On each compound profile, pathways are divided into two groups. Key Pathways are those supported by more than one relevant cited source, or by a direct mechanistic link to the compound's assigned Level 1 (L1) roles — either is sufficient on its own. These are the load-bearing pathways for that compound's classification. Each Key Pathway entry is grouped under its Level 2 (L2) role, with the parent L1 shown as a label alongside, and includes a one-sentence summary of the specific evidence context.

Expanded Pathways are secondary or context-dependent interactions supported by cited literature but not central to the compound's primary profile. These appear as a flat alphabetical list without narrative, and link to the pathway's own page in the Atlas.

Pathway integrity

A pathway may only appear on a compound profile if the compound-pathway relationship is supported by cited peer-reviewed literature. No pathway claim appears without a citation anchor. If a pathway interaction is plausible but not yet citation-supported, it is not listed.

Navigating via pathways

Each pathway in the Atlas links back to all compounds mapped to it. For readers who already know they are interested in specific mechanisms — NF-κB, PI3K–AKT–mTOR, AMPK signalling — the Pathway Atlas provides a direct route to all compounds studied in that context.

05 — Pharmacokinetics

Pharmacokinetics and administration

Biological evidence establishes that a compound interacts with a pathway relevant to cancer biology. It does not, on its own, establish how much of that compound reaches circulation, how long it stays active, what it competes with for clearance, or what dose the underlying research actually used. That is a separate, practical layer, and every compound profile addresses it directly in its Pharmacokinetics and Administration section.

This section exists because the gap between what a compound does in a laboratory setting and what a standard oral dose delivers in a person is often the single most important piece of context for interpreting the evidence above it. It is presented in six fixed subsections, in this order.

Absorption

How the compound is taken up into circulation, and what measurably changes that — co-administration with dietary fat, first-pass hepatic metabolism, particle size, or formulation type. Where a factor is documented to meaningfully shift plasma exposure, it is stated explicitly.

The Concentration Gap

How the concentrations required to produce an effect in cell studies compare with what a standard oral dose actually achieves in human plasma. Where this gap is large, it is stated as a specific figure, not a vague caveat — this is the section that gives the In Vitro evidence above its necessary context.

Clinical Dose Context

The dose range evaluated in the cited research, stated as a collapsed range only — not a mini summary of individual studies, and never tied to an outcome claim. This is the one place on a compound profile where a dose figure appears. The Evidence Summary above it is deliberately free of dose numbers; this section is where that information lives instead.

Formulation Effects

Where more than one formulation of a compound exists with meaningfully different human pharmacokinetic data, this subsection compares them directly — by mechanism, relative bioavailability, and, where relevant, which body compartment each is better suited to reach. Not every compound has multiple formulations with distinct clinical data; where that's the case, this subsection is brief.

Metabolism

The primary enzymes or clearance pathways responsible for processing the compound, and — where relevant — any documented effect the compound itself has on those same pathways, such as enzyme inhibition or induction. This is what determines interaction risk with other substances sharing the same clearance route.

Co-Dosing Considerations

Metabolism data is summarised as one of three flags — Avoid, Caution, or Monitor — applied to specific interacting medications or other nutraceuticals rather than left as general caution language. Each flag is set to the most cautious guidance the cited evidence supports: Avoid where a source documents a clinically significant interaction or recommends against combining (and, for anticoagulant or chemotherapy interactions, where the potential harm is severe); Caution where the evidence supports clinician review; and Monitor where a specific parameter, such as liver enzymes, warrants watching. These flags describe the level of caution the research raises — they are not instructions. Whether to combine, separate, or avoid a supplement and a medication is a decision for the treating physician or oncology team, who has the full treatment picture.

06 — Timing

Reported onset and persistence

Compound profiles that include relevant pharmacokinetic and time-course data (see 05 — Pharmacokinetics, above) address two different timelines, and they answer two different questions. Confusing them is one of the easiest ways to misread how a compound behaves, so this is treated as its own concept rather than folded into pharmacokinetics.

Two different clocks

The first clock is pharmacological: how quickly a compound's direct, measurable effects begin after dosing, and how long they last before fading. In the studies reviewed this clock is usually fast — reported effects often begin within hours — and usually short, fading within about a day without repeated dosing. These timings vary by compound, formulation, dose and measured endpoint.

The second clock is biological: how long sustained exposure takes to produce a downstream change in tissue behaviour, and how long that change persists once dosing stops. This clock is slower to start, typically building over one to two weeks of consistent use, and slower to fade — sometimes persisting for a period after the compound itself has left the body.

These two clocks are frequently misread as contradictory, because a compound can clear the bloodstream within days while the biological changes it triggered are still resolving. They are not contradictory — they are different questions, tracked on their own timelines.

What this means for how a compound is used

Where a compound's studied effects depended on the second, slower clock, the studies reporting them generally used repeated, sustained dosing rather than occasional use. Where this is the case, the compound's profile states it — describing how the compound was administered in the research, not recommending a dosing pattern. Any washout before an interacting medication, a procedure, or a change in treatment is a matter for the treating clinician.

07 — Citations

Citation standards

Every factual claim about a compound's biological activity on this site has citation support in the underlying data. Citations are formatted in Vancouver style and each must include a publicly accessible URL — typically a DOI link, PubMed record, or publisher page. References are not decorative; they are the mechanism by which any claim on this site can be independently verified.

A citation indicates that this is what the referenced researchers reported, in the study or review cited. It does not indicate that the finding is definitive, that it has been replicated, or that it translates to human clinical outcomes. The citation is a pointer to the source, not an endorsement of certainty.

What "citation-backed" means on this site

• The referenced study or review exists and is publicly accessible via the linked URL.
• The claim made reflects what that source actually reports — not a paraphrase that overstates the finding.
• The evidence tier assigned to the claim matches the study type: human trials are labelled as human evidence; cell-line studies are labelled as in vitro.
• Where a claim is supported by a review article rather than a primary study, the citation points to the review.

What it does not mean

• That the cited study is free of limitations — no study is, and limitations in the underlying research are limitations in what this site can claim.
• That the finding has been replicated or constitutes scientific consensus.
• That independent quality assessment of each cited paper has been conducted beyond confirming its relevance and tier classification.

References on each compound profile are collected from the citation links attached to that compound's pathway mappings, deduplicated, and sorted alphabetically. The reference list is expandable and links directly to each source.

08 — Formulation

Formulation and sourcing

For many nutraceuticals, the gap between what a compound can do in research and what a standard retail product delivers is not a minor detail — it is the central practical question. Oral bioavailability, first-pass metabolism, lipophilicity, particle size, delivery matrix, and co-formulation all affect how much of an active compound reaches systemic circulation, and at what concentration.

Standard curcumin and Theracurmin are not interchangeable. Berberine hydrochloride and dihydroberberine differ materially in absorption efficiency. Quercetin and enzymatically modified isoquercitrin (EMIQ) produce substantially different plasma profiles. These differences are documented in human pharmacokinetic studies, and they affect whether the doses evaluated in research are achievable with the oral products available in the retail market.

Formulation information on compound profiles

The Formulation Effects subsection of Pharmacokinetics and Administration (see 05, above) addresses this directly — comparing formulations by mechanism, relative bioavailability, and the impact of enhanced-bioavailability formulations where human data exist, alongside the practical gap between research dosing and standard retail dosing covered under Absorption and Clinical Dose Context. Where a specific formulation type has meaningfully different clinical data, this is noted explicitly.

The Sourcing Guide

Each compound profile links to a dedicated Sourcing page where specific products and formulations are reviewed in greater detail — including, if known, the product's third-party testing, standardisation, manufacturing quality, and formulation type. We list a handful of products per nutraceutical with links to identified online retailers. The highlighted Featured Product is, in our opinion, the retail option that most closely met our selection criteria among the products reviewed.

Where affiliate relationships exist, they are disclosed in full in the Affiliate Disclosure.