Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Blends & Stacks/Ipamorelin + CJC-1295 (no DAC)
Growth Hormone Blend
Ipa/CJC · CJC-1295 without DAC · Mod GRF(1-29) + ipamorelin
Two pituitary receptors, one amplified pulse. The most pharmacologically defensible combination in circulation — and the one where the "no DAC" specification does all the work.
This combination has better pharmacological grounding than anything else on this site. GHRH analogues and ghrelin-receptor agonists act on two distinct pituitary receptors, and their combined effect on GH release is synergistic rather than additive — a principle established in endocrine pharmacology, not extrapolated from a forum.[3]
Ipamorelin supplies the GHS-R1a arm: it stimulates GH release and suppresses somatostatin, the brake. CJC-1295 without DAC — more accurately Mod GRF(1-29), a tetrasubstituted GHRH(1-29) fragment — supplies the GHRH arm. One releases the brake, the other presses the accelerator, and the result is a single amplified pulse that decays within an hour or two, leaving the axis to recover as it normally would.
What none of that establishes is a clinical outcome. There is no trial of this combination for body composition, recovery, sleep or anything else. Ipamorelin's clinical development was discontinued; CJC-1295 never had a completed development programme. Everything downstream of "it produces a bigger GH pulse" is inference.
If a vendor sells "CJC-1295" without specifying, assume nothing. The DAC version produces a sustained IGF-1 elevation over days — a completely different exposure profile with a completely different risk calculus. The pulsatile arguments made for this stack apply only to the no-DAC form.
Two receptors, one somatotroph. Pituitary somatotrophs express both the GHRH receptor and GHS-R1a. GHRH signalling drives cAMP-mediated GH synthesis and release; ghrelin-receptor signalling acts through a separate pathway and additionally suppresses hypothalamic somatostatin release. Stimulating both simultaneously produces a GH response greater than the sum of each alone.
Why the short half-life matters. A pulse is not the same exposure as a plateau. GH receptor signalling is pulse-sensitive, and continuous elevation drives receptor desensitisation and sustained IGF-1 elevation. Mod GRF(1-29) has a half-life of roughly half an hour; ipamorelin around two hours. Together they produce a discrete pulse that ends.
Fasted, pre-sleep timing. Insulin and elevated glucose suppress GH release, so a fed state directly antagonises the mechanism. The largest physiological GH pulse occurs in early slow-wave sleep, so dosing before sleep reinforces an existing pulse rather than creating an out-of-phase one.
Ceiling effects. Somatotroph GH stores are finite. Above some dose the pulse cannot get larger and only the side-effect burden grows — the mechanistic argument against escalation, and the reason stacking a third secretagogue on top is not three times the effect.
A blend is not a compound. It is several compounds sharing a vial, and each one carries its own evidence base, dose-response curve and risk profile. Study them individually before studying them together.
| Component | Share of blend | Role in the blend | Monograph link |
|---|---|---|---|
| Ipamorelin Selective GHS-R1a agonist |
~5 mg of 10 (1:1) | Ghrelin receptor agonism plus somatostatin suppression — releases the brake on GH secretion. Selective: no meaningful cortisol or prolactin rise. | Monograph |
| CJC-1295 (no DAC) Mod GRF(1-29), tetrasubstituted GRF(1-29) |
~5 mg of 10 (1:1) | GHRH receptor agonism — presses the accelerator. Four amino acid substitutions confer DPP-IV resistance while keeping the half-life short enough to produce a pulse rather than a plateau. | Monograph |
The "no DAC" specification is not a detail — it is the entire design. CJC-1295 with DAC (drug affinity complex) binds albumin and persists for six to eight days, producing a sustained elevation of GH and IGF-1 rather than a pulse. That flattens the physiological pulse architecture that GHRH-analogue dosing is supposed to preserve, and it is why the pulsatile-preservation argument does not apply to the DAC version.
Because the two components have similar half-lives in the no-DAC form, they are conventionally dosed 1:1 and co-administered in a single injection. Pre-blended vials fix that ratio; separate vials do not.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Established endocrine pharmacology: combined stimulation of the GHRH receptor and GHS-R1a produces greater GH release than either alone. Among the blends here that have never been trialled as a combination, this is the strongest study-tier claim — though note that CagriSema outranks it outright, having been tested as a combination in humans through phase 3.
Characterised as the first selective GH secretagogue — high GH-releasing potency without meaningful ACTH, cortisol or prolactin elevation.
Clinical pharmacology work on CJC-1295 demonstrated dose-dependent increases in GH and IGF-1. Most of this data concerns the DAC version, where sustained elevation is the point.
No study has assessed body composition, recovery, sleep or any clinical endpoint for ipamorelin + CJC-1295 in humans.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The dominant use case. A larger GH pulse is documented; whether that translates into measurable body-composition change in a non-GH-deficient adult has never been tested for this combination.
GH secretion and slow-wave sleep are bidirectionally coupled. The most consistently reported subjective effect and the least studied.
From GH-driven collagen synthesis. Inferred.
The rationale for including the stack alongside aggressive fat loss.
Proposed to support basal metabolic rate, lean mass and recovery by a route independent of thyroid hormone. It is not fully independent — thyroid hormone is permissive for GH secretion and action, so an under-replaced patient is stimulating a blunted axis.
Preserved pulsatility and intact feedback should in principle protect against the receptor downregulation seen with continuous GH. Not characterised over long horizons.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most consistent report for this stack by a wide margin.
Widely reported and inseparable from the sleep improvement reported alongside it.
Reported over months. Consistent with GH-driven collagen effects; unmeasured.
Near-universal and transient.
Dose-related, usually settling within weeks. The most common complaint.
Frequently reported with pre-sleep dosing.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No meaningful cortisol or prolactin elevation, unlike GHRP-6 and hexarelin.
Sustained GH and IGF-1 elevation produces insulin resistance, fluid retention, arthralgia and carpal tunnel symptoms regardless of the upstream stimulus. These are documented for the axis, not novel to this stack.
Ipamorelin development was discontinued; CJC-1295 never completed a development programme. There is no chronic-use safety dataset for either, alone or combined.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The standard concern with sustained GH-axis stimulation, and the reason approved GH-axis drugs contraindicate active malignancy. IGF-1 is measurable; almost nobody using this stack measures it.
Directly relevant when the stack sits alongside a glucagon-receptor agonist that pushes hepatic glucose output in the same direction.
If a vendor supplies the DAC form under an ambiguous label, the exposure profile changes from a nightly pulse to continuous multi-day elevation without the user knowing.
GH and IGF-1 raise peripheral T4 → T3 conversion and lower circulating T4. In GH therapy this is documented well enough that it unmasks central hypothyroidism and commonly requires a levothyroxine dose increase. A replaced patient may drift under-replaced and blame the peptide rather than the thyroid dose.
Finite somatotroph capacity means dose increases beyond saturation add adverse effects without adding pulse amplitude.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most common complaint, dose-related.
The recognisable GH-excess signal, reported at higher doses.
Transient, benign, near-universal.
Reported inconsistently; usually attributed to too high a dose.
A counter-report to the ipamorelin selectivity claim, suggesting selectivity may be dose-dependent.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Insulin suppresses GH release; the largest physiological pulse is early in slow-wave sleep. Reinforcing that pulse fasted is the coherent design and is what almost every protocol converges on.
Convention rather than a finding, based on the similar half-lives of the two components in the no-DAC form.
The meaningful exposure variable is downstream IGF-1 within the age-adjusted reference range. This is what the approved GH-axis drugs are monitored on.
Multi-daily dosing increases total exposure and IGF-1 without increasing the amplitude of the pulse that matters.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most widely circulated dose — the "100/100" convention. Single subcutaneous injection two hours after the last meal, immediately before sleep.
Higher-dose community range. Ceiling effects make the additional pulse gain questionable.
The pulse-mimicking approach. Higher total exposure and correspondingly higher IGF-1.
The common cycling pattern, not derived from any pharmacological finding.
| Approach | Ipamorelin | CJC-1295 no DAC | Frequency |
|---|---|---|---|
| Standard "100/100" | 100 mcg | 100 mcg | Nightly, fasted |
| Higher-end | 200 – 300 mcg | 200 – 300 mcg | Nightly, fasted |
| Multi-pulse | 100 mcg | 100 mcg | 2–3× daily, fasted |
| With tesamorelin instead of CJC | 250 mcg | 1–2 mg tesamorelin | Nightly, fasted |
Pre-blended vials state a combined milligram figure. A 10 mg blend vial at a 1:1 ratio delivers 5 mg of each component, so a "200 mcg total" dose is 100 mcg of each — which is what the "100/100" convention actually means. The blend calculator handles the split.
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Acromegaly — chronic growth hormone excess from a pituitary adenoma — is treated with octreotide, a somatostatin analogue that suppresses GH and normalises IGF-1. Nobody using a secretagogue stack is producing acromegaly; the doses and duration are not comparable. But the direction of travel is the same one, and acromegaly is what the far end of it looks like: cardiomyopathy, hypertension, sleep apnoea, insulin resistance, arthropathy and shortened life. Worth reading before assuming more GH is straightforwardly better.
Tesamorelin is an approved GHRH analogue with a real label and a real safety dataset. Swapping it in gives the same two-receptor logic with a far better-characterised GHRH arm — at the cost of daily rather than pulse-matched kinetics.
Lean-mass preservation rationale. The unspoken counterpart is that GH and glucagon agonism both worsen glucose handling.
GH-driven collagen synthesis alongside BPC-157/TB-500. The BPC-157 GH-receptor upregulation finding is the specific hook.
The most consequential and most easily avoided antagonism in this stack.
Finite somatotroph capacity. More compounds do not mean more GH; they mean more IGF-1 exposure risk.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most common growth-hormone combination in circulation, often supplied pre-blended.
The version used in the Gold Standard protocol, which uses tesamorelin rather than CJC-1295.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Neither component reached a completed development programme for GH indications.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Measure baseline IGF-1, dose to keep it within the age-adjusted reference range, administer once nightly fasted, and cycle rather than run indefinitely. This is what the approved GH-axis drugs are monitored on and is directly transferable.
Given the documented insulin-resistance effect of GH elevation, HbA1c and fasting glucose before and during use is the minimum defensible monitoring — particularly in any stack containing a glucagon agonist.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The standard circulating pattern.
Grouped in the neuro-cognitive and endocrine axis pillar and introduced after the metabolic and mitochondrial foundations.
One result organises this entire section. In cancer cachexia, the ghrelin agonist anamorelin was tested in two phase 3 trials against co-primary endpoints of lean body mass and handgrip strength. Lean mass rose significantly. Handgrip strength did not move. That is the yardstick for every claim below: growth hormone reliably changes what a scale and a DEXA report, and much less reliably changes what a person can do.
Neither component is approved, and the combination has never been studied as a combination. Adult growth hormone deficiency is a specific endocrine diagnosis made on a provocative test and treated with recombinant human GH under endocrinology supervision. Almost nobody using this stack has that diagnosis, and the vocabulary of the diagnosis is routinely borrowed to describe ordinary age-related decline.
Pathophysiology
True adult GH deficiency follows pituitary disease, surgery, radiotherapy or trauma. It produces reduced lean mass, increased visceral fat, reduced bone density, impaired quality of life and an adverse lipid profile, and it is diagnosed on a provocative stimulation test — not on a symptom list and not on a single IGF-1 level.
Mechanistic rationale
A secretagogue works by stimulating a pituitary that still functions. In genuine GH deficiency the pituitary is the problem, so the compound is acting on the broken part. Recombinant GH replaces the hormone directly, which is why it is the treatment. This distinction is the single most useful thing on this page: the population with the real diagnosis is the population a secretagogue helps least.
Community reports
Community discussion frequently describes symptoms of "low GH" and treats them as equivalent to the diagnosis. Fatigue, poor sleep, central weight gain and low mood are common to a great many conditions, most of which are more common than pituitary disease and several of which are treatable.
Components carrying the argument: Neither — this is the case against the stack
Pathophysiology
Age-related muscle loss involves reduced fibre number and size, motor unit remodelling, and anabolic resistance to protein and loading. Function — strength, gait speed, ability to rise from a chair — is what predicts falls, independence and mortality. Mass alone predicts them far less well.
Mechanistic rationale
GH increases lean body mass in trials, reliably and measurably. It increases strength much less convincingly, and part of the mass gain is fluid rather than contractile tissue. The ROMANA trials of a ghrelin agonist in cancer cachexia are the cleanest illustration: lean body mass rose significantly against placebo across two phase 3 trials, and handgrip strength did not differ in either. That is the same receptor family, tested properly, with the endpoints separated.
Community reports
Users report weight on the scale, fuller-looking muscle and better pumps. Those are the effects most consistent with increased water and glycogen, which is also what a GH-driven mass gain looks like early. Strength reports are notably less consistent.
Components carrying the argument: Ipamorelin (ghrelin) + CJC-1295 (GHRH) → IGF-1
Pathophysiology
The largest natural GH pulses occur during slow-wave sleep. That association is well established and is the basis of the sleep claim.
Mechanistic rationale
Deep sleep drives GH, not the reverse. A secretagogue given at night is attempting to amplify a pulse that depends on sleep architecture the compound does not create. If sleep is fragmented — by apnoea, alcohol, shift work or a phone — the upstream problem is the sleep. Ghrelin signalling does have some independent effects on sleep in animal work, so the claim is not empty; it is just far weaker than the direction people assume.
Community reports
Deeper sleep is the single most consistently reported subjective effect of GH secretagogues. It is also among the most placebo-susceptible endpoints in this library, and untreated obstructive sleep apnoea is common and routinely missed in exactly this demographic.
Components carrying the argument: Ipamorelin — ghrelin receptor
Pathophysiology
Osteoporosis is reduced bone mass with microarchitectural deterioration, and the endpoint that matters is fracture, not density.
Mechanistic rationale
GH raises IGF-1, and IGF-1 is genuinely involved in bone formation, so turnover markers move. Turnover markers are not fracture reduction, and no secretagogue has ever demonstrated the latter. Teriparatide — a 34-residue parathyroid hormone fragment — has randomised fracture data and has been approved since 2002. If bone is the goal, the peptide that treats it already exists.
Community reports
Bone is rarely the stated reason for use and appears mostly as a supporting argument for longevity framing.
Components carrying the argument: IGF-1 mediated; effect size unproven
Pathophysiology
Visceral adipose tissue is metabolically active and independently associated with insulin resistance, dyslipidaemia and cardiovascular risk in a way subcutaneous fat is not.
Mechanistic rationale
GH is lipolytic and preferentially mobilises visceral fat, which is a real effect. Note where it has been demonstrated properly: tesamorelin, a stabilised GHRH analogue, is approved for reducing visceral adipose tissue in HIV-associated lipodystrophy on randomised trial data. Same axis, same mechanism, one indication where it was actually tested.
Community reports
Reduced waist measurement is commonly reported and is plausible. It is also what a modest calorie deficit produces, and people who start a peptide protocol rarely change nothing else.
Components carrying the argument: GH-driven lipolysis
Pathophysiology
Growth hormone is a counter-regulatory hormone. It antagonises insulin action in muscle and liver, raises hepatic glucose output, and increases free fatty acid flux.
Mechanistic rationale
GH is diabetogenic. This is not a rare adverse effect; it is a core property of the hormone, and it is why impaired glucose tolerance and frank diabetes are features of acromegaly. Sustained secretagogue use raises fasting glucose and HbA1c in some people, in a population frequently pursuing metabolic improvement. Fasting glucose and HbA1c are inexpensive tests and are almost never checked by people using these compounds.
Community reports
Rising fasting glucose is reported occasionally and usually attributed to diet. Carpal tunnel symptoms, joint aching and fluid retention are also commonly described — all classic GH effects, all dose-related.
Components carrying the argument: GH itself — unavoidable if the stack works
Pathophysiology
Acromegaly is chronic GH excess from a pituitary adenoma. It causes cardiomyopathy, hypertension, sleep apnoea, insulin resistance, arthropathy, increased colorectal neoplasia, and it shortens life.
Mechanistic rationale
Nobody using a secretagogue stack is producing acromegaly — the doses and duration are not comparable, and that should be said plainly. But the direction of travel is the same one, and it is worth knowing that an entire drug class exists to reverse it. Octreotide is a somatostatin analogue prescribed to suppress the hormone this stack is designed to raise.
Community reports
Rarely raised. The features people do report at higher doses — fluid retention, carpal tunnel, joint aching, coarsening — are the mild end of the same spectrum.
Components carrying the argument: The axis itself
Pathophysiology
Growth hormone alters deiodinase activity and peripheral conversion of T4 to T3, and can reduce thyroxine-binding globulin. In someone with limited thyroid reserve, GH can unmask hypothyroidism that was previously compensated.
Mechanistic rationale
Thyroid function tests can move on a GH secretagogue without any change in thyroid function, and a person on levothyroxine may need their dose reviewed. Both effects are well described in GH replacement literature and neither is widely known in the community using these compounds.
Community reports
Fatigue or cold intolerance appearing after starting a GH protocol is usually blamed on the protocol or on a "detox". In someone with marginal thyroid reserve it can be unmasked hypothyroidism, and the two are indistinguishable without a blood test.
Components carrying the argument: GH effect on deiodinases and binding proteins
Pathophysiology
IGF-1 signalling promotes cell proliferation and inhibits apoptosis. Epidemiological work associates higher circulating IGF-1 with incidence of several common cancers, though association is not causation and the effect sizes are modest.
Mechanistic rationale
The entire purpose of this stack is to raise IGF-1 systemically and keep it raised. No human study has shown that a secretagogue causes cancer, because none has looked. Anyone with a current or past malignancy should be discussing this with an oncologist rather than reading a website.
Community reports
Rarely raised before use. IGF-1 is a cheap blood test and is the one measurement that would tell a user whether the compound is doing anything at all — and it is seldom taken.
Components carrying the argument: IGF-1, systemically and continuously
| Claim | Does GH do it? | Evidence | The thing to know |
|---|---|---|---|
| Increase lean mass | Yes | Human (GH) | Part of it is fluid |
| Increase strength / function | Weakly at best | Human | ROMANA: mass rose, handgrip did not |
| Improve deep sleep | Unclear | Association only | Sleep drives GH, not the reverse |
| Reduce visceral fat | Yes | Human (tesamorelin) | Proven in one indication, where it was tested |
| Improve bone | Markers only | None for fracture | Teriparatide has the fracture data |
| Raise blood glucose | Yes | Established | GH is diabetogenic — check HbA1c |
| Move thyroid labs | Yes | Established | Without changing thyroid function |
| Raise IGF-1 | Yes — that is the point | Established | Cheap test, seldom taken |
For diagnosed adult GH deficiency: recombinant human GH under endocrinology supervision, after a provocative test. Not on symptoms, and not on an IGF-1 level alone.
For age-related decline, which is what almost everyone here is actually treating: progressive resistance training and 1.2–1.6 g/kg/day of protein distributed across meals have the strongest evidence for preserving and rebuilding muscle in older adults, and they improve function rather than only mass. Nothing on this page substitutes for them.
For sleep: cognitive behavioural therapy for insomnia is first-line and outperforms hypnotics at follow-up. Screening for obstructive sleep apnoea matters more than any compound here — it is common, routinely missed, treatable, and it independently wrecks both GH secretion and daytime function.
For bone: teriparatide or abaloparatide for anabolic effect, bisphosphonates or denosumab for antiresorptive, adequate vitamin D and calcium, and progressive loading.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Available pre-blended (commonly 10 mg total, 5 mg of each) or as separate vials. Separate vials allow the ratio to be adjusted; blends do not. Reconstituted with bacteriostatic water; because doses are in the low hundreds of micrograms, dilution should be chosen so the dose lands on a readable syringe mark.
Lyophilised: −20 °C long-term. Reconstituted: 2–8 °C, protected from light.
Blend: commonly 10 mg total. Separate: ipamorelin 5–10 mg, CJC-1295 no DAC 2–5 mg.
Confirm the product is the no-DAC form. The distinction is not visible in the vial and is the single most important product characteristic for this stack.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Not approved for human use. Neither ipamorelin nor CJC-1295 has marketing approval in any jurisdiction. Both are supplied as research chemicals.
Several peptide GH secretagogues were affected by the FDA's April 2026 restructuring of the Section 503A compounding categories. None was among the seven substances reviewed at the July 2026 advisory committee meeting, and no listing decision has been made for them.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: component status: both ipamorelin and CJC-1295 rejected by PCAC in 2024. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
GHRH analogues, GHRPs and ghrelin-receptor agonists are all explicitly named on the WADA Prohibited List under S2. This stack is prohibited at all times, in and out of competition.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
