Peptides & growth hormone

Insulin

Insulin is the peptide hormone the pancreas releases to move glucose out of the blood and into muscle, fat and liver. As a drug, it is made by recombinant DNA technology and injected to treat diabetes. Products range from rapid-acting analogs taken with meals to long-acting analogs that cover a full day or more.

Outside medicine, some bodybuilders inject insulin because it suppresses muscle protein breakdown and drives glucose and nutrients into muscle. The single most important fact about it is that hypoglycemia (low blood sugar) is its most common adverse reaction, and severe hypoglycemia can cause seizures, unconsciousness and death. Every insulin label carries this warning, and the physiology is the same whether or not the user has diabetes.

This page summarizes what the FDA labels, clinical trials, poison-center data and published case reports show. It is for education only and is not medical advice.

Property Detail
Drug class Peptide hormone; human insulin and insulin analogs
Example products Humalog (lispro), NovoLog (aspart), Humulin R (regular), Humulin N (NPH), Lantus (glargine), Tresiba (degludec)
Route Subcutaneous injection; regular insulin and some rapid-acting analogs also IV under medical supervision
Strength Most products 100 units/mL (U-100); some also come in concentrated forms
Approved use To improve glycemic control in adults and children with diabetes mellitus
Half-life (labels) Short and type-dependent: about 1–1.5 h after subcutaneous lispro or regular insulin; about 25 h for degludec at steady state
Most common adverse reaction Hypoglycemia, which can be life-threatening
US status Analogs are prescription-only; Humulin R U-100 and Humulin N carry over-the-counter labels; not listed in Schedule III
WADA status Prohibited at all times (S4.4.2, insulins and insulin-mimetics)

What it is

Human insulin is a two-chain peptide of about 5.8 kDa. The Humulin R label lists its formula as C₂₅₇H₃₈₃N₆₅O₇₇S₆ with a molecular weight of 5.808 kDa, produced in a non-pathogenic laboratory strain of E. coli (Humulin R label).

Insulin analogs are modified versions of the human molecule. The changes do not alter how insulin acts once in the blood; they change how fast it leaves the injection site. Each label describes the modification:

Insulin Change vs human insulin (label) Effect on absorption
Regular (Humulin R) None; identical to human insulin Reference
NPH (Humulin N) Same molecule, crystallized with protamine and zinc into a cloudy suspension Crystals dissolve slowly, giving an intermediate profile
Lispro (Humalog) The two amino acids at B28 and B29 are swapped Absorbed faster than regular insulin
Aspart (NovoLog) One amino acid at B28 replaced by aspartic acid Absorbed faster than regular insulin
Glargine (Lantus) One amino acid changed at A21 and two arginines added to the end of the B chain; formulated at pH ≈4 Slow, prolonged absorption with no pronounced peak
Degludec (Tresiba) B30 removed; a glutamic acid plus C16 fatty acid side chain attached at B29 Forms multi-hexamers that make a slow-release depot; also binds albumin

Sources: Humalog, NovoLog, Humulin N, Lantus and Tresiba labels.

Mechanism

Every label describes the same core action. Insulin lowers blood glucose by:

  • increasing glucose uptake into skeletal muscle and fat;
  • suppressing glucose production by the liver;
  • inhibiting the breakdown of fat (lipolysis) and of protein (proteolysis), and enhancing protein synthesis.

Insulin also shifts potassium from the blood into cells, which is why the labels warn about hypokalemia (low blood potassium).

Insulin is related to, but different from, insulin-like growth factor 1. See IGF-1, IGF-1 LR3 and growth hormone for those pages.

Insulin types compared

Insulins are grouped by how quickly they start working and how long they last after a subcutaneous injection. The labels stress that these timings are only general guidelines. They vary considerably between people and in the same person, with injection site, blood flow, temperature, exercise and dose.

Type Example (FDA label) Onset Peak effect Duration of effect Labeled meal timing
Rapid-acting NovoLog (aspart) Not given as a number 1–3 h 3–5 h 5–10 minutes before a meal
Rapid-acting Humalog (lispro) Faster than regular insulin Serum peak 30–90 min Shorter than regular insulin Within 15 minutes before or right after a meal
Short-acting Humulin R (regular) ≈30 min (range 10–75 min) ≈3 h (range 20 min–7 h) ≈8 h (range 3–14 h); ≈18 h with large doses in obese subjects About 30 minutes before a meal
Intermediate-acting Humulin N (NPH) Slower than regular insulin Median 6.5 h (range 2.8–13 h) Median 14.5 h (range 9.5–19.3 h) in a Lantus label comparison Not tied to meals
Long-acting Lantus (glargine) Slow, prolonged absorption No pronounced peak Median 24 h (range 10.8 to over 24 h) Once daily
Long-acting Tresiba (degludec) Appears in blood ≈1 h after first dose Median 12 h at steady state At least 42 h after the last of 8 daily doses Once daily

Two details from the Humulin R label matter for safety. First, in obese subjects given larger doses, the effect lasted about 18 hours instead of about 8. Second, intravenous regular insulin starts working in about 10–15 minutes (Humulin R label). A “short-acting” insulin can therefore keep lowering glucose well into the night or the next day.

Pharmacokinetics

Insulin is absorbed from the injection site, then cleared mainly by the liver, with uptake and breakdown also in the kidney, muscle and fat. Its half-life after subcutaneous injection mostly reflects how fast it leaves the depot, not how fast the body clears it.

Product Time to peak concentration Apparent half-life Other label data
Humalog (lispro) 30–90 min (healthy volunteers) ≈1 h Absolute bioavailability 55–77%
NovoLog (aspart) Median 40–50 min 81 min Mean peak 82 mU/L vs 36 mU/L for regular insulin at the same dose
Humulin R (regular) 36–150 min; ≈3 h with 50–100 unit doses in obese subjects ≈1.5 h (range 40 min–7 h); ≈20 min to 1 h when given IV Bioavailability 48–89%
Humulin N (NPH) Median ≈4 h (range 1–12 h) ≈4.4 h (range 1–84 h) Label notes a true half-life cannot be estimated accurately
Tresiba (degludec) Median 9 h at steady state ≈25 h Over 99% bound to albumin; steady state after 3–4 days

Sources: the Humalog, NovoLog, Humulin R, Humulin N and Tresiba labels.

Approved medical use

Every insulin label reviewed here has essentially the same indication: to improve glycemic control in adults and children with diabetes mellitus. Tresiba is approved from 1 year of age. Doses are individualized from blood glucose monitoring, metabolic needs and the treatment goal, and labels call for any change in insulin regimen to be made under close medical supervision.

The benefit of insulin-based intensive therapy is well established in type 1 diabetes. In the Diabetes Control and Complications Trial (DCCT), 1,441 patients were randomized to intensive or conventional insulin therapy and followed for a mean of 6.5 years (DCCT, NEJM 1993):

Outcome Effect of intensive therapy
New retinopathy (primary-prevention cohort) −76% (95% CI 62–85%)
Retinopathy progression (secondary-intervention cohort) −54% (95% CI 39–66%)
Microalbuminuria −39% (95% CI 21–52%)
Clinical neuropathy −60% (95% CI 38–74%)
Severe hypoglycemia Increased two- to threefold

The DCCT shows the central trade-off of insulin: pushing glucose lower brings benefits and more hypoglycemia at the same time.

What the research shows on muscle

Insulin and muscle protein

The best summary of insulin’s direct effect on human muscle is a 2016 meta-analysis of insulin-infusion studies, with 25 studies and 173 people in the pooled analysis (Abdulla et al., Diabetologia 2016):

Measure Result with insulin
Muscle protein synthesis, overall No significant effect
Muscle protein synthesis, when amino acid supply was raised Increased
Muscle protein breakdown Reduced, regardless of amino acid supply
Net protein balance Improved

The authors concluded that insulin has a “permissive” role in muscle protein synthesis when amino acids are elevated, and a clear role in reducing breakdown. These are short, tightly controlled clamp studies in which glucose was infused to prevent hypoglycemia.

No trials of insulin as a muscle-building drug

We found no randomized controlled trials testing injected insulin for muscle size, strength or performance in healthy or trained people. The rationale for non-medical use rests on the protein-turnover physiology above, not on outcome trials. Any claim of specific muscle gains from insulin is unsupported by controlled human data.

Side effects and risks

Hypoglycemia

The labels call hypoglycemia the most common adverse reaction of all insulins. They state that severe hypoglycemia can cause seizures, may lead to unconsciousness, and may be life-threatening or cause death. It can also impair concentration and reaction time, for example while driving (Humulin R label).

According to the labels, risk is highest when the insulin’s glucose-lowering effect is at its maximum. It rises with:

  • changes in meal pattern, such as skipped or delayed meals or a different carbohydrate content;
  • changes in physical activity;
  • changes in other medications;
  • kidney or liver impairment.

Warning symptoms can be blunted after repeated hypoglycemia, in long-standing diabetes, with nerve damage, and with beta-blockers.

The American Diabetes Association classifies hypoglycemia in three levels (ADA Standards of Care 2026):

Level Definition
Level 1 Glucose under 70 mg/dL (3.9 mmol/L) and at least 54 mg/dL (3.0 mmol/L)
Level 2 Glucose under 54 mg/dL (3.0 mmol/L); the threshold at which neuroglycopenic symptoms (confusion, impaired thinking) begin, requiring immediate action
Level 3 A severe event with altered mental or physical status that needs another person’s help to treat, at any glucose level

Even under medical supervision, severe events are common. In the Lantus trials, severe symptomatic hypoglycemia (needing another person’s help) occurred in these shares of patients (Lantus label):

Study population Duration Lantus Comparator
Type 1 diabetes, adults (3 trials) 16–28 weeks 6.5–10.6% NPH 5.2–15.0%
Type 1 diabetes, children 26 weeks 23.0% NPH 28.6%
Type 2 diabetes, adults (3 trials) 28 weeks–5 years 0.4–7.8% NPH 1.1–11.9%
ORIGIN trial, adults with cardiovascular disease or risk factors Median 6.2 years 5.6% Standard care 1.8%

At the population level, a CDC surveillance study estimated 97,648 US emergency department visits a year (95% CI 64,410–130,887) for insulin-related hypoglycemia and errors in 2007–2011 (Geller et al., JAMA Intern Med 2014). Almost one-third (29.3%) led to hospitalization. Severe neurologic effects were documented in an estimated 60.6% of visits, and more than half had a blood glucose of 50 mg/dL or lower. The most common triggers were reduced food intake and injecting the wrong insulin product.

Hypokalemia

All insulins move potassium into cells and can cause hypokalemia. The Humalog label warns that untreated hypokalemia may cause respiratory paralysis, ventricular arrhythmia and death (Humalog label). The labels call for potassium monitoring with intravenous use and in people at risk, such as those taking potassium-lowering drugs.

Other label warnings

  • Hypersensitivity. Severe generalized allergy, including anaphylaxis, can occur.
  • Lipodystrophy and cutaneous amyloidosis. Repeated injection in one area can thicken or thin the fat under the skin, or cause amyloid deposits. Injecting into these areas can reduce absorption, and switching to an unaffected site can then cause hypoglycemia.
  • Weight gain and edema. Both are listed adverse reactions; fluid retention and heart failure are a specific concern when insulin is combined with thiazolidinediones (PPAR-gamma agonists).
  • Never share pens, needles or syringes. Sharing risks transmission of blood-borne infections.
  • Medication errors. The labels warn about accidental mix-ups between insulin products.

Contraindications are use during an episode of hypoglycemia and hypersensitivity to the product.

Interactions

The Humalog label groups interactions as follows (Humalog label):

Effect Examples from the label
Increase hypoglycemia risk Other diabetes drugs, ACE inhibitors, ARBs, fibrates, fluoxetine, MAO inhibitors, salicylates, octreotide, sulfonamide antibiotics
Reduce insulin’s effect Corticosteroids, danazol, diuretics, estrogens, glucagon, niacin, progestogens, somatropin (growth hormone), sympathomimetics such as albuterol, thyroid hormones
Raise or lower the effect Alcohol, beta-blockers, clonidine, lithium
Mask hypoglycemia symptoms Beta-blockers, clonidine, guanethidine, reserpine

Several drugs on this list, including growth hormone, albuterol and danazol, are also found in non-medical performance-drug use. Combining them with insulin changes glucose control in ways that are hard to predict.

Overdose and poison-center data

The labels state that excess insulin may cause hypoglycemia and hypokalemia, that severe episodes with coma, seizure or neurologic impairment may be treated with glucagon or IV glucose, and that hypoglycemia may recur after apparent recovery, so sustained carbohydrate and observation may be needed (Humulin R label).

Published data on overdoses:

  • Poison-center trends. Nine US poison centers covering four states recorded 3,819 insulin exposures in 2000–2009. Annual exposures rose 279% over the decade, and 68% were unintentional therapeutic errors (Spiller et al., Ann Pharmacother 2011).
  • Unintentional errors. In 642 unintentional insulin overdoses handled by three poison centers, hypoglycemia occurred in 15.9%, and 17.4% were treated in an emergency department. No major outcomes or deaths were recorded (Beuhler et al., Clin Toxicol 2013). These were mostly people with diabetes and a dosing mistake, not large deliberate overdoses.
  • Large overdoses. A systematic review of 45 published insulin overdose cases (1986–2017) found that 44 were hospitalized, for a median of 94 hours (range 12–721 h), and one-third needed intensive care. Complications included intermittent cerebral impairment (73%), hypokalemia (49%), other electrolyte disturbances (42%) and cardiac toxicity (9%). One patient had lasting hypoglycemic brain damage and one died (Johansen and Christensen, Basic Clin Pharmacol Toxicol 2018). IV glucose was sometimes needed for up to a week.
  • Deaths. A forensic literature review of 109 overdose cases involving insulin or oral glucose-lowering drugs, examined after death, found insulin in 95.4%. Of these, 65% were suicides, 23% accidents and 12% homicides. The most common microscopic finding was neuronal depletion or necrosis in 29.1% (Manetti et al., Biomedicines 2022).

Use outside medicine

How common it is

In a 2009 online survey of strength athletes, researchers described 41 non-diabetic insulin users (Ip et al., Curr Sports Med Rep 2012):

  • 95.1% also used anabolic steroids, and they averaged 16.2 performance drugs a year;
  • 56.8% reported hypoglycemia, and one reported losing consciousness;
  • 37.8% obtained insulin from community pharmacies, and 80.6% said it was “easy” to get.

In an Italian study of 92 recreational bodybuilders, 43% regularly used hormones. Of those, 38% used insulin, usually alongside steroids. HDL cholesterol was lower in insulin or growth hormone users, and insulin use was specifically linked to a higher ALT-to-AST liver enzyme ratio (Di Girolamo et al., Sports Med Open 2024).

Case reports of harm

Published cases describe the same pattern: severe, sometimes treatment-resistant hypoglycemia in young, otherwise healthy men.

  • Switzerland, 1998. A 30-year-old bodybuilder injected short-acting insulin before an international competition. He lost consciousness, had convulsions and was intubated. Glucose stayed low despite IV glucose until he received more glucose and glucagon in intensive care (Konrad et al., 1998).
  • 1994. A case of self-induced insulin hypoglycemia in a bodybuilder was reported in Archives of Internal Medicine (Reverter et al., 1994).
  • UK, 2003. Clinicians reported a case to highlight the dangers of insulin use by bodybuilders, noting that its appeal was that it was undetectable by the tests of the time (Evans and Lynch, BJSM 2003).
  • France, 2019. A 30-year-old bodybuilder arrived in a coma from severe hypoglycemia of unknown cause. He needed repeated glucose infusions, and the cause was later traced to hidden insulin injections (Heidet et al., J Emerg Med 2019).

The label risk factors help explain why these cases occur. Hypoglycemia risk rises with skipped or changed meals, more physical activity and drugs that alter insulin’s effect, and users outside medicine often face all three without glucose monitoring. Larger doses can also act much longer than the “typical” times in the table above.

“Insulin can’t be detected.” This was true of routine testing in the early 2000s, but anti-doping labs have since validated mass-spectrometry methods that identify synthetic insulin analogs (lispro, aspart, glulisine, glargine metabolite, degludec) in urine (Thomas et al., Metabolites 2021). Human insulin itself is identical to the body’s own and remains harder to distinguish.

  • United States. Insulin is not listed as a controlled substance in Schedule III (21 CFR 1308.13). The insulin analogs are prescription-only, while Humulin R U-100 and Humulin N are published on DailyMed as over-the-counter drug labels.
  • Sport. WADA lists insulins and insulin-mimetics under S4.4.2, metabolic modulators, prohibited in and out of competition. They are non-Specified substances (WADA 2026 Prohibited List).

Key takeaways

  • One hormone, many speeds. Rapid-, short-, intermediate- and long-acting insulins differ mainly in how fast they leave the injection site, from about 3–5 hours of effect for aspart to more than 42 hours for degludec.
  • Hypoglycemia is the defining risk. Labels call it the most common adverse reaction of all insulins, and it can cause seizures, coma and death. Even in supervised trials, severe events affected 6.5–10.6% of Lantus-treated adults with type 1 diabetes within 16–28 weeks.
  • Effects can outlast expectations. Large doses of regular insulin acted for about 18 hours instead of about 8, and hypoglycemia can recur after apparent recovery.
  • Muscle evidence is physiological, not clinical. Insulin reduces muscle protein breakdown, but no controlled trials show it builds muscle or improves performance in healthy people.
  • Documented harm in non-medical use. Most surveyed non-diabetic users reported hypoglycemia, and case reports describe coma, seizures and intubation in young bodybuilders.
  • Banned in sport. WADA prohibits all insulins at all times, and synthetic analogs can now be detected in urine.

Sources

  1. Eli Lilly and Company. Humulin R (insulin human) injection, prescribing information. DailyMed.
  2. Eli Lilly and Company. Humulin N (insulin isophane human) injectable suspension, prescribing information. DailyMed.
  3. Eli Lilly and Company. Humalog (insulin lispro) injection, prescribing information. DailyMed.
  4. Novo Nordisk. NovoLog (insulin aspart) injection, prescribing information. DailyMed.
  5. Sanofi-Aventis U.S. Lantus (insulin glargine) injection, prescribing information. DailyMed.
  6. Novo Nordisk. Tresiba (insulin degludec) injection, prescribing information. DailyMed.
  7. Diabetes Control and Complications Trial Research Group; Nathan DM, Genuth S, Lachin J, et al. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329(14):977–986. PubMed.
  8. American Diabetes Association Professional Practice Committee for Diabetes. 6. Glycemic goals, hypoglycemia, and hyperglycemic crises: Standards of Care in Diabetes–2026. Diabetes Care. 2026;49(Suppl 1):S132–S149. PubMed.
  9. Abdulla H, Smith K, Atherton PJ, Idris I. Role of insulin in the regulation of human skeletal muscle protein synthesis and breakdown: a systematic review and meta-analysis. Diabetologia. 2016;59(1):44–55. PubMed.
  10. Geller AI, Shehab N, Lovegrove MC, et al. National estimates of insulin-related hypoglycemia and errors leading to emergency department visits and hospitalizations. JAMA Intern Med. 2014;174(5):678–686. PubMed.
  11. Spiller HA, Borys DJ, Ryan ML, et al. Unintentional therapeutic errors involving insulin in the ambulatory setting reported to poison centers. Ann Pharmacother. 2011;45(1):17–22. PubMed.
  12. Beuhler MC, Spiller HA, Aleguas A. Demographics and outcome of unintentional insulin overdoses managed by three poison centers. Clin Toxicol (Phila). 2013;51(8):789–793. PubMed.
  13. Johansen NJ, Christensen MB. A systematic review on insulin overdose cases: clinical course, complications and treatment options. Basic Clin Pharmacol Toxicol. 2018;122(6):650–659. PubMed.
  14. Manetti AC, Visi G, Spina F, et al. Insulin and oral hypoglycemic drug overdose in post-mortem investigations: a literature review. Biomedicines. 2022;10(11):2823. PubMed.
  15. Ip EJ, Barnett MJ, Tenerowicz MJ, Perry PJ. Weightlifting’s risky new trend: a case series of 41 insulin users. Curr Sports Med Rep. 2012;11(4):176–179. PubMed.
  16. Di Girolamo FG, Biasinutto C, Mangogna A, et al. Metabolic consequences of anabolic steroids, insulin, and growth hormone abuse in recreational bodybuilders: implications for the World Anti-Doping Agency passport. Sports Med Open. 2024;10(1):28. PubMed.
  17. Konrad C, Schüpfer G, Wietlisbach M, Gerber H. [Insulin as an anabolic: hypoglycemia in the bodybuilding world]. Article in German. Anasthesiol Intensivmed Notfallmed Schmerzther. 1998;33(7):461–463. PubMed.
  18. Reverter JL, Tural C, Rosell A, Domínguez M, Sanmartí A. Self-induced insulin hypoglycemia in a bodybuilder. Arch Intern Med. 1994;154(2):225–226. PubMed.
  19. Evans PJ, Lynch RM. Insulin as a drug of abuse in body building. Br J Sports Med. 2003;37(4):356–357. PubMed.
  20. Heidet M, Abdel Wahab A, Ebadi V, et al. Severe hypoglycemia due to cryptic insulin use in a bodybuilder. J Emerg Med. 2019;56(3):279–281. PubMed.
  21. Thomas A, Benzenberg L, Bally L, Thevis M. Facilitated qualitative determination of insulin, its synthetic analogs, and C-peptide in human urine by means of LC-HRMS. Metabolites. 2021;11(5):309. PubMed.
  22. World Anti-Doping Agency. The 2026 Prohibited List. WADA.
  23. US Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.