Considering testosterone propionate? It’s the fastest-acting testosterone ester, but frequent injections and unique characteristics require understanding before use.

You’ve heard propionate is different from other testosterone esters. Faster-acting. Requires more frequent injections.

You’re unclear whether the benefits justify the injection frequency, how to dose it properly, and how it compares to longer esters like enanthate or cypionate.

You’ve been told:

• “Propionate gives faster results than other esters”
• “It’s better for cutting because less water retention”
• “Daily injections are mandatory”
• “Side effects are worse than long esters”

Some true, some false. The truth: Testosterone propionate has a 2-3 day half-life (shortest common ester), requires every-other-day or daily injections for stable levels, kicks in within 24-48 hours (much faster than enanthate/cypionate), and clears the system quickly (beneficial for side effect management and faster PCT start). The testosterone molecule is identical to other esters—only the release speed differs. Typical cycles use 200-500mg/week split into frequent doses for 8-12 weeks. Side effects match other testosterone forms but injection frequency creates more injection site irritation. Best for those wanting precise control and willing to inject frequently.

In this comprehensive guide, I’ll explain what testosterone propionate is (the short ester and pharmacokinetics), detail typical cycle protocols (dosing, frequency, duration for different goals), compare to other testosterone esters (propionate vs. enanthate vs. cypionate), reveal all side effects (same hormone, same effects), provide injection strategies (managing frequent administration), and show PCT timing advantages (faster recovery initiation).

Whether you’re considering propionate for your first cycle or switching from longer esters, complete understanding is essential.

Let’s examine testosterone propionate scientifically and practically.

Technical Specifications

Quick reference.

Full name: Testosterone Propionate

Class: Anabolic androgenic steroid

Administration: Intramuscular injection only

Half-life: Approximately 2-3 days

Onset of action: Rapid (24-48 hours post-injection)

Detection time: 2-3 weeks (shorter than long esters)

Ester length: Short (3-carbon chain)

What Is Testosterone Propionate?

The compound explained.

The Basic Definition

What it is:

• Synthetic testosterone hormone
• Injectable formulation
• Testosterone molecule + propionate ester attached
• Short-acting testosterone

What the ester does:

• Propionate = 3-carbon ester chain
• Smallest commonly used testosterone ester
• Determines release speed and duration
• Time-release mechanism

How it works:

• After injection, depot forms in muscle
• Esterases (enzymes) cleave propionate ester
• Free testosterone released into bloodstream
• Faster cleavage than longer esters = quicker release
• Rapid absorption

The half-life:

• Approximately 2-3 days
• Much shorter than enanthate (7-10 days) or cypionate (8-12 days)
• Requires frequent re-administration
• Short duration

Testosterone Propionate vs. Other Esters

The critical understanding:

• All testosterone esters = same testosterone molecule
• Propionate, enanthate, cypionate release IDENTICAL testosterone
• Only difference: Speed and duration of release
• Same hormone, different delivery

The comparison:

Testosterone propionate:

• Half-life: 2-3 days
• Injection frequency: Every other day or daily
• Onset: 24-48 hours
• Time to steady state: 1-2 weeks
• Fast-acting

Testosterone enanthate:

• Half-life: 7-10 days
• Injection frequency: 1-2x weekly
• Onset: 4-6 weeks to steady state
• Time to steady state: 4-6 weeks
• Slow-acting

Testosterone cypionate:

• Half-life: 8-12 days
• Injection frequency: 1-2x weekly
• Onset: 4-6 weeks to steady state
• Time to steady state: 4-6 weeks
• Slow-acting (similar to enanthate)

The functional implications:

• Propionate: Precise control, rapid results, frequent injections
• Enanthate/Cypionate: Convenience, stable long-term, infrequent injections
• Control vs. convenience trade-off

Medical vs. Performance Use

Medical use (TRT):

• Rarely used for modern TRT
• Reason: Injection frequency burden (EOD or daily)
• Longer esters preferred (weekly dosing easier for patients)
• Uncommon for therapy

Performance use:

• Popular among experienced users
• Preferred for cutting cycles (perceived less water retention due to stable levels)
• Favored when control and rapid adjustment needed
• Athletic application

How Testosterone Propionate Works

The anabolic mechanisms.

Muscle Growth Pathways

Mechanism 1: Protein synthesis enhancement

• Testosterone binds to androgen receptors in muscle cells
• Activates genetic transcription
• Increases protein production within muscle fibers
• Anabolic signaling

Mechanism 2: Nitrogen retention

• Positive nitrogen balance essential for muscle growth
• Testosterone increases nitrogen retention in muscle tissue
• More nitrogen = more protein building blocks available
• Anabolic environment

Mechanism 3: IGF-1 elevation

• Testosterone increases insulin-like growth factor 1
• IGF-1 promotes muscle growth and recovery
• Synergistic muscle-building effect
• Growth factor amplification

Mechanism 4: Anti-catabolic effects

• Suppresses cortisol (catabolic hormone)
• Blocks cortisol receptors in muscle
• Prevents muscle breakdown
• Muscle preservation

Mechanism 5: Satellite cell activation

• Activates muscle stem cells (satellite cells)
• These cells fuse to existing muscle fibers
• Enables new muscle growth beyond natural limits
• Muscle expansion potential

Performance Enhancement

Strength increase:

• Neural adaptations (improved muscle recruitment)
• Increased muscle contractile proteins
• Enhanced ATP production
• Power output boost

Recovery enhancement:

• Faster glycogen replenishment
• Accelerated muscle protein synthesis
• Reduced muscle damage and inflammation
• Training frequency increase possible

Red blood cell production:

• Stimulates erythropoiesis (RBC production)
• Increased oxygen-carrying capacity
• Better muscular endurance
• Cardiovascular benefit

Typical Testosterone Propionate Cycles

Dosing protocols.

The Injection Frequency Requirement

Why frequent injections necessary:

• 2-3 day half-life
• Levels drop significantly after 48-72 hours
• Must re-inject to maintain stable blood levels
• Pharmacokinetic necessity

The options:

Every other day (EOD):

• Minimum acceptable frequency
• Some fluctuation between doses
• Example: Monday, Wednesday, Friday, Sunday (rotating)
• Standard approach

Daily:

• Most stable blood levels
• Minimal fluctuation
• Example: Same time each day
• Optimal stability

The comparison:

• EOD: 3.5 injections per week (if cycling Sun, Tues, Thurs, Sat)
• Daily: 7 injections per week
• Significantly more injections than long esters

Beginner Cycle (First Steroid Use)

The conservative approach:

• Testosterone-only (no other compounds)
• Learn individual response
• Propionate not typically recommended for first cycle (injection frequency burden)
• Usually advised to use enanthate/cypionate instead

If using propionate for first cycle:

• Dose: 300-400mg per week total
• Frequency: 50mg EOD or 100mg EOD
• Duration: 8-10 weeks
• Conservative protocol

Example (350mg/week):

• 50mg every other day
• 7 injections over 2 weeks = 350mg total weekly
• EOD schedule

Example (400mg/week):

• 100mg Monday, Wednesday, Friday, Sunday (rotating)
• Simpler schedule

Intermediate Cycle

Experienced users:

• Multiple cycles completed
• Understand personal response
• Knowledge required

Typical protocol:

• Dose: 400-600mg per week
• Frequency: EOD or daily
• Duration: 8-12 weeks
• Standard approach

Example (500mg/week):

• 100mg Monday, Wednesday, Friday
• 100mg Sunday (4th injection)
• Rotating weekly pattern
• 500mg total weekly

Stacking:

• Often combined with other compounds
• Propionate as testosterone base (200-400mg/week)
• Plus cutting compounds (e.g., 350mg trenbolone acetate weekly, 50mg anavar daily)
• Multi-compound protocol

Advanced Cycle (Not Recommended)

High-level use:

• Professional bodybuilders
• Years of experience
• High risk
• Extreme application

Typical advanced:

• Dose: 600-1000mg+ per week
• Stacked with multiple compounds
• Duration: 8-16 weeks
• Health risk escalation

Bulking vs. Cutting

Bulking (muscle gain):

• Dose: 400-600mg/week
• Caloric surplus
• Combines well with bulking compounds
• Mass building

Cutting (fat loss):

• Dose: 300-500mg/week
• Caloric deficit
• Preferred for cutting due to less water retention (myth, but perceived)
• Often stacked with cutting compounds (tren, masteron, anavar)
• Fat loss with muscle preservation

The “less water retention” myth:

• Propionate doesn’t inherently cause less water retention
• Perceived difference due to more stable levels (EOD/daily dosing prevents spikes)
• Any testosterone causes water retention at supraphysiological doses
• Psychological more than pharmacological

Side Effects of Testosterone Propionate

Identical to other testosterone esters.

The Important Clarification

Same hormone = same side effects:

• Propionate releases same testosterone as enanthate/cypionate
• Side effect profile identical
• Only differences: Injection site reactions (more frequent) and timeline
• No unique side effects

Side Effect 1: Elevated Hematocrit

The mechanism:

• Testosterone stimulates erythropoietin production
• Increases red blood cell production in bone marrow
• Elevates hematocrit percentage (RBC concentration)
• Blood becomes more viscous
• Hematological effect

The risk:

• Thick blood strains cardiovascular system
• Increased clotting risk
• Stroke and heart attack risk elevated
• Cardiovascular danger

Management:

• Regular blood donation (reduces RBC count)
• Hydration
• Monitor bloodwork (target <52% hematocrit)
• Proactive control

Side Effect 2: Elevated Blood Pressure

The mechanism:

• Sodium and water retention
• Increased blood volume
• Elevated hematocrit contributes (viscous blood)
• Hypertension

The impact:

• Systolic can increase 10-20+ mmHg
• Chronic hypertension damages organs
• Health concern

Management:

• Monitor blood pressure regularly
• Reduce sodium intake
• Cardiovascular exercise
• Medications if needed (ARBs, ACE inhibitors)
• Blood pressure control

Side Effect 3: Cholesterol Disruption

The mechanism:

• Supraphysiological androgens alter hepatic lipid metabolism
• HDL (good cholesterol) decreases 20-40%
• LDL (bad cholesterol) increases 10-30%
• Atherogenic lipid profile

The risk:

• Atherosclerosis acceleration
• Cardiovascular disease risk
• Long-term danger

Management:

• High-fiber diet
• Omega-3 supplementation
• Regular cardio exercise
• Cannot fully prevent, only mitigate
• Damage control

Side Effect 4: Gynecomastia

The mechanism:

• Testosterone aromatizes to estradiol (estrogen)
• Elevated estrogen stimulates breast tissue growth
• Aromatization pathway

Prevention:

• Aromatase inhibitors (anastrozole, exemestane)
• Block testosterone → estrogen conversion
• Dose based on bloodwork
• AI use

Early intervention:

• SERMs (Nolvadex, raloxifene) if lumps develop
• Can reverse early-stage gyno
• Time-sensitive treatment

Side Effect 5: Acne

The mechanism:

• Testosterone (and DHT) stimulate sebaceous glands
• Increased sebum production
• Oily skin, clogged pores
• Bacterial growth and inflammation
• Androgenic skin effect

Management:

• Good hygiene
• Topical treatments (benzoyl peroxide)
• Oral antibiotics if severe
• Symptomatic control

Side Effect 6: Hair Loss

The mechanism:

• Testosterone converts to DHT
• DHT binds scalp follicle receptors
• Follicle miniaturization (if genetically prone)
• Progressive thinning and loss
• DHT-mediated

Who’s affected:

• Only those with male pattern baldness genes
• Family history = high risk
• Genetic predisposition

Prevention attempts:

• Finasteride or dutasteride (5α-reductase inhibitors)
• Block testosterone → DHT conversion
• Partially effective
• Limited prevention

Reversibility:

• Lost follicles don’t regenerate
• Permanent
• Irreversible

Side Effect 7: Virilization in Women

The effects:

• Voice deepening (permanent)
• Clitoral enlargement (permanent)
• Facial/body hair growth (permanent)
• Male pattern baldness
• Menstrual irregularities
• Masculinization

The recommendation:

• Women should avoid testosterone entirely
• Use anavar, primobolan instead if considering steroids
• Not appropriate for women

Side Effect 8: Natural Testosterone Suppression

The mechanism:

• Exogenous testosterone detected by brain
• Hypothalamic-pituitary-testicular axis shutdown
• LH and FSH production cease
• Testicular testosterone production stops
• Testicular atrophy
• HPT axis suppression

The timeline:

• Suppression begins within days
• Complete shutdown within 2-4 weeks
• Rapid and total

Recovery:

• With PCT: 4-8 weeks typically
• Without PCT: 6-12+ months
• PCT essential

Side Effect 9: Injection Site Irritation (Unique to Propionate)

The problem:

• Propionate causes more injection site pain than longer esters
• Reason: Shorter ester more “sharp” (anecdotal, mechanism unclear)
• Frequent injections compound issue
• Local discomfort

The manifestations:

• Post-injection pain (PIP)
• Redness and swelling
• Hardened lumps at injection sites
• Injection site reactions

Management:

• Rotate injection sites extensively (8+ sites)
• Warm oil before injection (body temperature)
• Inject slowly
• Massage area after injection
• Minimize irritation

The site rotation:

• Glutes (left and right, upper and lower = 4 sites)
• Quads (left and right, vastus lateralis = 2 sites)
• Delts (left and right = 2 sites)
• Ventrogluteal (left and right = 2 sites)
• Total: 10 potential sites
• Extensive rotation necessary

Advantages of Testosterone Propionate

Why choose the short ester.

Advantage 1: Rapid Onset

The benefit:

• Effects felt within 24-48 hours
• Results visible within 1-2 weeks
• No 4-6 week buildup period
• Immediate feedback

Comparison:

• Propionate: Effects in days
• Enanthate/Cypionate: Effects in weeks
• Speed advantage

Advantage 2: Precise Control

Dose adjustability:

• Can adjust dose daily/EOD
• See results of change within days
• Rapid titration

Side effect management:

• If sides occur, stop immediately
• Clears system in 3-5 days
• Sides resolve quickly
• Quick abort option

Estrogen management:

• Easier to dial in AI dose
• Changes in testosterone reflect in estrogen faster
• Fine-tuning possible

Advantage 3: Faster PCT Initiation

The timing:

• Wait 3-4 days after last injection
• Then start PCT
• Short clearance

Comparison:

• Propionate: PCT starts 3-4 days post-cycle
• Enanthate/Cypionate: PCT starts 2 weeks post-cycle
• 10-day advantage

The benefit:

• Less time in low-testosterone state
• Faster recovery initiation
• Less muscle loss during transition
• Recovery advantage

Advantage 4: Short Cycles Viable

The possibility:

• 6-8 week cycles effective with propionate
• Reaches peak levels quickly
• Makes short cycles worthwhile
• Flexibility

Comparison:

• Propionate: 6 weeks viable
• Enanthate: Minimum 10-12 weeks (4-6 week buildup wastes time)
• Short-cycle option

Disadvantages of Testosterone Propionate

The downsides.

Disadvantage 1: Injection Frequency

The burden:

• EOD minimum (3.5x weekly)
• Daily optimal (7x weekly)
• Compared to 1-2x weekly for long esters
• Time and discipline demand

The lifestyle impact:

• Traveling complicated
• Busy schedules challenged
• Forgetfulness problematic
• Inconvenient

Disadvantage 2: Injection Site Issues

The problems:

• More frequent injections = more scar tissue
• Propionate causes more PIP than long esters
• Site rotation essential
• Potential site exhaustion with long-term use
• Local complications

Disadvantage 3: Cost

The economics:

• Propionate often more expensive per mg
• Need more frequent vials
• More syringes and supplies
• Higher cost

Disadvantage 4: Not Ideal for Beginners

The complexity:

• Injection frequency overwhelming for first-time users
• Long esters simpler to manage
• Beginners should start with enanthate/cypionate
• Steeper learning curve

Post-Cycle Therapy (PCT) for Propionate

Recovery protocol.

The Timing Advantage

When to start:

• 3-4 days after last propionate injection
• Much faster than long esters (2 weeks wait)
• Quick PCT initiation

Why this works:

• 2-3 day half-life
• After 3-4 days (1.5-2 half-lives), levels low enough
• PCT drugs can work effectively
• Optimal timing

Standard PCT Protocol

The drugs:

• Clomid: 50mg daily for 4-6 weeks
• Nolvadex: 20mg daily for 4-6 weeks
• Often both used together
• SERM therapy

The mechanism:

• Block estrogen receptors in pituitary
• Stimulate LH and FSH release
• Restart testicular testosterone production
• Natural recovery

Monitoring

Bloodwork timeline:

• 4-6 weeks after PCT completion
• Check testosterone, LH, FSH, estradiol
• Verify recovery successful
• Confirmation testing

Propionate vs. Enanthate/Cypionate: Which to Choose?

The decision framework.

Choose Propionate If:

You want maximum control:

• Ability to adjust rapidly
• Quick side effect cessation if needed
• Precision priority

You’re experienced:

• Comfortable with frequent injections
• Understand protocols
• Knowledge prerequisite

You’re running short cycles:

• 6-8 week cycles
• Don’t want to waste time on buildup
• Time efficiency

You want faster PCT:

• Minimize low-T transition period
• Quicker recovery
• Recovery speed

You don’t mind frequent injections:

• Discipline to inject EOD or daily
• Lifestyle accommodates
• Commitment present

Choose Enanthate/Cypionate If:

You want convenience:

• 1-2x weekly injection acceptable
• Prefer simpler protocol
• Ease priority

You’re a beginner:

• First cycle should be simple
• Learn basics before complexity
• Foundational learning

You’re running long cycles:

• 12-16+ weeks
• Buildup time less significant
• Extended duration

You want stable long-term levels:

• Once steady state reached, very stable
• Less daily fluctuation
• Long-term stability

The Hybrid Approach

Kickstart with propionate:

• Weeks 1-4: Propionate (rapid onset)
• Weeks 5-12: Switch to enanthate (convenience)
• Best of both worlds

The benefit:

• Immediate results from propionate
• Then convenience of long ester
• Strategic combination

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This article is informational only. We do not condone or recommend steroid use. If considering any hormone therapy, work with qualified medical professionals and understand the serious health risks involved.

REFERENCES

SECTION 1 — Pharmacokinetics: half-life, ester mechanism, and injection timing

[1] Amory JK et al. — PubMed/Steroids, 1987 Pharmacokinetic characterization of testosterone propionate in normal men after a single 25mg intramuscular dose; stable isotope-labeled testosterone propionate transferred gradually from the IM injection site to systemic circulation; plasma levels maintained 2–4 ng/ml between 3 and 36 hours; plasma testosterone was maintained above physiological levels for approximately 48 hours; foundational PK data confirming the short-acting nature of propionate and the requirement for re-injection every 2–3 days https://pubmed.ncbi.nlm.nih.gov/3782423/

[2] Pastuszak AW et al. — PMC/Andrology, 2022 Comprehensive pharmacokinetics review of testosterone therapy formulations; testosterone propionate has a short half-life (~2 days), requiring injection every 2–3 days to maintain therapeutic levels; longer esters (enanthate, cypionate) have 4.5-day and 8-day half-lives respectively, enabling weekly dosing; all testosterone esters release the same bioidentical testosterone after enzymatic ester cleavage; ester chain length dictates release rate and duration, not the identity of the hormone released; short-acting IM testosterone formulations associated with supraphysiological peak concentrations and higher erythrocytosis risk https://pmc.ncbi.nlm.nih.gov/articles/PMC9293229/

[3] Wikipedia — Pharmacokinetics of Testosterone Encyclopedic summary of published testosterone pharmacokinetic data; elimination half-life of testosterone propionate as oil solution by IM injection: 0.8 days; testosterone enanthate: 4.5 days; testosterone cypionate: ~8 days; testosterone undecanoate: 20.9–33.9 days; bioavailability by IM injection approximately 95%; 97–99.5% of circulating testosterone bound to plasma proteins; confirms the comparative ester half-life data used throughout the article https://en.wikipedia.org/wiki/Pharmacokinetics_of_testosterone

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SECTION 2 — Anabolic mechanisms: how testosterone builds muscle

[4] Bhasin S et al. — PubMed/Endocrine Reviews, 2025 Comprehensive mechanistic review; testosterone induces hypertrophy of type I and II muscle fibers; promotes differentiation of mesenchymal progenitor cells into myogenic lineage via AR-mediated pathway; liganded AR binds β-catenin, translocates to nucleus, upregulates follistatin to block TGF-β and promote myogenesis; increases myoblast proliferation through polyamine biosynthesis; stimulates GH and IGF-1 secretion; inhibits muscle atrophy genes; anti-catabolic mechanism via androgen receptor-mediated inhibition of ubiquitin-proteasome degradation pathways https://pubmed.ncbi.nlm.nih.gov/41355050/

[5] Bhasin S et al. — PMC/Frontiers in Physiology, 2021 Review of AAS mechanisms on skeletal muscle hypertrophy, metabolic and cardiovascular health; AAS increase muscle protein synthesis and accretion via genomic pathways (AR binding → nuclear translocation → enhanced transcription of anabolic genes) and non-genomic pathways (membrane receptor activation → mTOR, PI3K/Akt signaling); satellite cell activation via AR in myonuclei and satellite cells; testosterone inhibits catabolic pathways including MAFbx/MuRF-1 ubiquitin ligases through Akt phosphorylation; chronic AAS use also has detrimental metabolic and cardiovascular effects https://pmc.ncbi.nlm.nih.gov/articles/PMC8087567/

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SECTION 3 — Side effects: erythrocytosis and cardiovascular risk

[6] Stojkov NJ et al. — PMC/Canadian Medical Association Journal, 2017 Review of testosterone-induced erythrocytosis; mechanism involves erythropoietin stimulation, hepcidin suppression (increasing iron availability), and estradiol-mediated hematopoietic stem cell effects; hematocrit begins to increase within one month; effect is dose-dependent and more pronounced in older men; short-acting parenteral testosterone depots associated with greater erythrocytosis risk due to supraphysiological peak concentrations; erythrocytosis leads to increased blood viscosity and thrombosis risk; FDA warns of venous thromboembolism, heart attack, and stroke risks https://pmc.ncbi.nlm.nih.gov/articles/PMC5647167/

[7] Saad F et al. — PMC/Steroids, 2015 Review of testosterone, HDL, and cardiovascular risk; supraphysiological androgen doses substantially decrease HDL-C — most pronounced in young men receiving high-dose anabolic androgens and athletes; dose, route, and age modulate the HDL effect; testosterone raises hepatic lipase activity, lowering HDL-C; may also reduce total cholesterol and LDL-C; overall lipid effect is atherogenic at supraphysiological doses; directly documents the lipid disruption pattern described in the article’s side effect profile https://pmc.ncbi.nlm.nih.gov/articles/PMC4527564/

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SECTION 4 — HPG axis suppression and PCT

[7] Matsumoto AM et al. — PubMed/Journal of Andrology, 1997 Study of testosterone cypionate at 100, 250, and 500mg/week doses; basal LH and FSH became undetectable within 2 weeks of starting 250 and 500mg doses, and within 5–6 weeks at 100mg; pituitary gonadotropin responses to LHRH disappeared more slowly; HPG axis suppression reversed following cessation of treatment; provides precise timeline data for suppression onset that directly supports the article’s HPG axis shutdown description https://pubmed.ncbi.nlm.nih.gov/9394096/

[8] Desai A et al. — PMC/Therapeutic Advances in Urology, 2022 Review of HPG axis suppression by TRT and AAS; exogenous testosterone exerts negative feedback on hypothalamus and pituitary, inhibiting GnRH → LH/FSH → intratesticular testosterone; inhibition of pulsatile GnRH leads to hypogonadotropic hypogonadism; severity proportional to duration and dose; SERMs (clomiphene, tamoxifen) block estrogen receptors in the pituitary, stimulating LH/FSH release and restarting endogenous testosterone production; PCT protocol rationale fully documented — directly supports the article’s PCT section explaining SERM mechanism https://pmc.ncbi.nlm.nih.gov/articles/PMC9243576/

[9] Rahnema CD et al. — PMC/Fertility and Sterility, 2014 Review of HPG axis recovery after TRT/AAS cessation; spontaneous recovery occurs in most cases with <1 year of use within 1 year of cessation; recovery of spermatogenesis took a mean of 10.4 months after AAS cessation, with FSH recovery at 19 months; longer duration associated with slower recovery; clomiphene citrate (CC) and hCG can accelerate HPG axis restoration; provides the evidence base for PCT timing and expected recovery duration following propionate and other testosterone cycles https://pmc.ncbi.nlm.nih.gov/articles/PMC4854084/