Antidepressants Stunt Growth (SSRIs & Height): Future NBAer to Jockey?

Research by Pratt et al. (2017) suggests that 7.8% of individuals between ages 12 and 19 used antidepressants from 2011-2014. (R)

Jack et al. (2020) report a continuous rise in the prescribing of antidepressants to adolescents in England; antidepressant prescriptions more than doubled from 2005-2017 among 12-17 year olds. (R)

Between April 2015-2021 the number of unique patients ages 5-12 increased 41% in England from 1,299 to 1,831. (R)

Although the benefits derived from antidepressant use are thought to outweigh the drawbacks (even in pediatrics) – something to consider is that antidepressants may stunt growth.

Do antidepressants stunt growth during adolescence?

Antidepressants (specifically SSRIs) may stunt growth by decreasing height gains – leading to a lower height in adulthood.

5 pieces of evidence suggest a growth stunting effect of antidepressants.

2 pieces of evidence suggest no growth stunting effect from antidepressants.

Nearly every study documented here has significant limitations and/or confounds such that it becomes difficult to definitively know whether SSRIs are legitimately stunting growth.

I personally side with evidence suggesting that antidepressants likely stunt growth (i.e. impair height gains) based on the fact that Weintrob et al. (2002) demonstrated a cause/effect impact of SSRI use on growth hormone (GH), IGF-1 secretion, and growth rate.

How did they do this? They monitored growth rate and hormones: (1) before antidepressant initiation, (2) during antidepressant treatment; (3) after antidepressant discontinuation; and (4) after antidepressant reinitiation (after discontinuation).

Growth hormone (GH) and/or IGF-1 appeared either suboptimally low or low (below the normal reference range relative to age) in all 4 patients during SSRI antidepressant use.

When SSRI antidepressants were discontinued: growth hormone (GH), IGF-1, and subsequent growth rate – all increased to the expected normal reference ranges.

Even in the study by Emslie et al. (1997) that found no significant change in height over an 8-week period of SSRI therapy – researchers reported “slower growth rate” in 20 long-term fluoxetine users.

Lastly, those who are exposed to antidepressants as a fetus and/or infant may experience suboptimal overall height and development because antidepressants can cause lower overall birth size (length/weight) and/or interfere with early development – which utlimately affects peak height.

How much do SSRIs actually stunt growth?

Assuming SSRI antidepressants actually stunt growth – the magnitude of growth stunting is likely contingent upon several variables:

1. Percentage of puberty on antidepressants (most important)
2. Dosage/potency of antidepressants administered
3. Specific stages of puberty during antidepressant use

The specific antidepressant used may matter as well – along with whether the individual is taking other medications (which might compound growth inhibition or offset it somehow).

Longer-term use of antidepressant use during puberty seems to have the strongest impact on height growth reduction followed by dosage (Calarge et al., 2019).

In other words, the greater the total percentage (%) of puberty you’re taking antidepressants – the more substantial the antidepressants will stunt height growth.

Dosage also likely matters insofar as higher dosages seem to suppress GH and IGF-1 release to a greater extent than lower doses.

The specific stages of puberty you’re in when using antidepressants might also matter to some extent – but this is merely my hypothesis and it hasn’t been confirmed.

Without considering the following: % of puberty on antidepressants (i.e. duration of use overlapping with puberty); dosage; and specific stages of puberty used – it’s probably difficult to estimate the degree to which antidepressants will stunt growth.

One large study reports SSRIs stunt growth ~1 cm per year.

Another moderate-sized study reports SSRIs stunt growth ~1.1 cm per 19 weeks (4.75 months).

A small case series of 4 pediatrics indicates that SSRIs stunt growth ~3.9 cm per year.

If we assume that puberty lasts 2 to 5 years (average), and a person uses SSRI antidepressants for the entire duration of puberty – what would the height reduction be?

Based on the above figures antidepressants could stunt height growth: 2 cm (0.79 inches) to 19.5 cm (7.68 inches) – on average – if the SSRI is administered throughout puberty.

Some researchers have also suggested that SSRIs may decrease the size of sex organs and gonads – based on the fact that testicular volume increased significantly after SSRIs were discontinued in one adolescent.

A conservative estimate for SSRI-induced growth stunting (assuming used throughout the entirety of puberty) would be ~2-5 cm (0.79-2 inches).

In other words, if you were on pace to be 6 feet – you may only end up ~5’10” and you might have slightly smaller sex organs and/or gonads (i.e. testicles/ovaries).

How Antidepressants Stunt Growth (Mechanisms)

Assuming antidepressants legitimately stunt growth, included below are the hypothesized mechanisms by which this stunting effect occurs.

The primary mechanism by which antidepressants likely stunt growth is via reduction of growth hormone (GH) and subsequent IGF-1 reductions.

It’s possible that antidepressants also interact with the melatonin system to suppress levels of gonadotropin-releasing hormone (GnRH) as well.

It’s also possible that changes in feeding habits (e.g. eating less food) while on non-serotonergic antidepressants result in low BMI and/or malnutrition such as to impair pubertal outcomes.

Growth hormone (GH) reductions

Growth hormone is understood to stimulate longitudinal growth during childhood and adolescence – and its secretion rapidly increases during puberty. (R1, R2)

Antidepressants alter serotonin signaling which is understood to decrease the secretion of growth hormone (GH).

Weintrob et al. (2002) observed that SSRIs inhibited GH secretion rapidly after treatment initiation in 4 adolescents. (R)

Interestingly, the discontinuation of SSRI therapy resulted in normalization of GH and growth rates whereas reinstatement of SSRI therapy (after cessation) resulted in decreased GH and growth rates.

This strongly supports the idea that SSRIs inhibit height growth by way of reducing GH secretion.

It was specifically suggested that SSRIs selectively impair the somatotrophic axis and reduce central alpha-2 adrenoreceptor-mediated growth hormone (GH) release.

IGF-1 reductions

SSRIs have been associated with reductions in concentrations of insulin-like growth factor-1 (IGF-1) during fetal development and in adulthood. (R1, R2)

Evidence suggests that dose-dependent changes in IGFs are related to dose-dependent pubertal gain in height. (R)

This means that if IGF-1 concentrations are abnormally low, pubertal height gains will not be as significant as if they were within the normal range.

It’s likely that IGF-1 reductions are an effect of reduced GH secretion – as GH induces growth predominantly through the stimulation of hepatic and peripheral IGF-1 secretion. (R)

Normalization of growth hormone (GH) concentrations such as with exogenous somatropin should theoretically normalize IGF-1 levels and subsequent height/growth rate if compromised by antidepressants.

Altered melatonin secretion (?)

Increasing serotonin reuptake inhibition may influence levels of melatonin.

Atypical concentrations of melatonin may affect: (1) sleep cycles; (2) circadian rhythms; and/or (3) puberty induction such as to decrease growth.

In fact, some think that high-dose melatonin may shrink testicles and decrease growth during puberty via interfering with the release of gonadotropin-releasing hormone (GnRH).

Why? Because in specific animals, significantly increasing melatonin with supplementation appears to suppress the release of hypothalamic gonadotropin-releasing hormone (GnRH) and impairs gonadal growth and overall development.

Carvalho et al. (2009) report that antidepressants increase melatonin levels – and this melatonin increase is a direct effect of antidepressant meds and not due to mood improvement resulting from treatment. (R)

However, it remains unclear as to whether the melatonin increase as a response to serotonergic antidepressants is significant enough to be a mechanism by which SSRIs decrease height potential.

Interestingly, research in animals suggest that the SSRI citalopram inhibits gonadotropin-releasing hormone (GnRH) synthesis in male zebrafish – which is consistent with the effect of melatonin. (R)

Keep in mind that just because SSRIs inhibit gonadotropin-releasing hormone (GnRH) in zebrafish does NOT automatically mean they have this same effect in humans – although the possibility warrants investigation.

Therefore, it’s theoretically possible that SSRI antidepressants: (1) increase melatonin synthesis (which in turn may reduce GnRH synthesis) and/or (2) directly decrease GnRH synthesis in humans during puberty – such as to reduce height and gonad development.

Increased body fat & weight gain (?)

It’s well-known that long-term serotonergic antidepressant therapy can cause weight gain – particularly in the context of an unhealthy lifestyle. (R)

Gafoor et al.: “Widespread utilization of antidepressants may be contributing to long term increased risk of weight gain and a population level.” (R)

It is known that obese children tend to be taller for their age but also fatter – and they end up maturing faster than normal weight children.

Despite being taller in childhood and maturing faster, obese children do NOT tend to attain taller height as adults since excessive adiposity (i.e. body fat) has an influence on the process of growth and puberty. (R)

Most evidence suggests that there’s no final height differences between obese and non-obese individuals after puberty. (R)

However, it’s possible that being overweight/obese might somehow prevent attainment of peak height potential due to adiposity-related hormone changes in puberty and/or chronic low-grade inflammation.

One study found that being overweight/obese seem to decrease adolescent growth spurt by a mean of 0.5 cm in girls and 0.9 cm in boys – but this could be due to prior gains associated with early growth resulting from being overweight/obese. (R)

In the event that being overweight/obese does somehow prevent the attainment of peak height (relative to genetic programming) – then antidepressant-induced weight gain could be an indirect mechanism by which growth ends up stunted.

Lower BMI & lower calorie intake?

Psychostimulants have been understood to suppress growth in part via an anorectic effect wherein appetite decreases and users don’t eat sufficient calories (macronutrients & micronutrients) to facilitate optimal pubertal growth.

However, this effect is unlikely with SSRI antidepressants given that SSRIs commonly promote body weight/fat gain – associated with higher calorie intake and higher BMI. (R)

It’s theoretically possible that non-serotonergic antidepressants (e.g. bupropion) could cause significant weight loss in select individuals due to an anorectic effect (i.e. appetite suppression) secondary to increased noradrenergic/dopaminergic tone and altered hormones.

Therefore, this could be a mechanism by which individuals who utilize non-serotonergic antidepressants during puberty (e.g. bupropion) end up with stunted growth.

It’s also possible that a subset of adolescents with severe depression (such that they have low appetite and/or calorie intake and low BMIs) – end up on antidepressants (e.g. SSRIs) because nothing else is helping.

If the SSRIs aren’t working well enough, appetite and BMIs may stay low despite using SSRIs and this could potentially lead to a “double whammy” effect wherein growth hormone (GH) is low but BMI/body fat are also low such as to stunt pubertal growth.

Note: There may be additional mechanisms by which antidepressants (particularly SSRIs) stunt growth beyond those mentioned above.

Is it “bad” if antidepressants stunt growth during puberty?

Probably. Among individuals with genetics for standard (i.e. average) or below-average height – any additional growth stunting may result in reduced self-esteem and dating difficulties, particularly for males.

There’s some evidence to suggest that: “there is a small psychological benefit for males to being taller as an adolescent.” (R)

Moreover, evidence from some research indicates that antidepressants reduce total height, increase BMI & body fat, and decrease development of gonads & sex organs.

In other words, antidepressant use could shrink testicles and reduce penis size – to varying degrees depending on specific pubertal years of treatment, dosage, and duration of overlap with puberty.

There may be a few rare outliers who are genetically predisposed to being abnormally tall/large (i.e. way above average height) that may benefit in some ways from a slight stunting of growth with antidepressants during puberty, however, most will not desire this effect.

Do non-SSRI antidepressants stunt growth too?

Possibly. The impact of non-SSRI antidepressants on pubertal growth hasn’t been formally studied – therefore evidence-based conclusions cannot be made.

Based on current data, one might infer that any non-SSRI antidepressant that appreciably inhibits the reuptake of serotonin and/or modulates serotonergic neurotransmission – has potential to stunt growth.

Why? Because inhibiting the reuptake of serotonin (even if not done specifically by an SSRI) seems to interfere with the secretion of growth hormone (GH) and IGF-1 (likely as a downstream effect of GH reduction).

Therefore, even tricyclic antidepressants (TCAs) could adversely modulate central alpha-2 adrenoreceptor-mediated GH secretion and/or somatotrophic axis activation to decrease pubertal height gains.

This also means that even “natural” (i.e. herbal) antidepressants like St. John’s Wort (Hypericum perforatum), Zembrin, Lavender, etc. – may have similar growth-stunting effects as SSRIs.

For this reason, you should NOT assume that just because something is “natural” or an “over-the-counter” supplement that it somehow is less risky than SSRIs with regards to its impact on growth in puberty.

Antidepressants that don’t target serotonin may be less likely to decrease height, however, the modulation of norepinephrine and dopamine (via reuptake inhibition) by psychostimulants is also associated with stunted growth. (R)

An antidepressant like bupropion (norepinephrine/dopamine-reuptake inhibitor) doesn’t appear to alter growth hormone (GH) secretion in humans – and therefore might be a safer choice for those concerned about growth stunting effects. (R)

However, even with a medication like bupropion, it’s possible that growth stunting could occur via alternative mechanisms similar to how it occurs with psychostimulants (e.g. appetite reduction, lower calorie intake, etc.).

A study by Mansoor et al. (2013) involving 334 adolescents (12-18 years old) with treatment-resistant depression found no significant differences between SSRI users and SNRI users in height gains during a 12-week treatment period. (R)

However, because there was no placebo control, it remains unclear as to whether both SSRIs and SNRIs were stunting growth relative to no treatment in this cohort.

Antidepressants Stunt Growth (Research)

Included below are studies that discussed, evaluated, or attempted to examine the effect of antidepressants on pubertal growth.

2019: SSRIs reduce longitudinal growth in risperidone-treated boys

Calarge et al.: “In risperidone-treated boys, SSRI use is associated with reduced longitudinal growth, particularly in those undergoing puberty.” (R)

Aim: Examine whether SSRIs inhibit longitudinal growth in children and adolescents, particularly in the early stages of puberty, using a sample of convenience comprising risperidone-treated boys.

Sample: Risperidone-treated boys (N=267) aged ~12.7 years – 71% whom had never used an SSRI – contributed to this analysis.

Design: 4 clinic-based studies in risperidone-treated 5-17 year-old males with no general medical conditions were combined for this analysis.

• Anthropometric measurements and psychotropic treatment history were compiled from medical/pharmacy records.
• Linear mixed effects regression analyses determined the association between SSRI use and change in age-sex-specific height and BMI – after adjusting for confounds.

Limitations: Based on data from 4 studies wherein SSRI treatment wasn’t randomized. Preexisting neuropsychiatric disorders (possible that these also interfere with growth – regardless of whether treated). Tanner staging based on genitalia. Risperidone use (most). Psychostimulant use (majority). Combined effect of SSRI x risperidone x psychostimulants. Unknown adherence to treatments. Possible insufficient statistical adjustment. Male-only sample (may not apply to females due to sex-specific metabolic effects).

What were the results?

After adjusting for: age; psychostimulant use; antipsychotic use; and time in the study – both the: (1) duration and (2) cumulative dose – of SSRI medications were inversely associated with height Z-score after age 11 (P < 0.0001).

After adjusting for baseline height, the duration of SSRI use had the strongest inverse association with height Z-score in Tanner stages 3 & 4 boys who used SSRIs continuously.

No association was observed with BMI Z-score.

How significant was the height reduction?

The effect was of a moderate magnitude: approximately 1 cm for every 1 year of treatment with SSRIs during adolescence.

Takeaway: SSRIs might moderately reduce longitudinal growth in pubertal boys. However, the limitations are relatively significant (risperidone use; psychostimulant use; non-randomized).

2017: Body composition in adolescents during treatment with SSRIs

Calarge et al.: “Although the participants only grew by 0.4 cm during the study period, which is to be expected given their age, SSRI use was still found to negatively impact longitudinal growth.” (R)

Aim: Examine the independent effect of depression, anxiety, and SSRI treatment on body composition in older adolescents (ages: 15-20).

Methods: Observe 264 healthy adolescents (15-20 years old) who remained unmedicated or who initiated SSRI therapy – over a ~1.5 year period.

Measures: Psychiatric functioning. Medication treatment. BMI. DEXA scan. Dietary intake. Physical activity.

Limitations: Possibly underpowered to detect a significant effect of depression or anxiety independently of SSRI use. Difficult to accurately determine symptom severity and medication adherence. Self-reports for dietary information and physical activity. SSRI use may be associated with more severe depression – thus making it difficult to know how much of the body composition change is actually from the SSRI.

What were the results?

Depression severity was inversely associated with BMI, fat mass index, and lean BMI.

Cumulative SSRI treatment duration & dose were positively associated with BMI, fat mass index, and lean BMI.

Anxiety severity and diagnosis were not significantly associated with any body composition changes.

Citalopram (Celexa) and escitalopram (Lexapro) were most strongly associated with increases in all body composition measures including visceral fat.

Weaker associations were observed with fluoxetine treatment – and sertraline didn’t differ from unmedicated (i.e. no SSRI) in its effect on body composition.

Did SSRIs significantly stunt growth?

Calarge et al. admitted that although participants grew ~0.4 cm during the ~1.5-year study period (which is to be expected), SSRIs still stunted longitudinal growth (i.e. height).

The strongest association with reduced longitudinal growth was with fluoxetine (Prozac).

Takeaway: SSRIs appear to increase BMI while simultaneously stunting growth.

2005: Fluoxetine for depression relapse prevention

Calarge & Kuperman discussed studies by Emslie et al. (1997) and Nilsson et al. (2004) – in which the effect of fluoxetine on the growth of adolescents was analyzed. (R)

Emslie et al. found zero significant differences in weight or height among fluoxetine users relative to placebo users – which differed from the findings of Nilsson et al.

It was mentioned that the older (average age) fluoxetine recipients in the Emslie et al. study may have led to a misleading conclusion that fluoxetine doesn’t negatively impact growth after 1 year.

Researchers also stated that “rounding” of height measurements by Nilsson et al. (2004) may not have been as big of a limitation as suggested due to the fact that this rounding would’ve been similar across all patients.

Emslie et al. replied to Calarge & Kuperman stating that the group with the longest exposure to fluoxetine contained only 20 patients.

Long-term fluoxetine use in these 20 patients was suggestive of slower height change (P = 0.065).

Emslie et al. emphasized that their findings do NOT demonstrate that fluoxetine doesn’t negatively impact pubertal growth – and they recommend monitoring height/weight in pediatric antidepressant users.

Nonetheless, Emslie et al. further analyzed the height/weight of their sample vs. expected height/weight – and found zero significant differences, however, the sample size was small.

Takeaway: Fluoxetine may cause slower height change – but there’s no strong evidence from this study to support this concept.

2004: Subchronic fluoxetine for MDD in children & adolescents

Nilsson et al.: “Clarification and determination of the clinical significance of the growth-rate reduction seen during fluoxetine treatment requires further investigation.” (R)

Researchers examined the effect of subchronic (i.e. low-dose) fluoxetine treatment in children & adolescents with major depressive disorder (MDD).

96 patients (9-17 years old) received either: (1) fluoxetine 10-60 mg/day (N=49) or (2) placebo (N=47) for a 19-week period.

There were notable differences between fluoxetine and placebo users from baseline in alkaline phosphatase and total cholesterol levels – but there were no significant differences in the rates of abnormal lab values for these markers.

Fluoxetine-treated patients gained significantly less height and weight than placebo users.

Height gain differences

• Fluoxetine height gain (average): ~1.0 cm
• Placebo height gain (average): ~2.1 cm

Weight gain differences

• Fluoxetine weight gain (average): ~1.2 kg
• Placebo weight gain (average): ~2.3 kg

Nilsson et al. concluded that “the growth of child and adolescent patients should be monitored” during treatment with fluoxetine – even at subchronic doses.

Limitations: Height not collected in standardized fashion. Measurements were rounded to the nearest inch (imprecise measurements could’ve skewed findings). Inaccuracies in collection of height data.

Takeaway: Fluoxetine treatment appears able to reduce height during puberty – even when administered for ~4.75 months at a low dose.

2002: Decreased growth during therapy with SSRIs

Weintrob et al.: “A decrease in growth rate, possibly secondary to suppression of growth hormone (GH) secretion may occur during SSRI therapy.” (R)

Aim: Examine growth and growth hormone (GH) secretion in 4 children treated with SSRIs for various psychiatric disorders.

Sample: 4 children (3 boys & 1 girl) ages 11-14 with OCD (obsessive-compulsive disorder) or Tourette syndrome – were evaluated in a “case study.”

Measures: Growth (height & bone age). Pubertal progression. Hormone levels (GH, prolactin, cortisol, free thyroxine).

Methods: Patients received SSRI treatment for 6 months to 5 years (doses: 20-100 mg/d) and all were evaluated at regular intervals for changes in: height, bone age, and puberty progression.

Limitations: Small sample. Mostly boys. OCD & Tourette syndrome may independently affect growth. OCD & Tourette syndrome patients only. Only fluoxetine & fluvoxamine. Other medications used prior to or along with SSRIs (e.g. risperidone, methylphenidate, etc.).

Specific cases

Case #1: 11-year-old girl on fluvoxamine (50 mg/d)

Therapy with fluvoxamine (i.e. Luvox) at a dosage of 50 mg/day was initiated for Tourette syndrome in a girl age 11 years 7 months.

During the 6 months of fluvoxamine treatment, the patient exhibited “growth arrest” despite the concomitant appearance of Tanner stage 2 pubertal signs and consistent weight gain.

Plasma prolactin & thyroid were in the normal range.

Growth hormone (GH) response to clonidine stimulation after estrogen priming was “borderline” at 9.4 ng/mL (413.6 pmol/L)

Insulin-like growth factor-1 (IGF-1) levels were low relative to this patient’s pubertal stage.

Fluvoxamine was discontinued at age 12 years 1 month and normal growth velocity of 6.6 cm/year was resumed.

Growth hormone level evaluation ~4 months after fluvoxamine discontinuation yielded a peak of 18.1 ng/mL (796.4 pmol/L).

Case #2: 13-year-old boy on fluoxetine (80 mg/d)

Therapy with fluoxetine (i.e. Prozac) at a dosage of 80 mg/day was initiated for OCD.

6 months after fluoxetine initiation, the boy exhibited a decrease in growth velocity to 1.4 cm/year followed by complete growth arrest for 4 months (age: 14-14.5 years).

Despite the growth arrest, the boy gained a consistent amount of weight – and was also overweight prior to treatment initiation.

Laboratory examinations revealed normal 24-hour cortisol, prolactin, and thyroid concentrations.

Peak growth hormone (GH) in response to clonidine stimulation was normal but the average 24-hour GH concentrations were low (~1.51 ng/mL) – and IGF-1 levels were also low.

Fluoxetine treatment was discontinued and ~1 month later: (A) GH concentration increased to ~3.18 ng/mL – and (B) IGF-1 levels increased – putting both within normal reference ranges.

After 6 months of fluoxetine cessation, growth velocity increased to 5.1 cm/year and testicular volume increased from 5 mL to 6-8 mL.

Treatment with fluoxetine was reinstated at age 15 years 11 months for 6 months but was subsequently stopped as a result of decreased growth velocity to 3 cm/year.

After fluoxetine cessation, the patient exhibited normal pubertal spurt of 5 to 6 cm/year corresponding to expected height percentile.

Case #3: 12-year-old boy on risperidone (1-1.5 mg/d) & fluvoxamine (100 mg/d)

This patient had been referred to the clinic for short stature and slow growth rate – after having been born small for gestational age at 31 weeks and a birthweight of 900 g.

The patient had taken methylphenidate but switched to a combination of risperidone and fluvoxamine to manage Tourette syndrome.

During 1-year follow-up on risperidone and fluvoxamine combination therapy, the patient exhibited decreased growth velocity from 4.5 cm/year to 2.4 cm/year with consistent weight gain.

Although cortisol, prolactin, and thyroid function were observed – the patient exhibited a subclinical deficit in GH levels and IGF-1 levels relative to pubertal stage.

Treatment with fluvoxamine couldn’t be stopped, however, therapy with somatropin (HGH analogue) was initiated at age 14.5 years which improved growth rate to 12 cm/year.

Case #4: 12-year-old boy on fluoxetine (20 mg/d)

This patient was referred for evaluation after being overweight/obese at age 12 years 9 months.

The patient had previously undergone treatment with methylphenidate (10 mg/d) for ADHD starting at age 7.

Upon referral, the patient was diagnosed with OCD and was treated with fluvoxamine (150 mg/d) but then switched to fluoxetine (20 mg/d).

Treatment with fluoxetine slowed the patient’s growth rate from 5.1 cm/year to 2.6 cm/year – with continuous weight gain.

Thyroid, prolactin, and cortisol concentrations were normal.

Growth hormone (GH) response to clonidine stimulation was suboptimal.

Because fluoxetine couldn’t be stopped, the patient received somatropin therapy at age 14 years 4 months and growth rate increased to 10 cm/year.

What did the authors conclude?

The 4 patients undergoing SSRI therapy exhibited growth attenuation/arrest despite normal weight gain.

The growth reduction was thought to be a byproduct of SSRI-mediated reductions in growth hormone (GH) secretion.

Weintrob et al. believe that SSRIs selectively impair activation of the “somatotrophic axis” by reducing central alpha-2 adrenoreceptor-mediated growth hormone (GH) release.

Somatotrophic axis impairment is further supported by the observed reduction in IGF-1 concentrations with normal weight gain, normal HPA axis function, and no chronic disease.

Excessive cortisol secretion as a cause of growth stunting was dismissed based upon the fact that cortisol levels were within normal ranges.

In 2 patients, growth rate appeared: (1) normal prior to SSRIs, (2) blunted after SSRIs, (3) normal after SSRI discontinuation, and (4) blunted after SSRI reinitiation – indicating a true cause/effect relationship (i.e. SSRIs causing stunted growth).

How significant were the height reductions?

In the patient taking 50 mg/day of fluvoxamine (Luvox) – complete growth arrest was observed from a growth rate of 6.6 cm/year; meaning that the antidepressant slowed growth by 6.6 cm/year.

In a patient on 80 mg/day of fluoxetine (Prozac) – pubertal growth rate decreased to 1.4 cm/year (within 6 months) followed by complete growth arrest (after 1 year).

Discontinuation of fluoxetine in this patient led to growth rate increasing to 5.1 cm/year.

This suggests that high-dose fluoxetine decreased growth rate by 3.7-5.1 cm/year.

In a patient on risperidone and fluvoxamine (100 mg/d) – growth rate decreased by 2.1 cm/year.

And in another patient on standard-dose fluoxetine (20 mg/d), growth rate decreased by 2.5 cm/year.

If we average the reductions in growth rate, we get an average growth reduction of 3.35 cm/year.

Keep in mind that the magnitude of growth stunting from antidepressants is likely contingent upon dosage and duration of use.

If we average the height reductions observed among the 4-person cohort, this yields an average height reduction of ~3.9 cm/year.

Assuming puberty lasts 2-5 years (average timeframe), this would yield a total height reduction ranging from 7.8 cm (3.07 inches) to 19.5 cm (7.68 inches) – along with decreased gonad size (i.e. testicles & ovaries).

Takeaway: SSRIs appear to stunt pubertal growth via interference with GH secretion.

Studies reporting no change in height from antidepressants

Two studies below found zero significant difference in height among fluoxetine users relative to placebo controls.

These studies support the idea that antidepressants do NOT significantly stunt growth during adolescence.

SSRI antidepressants could stunt growth if taken during pregnancy…

Another way in which antidepressants could stunt growth is by way of causing preterm delivery and/or fetal growth restriction.

Toh et al.: “Women treated with SSRIs in late pregnancy had a higher frequency of delivering SGA infants, and women receiving non-SSRI antidepressants were more likely to deliver premature and SGA offsprings.” (R)

• Researchers examined the association between prenatal exposure to antidepressants and: preterm delivery and fetal growth restriction.
• A total of 192 SSRI users & 59 non-SSRI antidepressant users were compared to 5,710 non-users (reference group) between 1998-2008.
• 3% of nonusers exhibited preterm delivery; 8.9% of SSRI users exhibited preterm delivery; and 15.3% of non-SSRI antidepressant users exhibited preterm delivery.
• Rates of delivering SGA (small gestational age) offspring were: 7.2% (nonusers); 10.9% (SSRI users); and 13.6% (non-SSRI antidepressant users).

It was concluded that women treated with SSRIs late in pregnancy had higher rates of delivering SGA infants and non-SSRI antidepressant users were more likely to deliver premature and SGA offspring.

SSRI use by pregnant women – especially later in pregnancy – can cause: preterm delivery; low birth weight; low birth weight for gestational age; gestational hypertension; preeclampsia; and various neonatal complications.

It is known that birth weight and length are strong predictors of adult height. (R)

For this reason, if SSRIs cause low birth weight/length or any other complications in pregnancy/delivery – this could result in stunted growth relative to if SSRIs were not used in pregnancy.

Takeaway: SSRIs may cause preterm delivery and low birth weight/length for gestational age – which would likely stunt growth in adulthood.

Variables that may influence impact of antidepressants on growth

Included below are variables that I hypothesize could determine the significance of a growth stunting effect resulting from antidepressants.

1. Percentage of SSRI & puberty overlap + specific stages of puberty

The percentage of puberty in which a person uses antidepressants and the specific stages of puberty in which antidepressants are used – is likely the biggest determinant of how significantly antidepressants will stunt growth.

Antidepressants used for 100% of puberty will likely yield the greatest growth suppression effect in most cases – whereas antidepressants used for just 5-10% of puberty may not yield a significant amount of growth suppression.

The stages of puberty may also matter to some extent – such that using an antidepressant for 6 months in Stage 1 or 2 of puberty might have a less significant impact on height development than using antidepressants for 6 months in Stage 3 or 4 of puberty.

2. Degree of hormonal change

The degree to which antidepressants alter hormones will likely determine the extent to which they alter pubertal growth.

Growth hormone (GH)

• Antidepressants seem to significantly reduce concentrations of growth hormone (GH) in many users.
• The greater the extent to which antidepressants reduce growth hormone – the stronger the height reduction effect.

Insulin-like growth factor-1 (IGF-1)

• Antidepressants seem to significantly reduce concentrations of IGF-1 (likely secondary to GH reduction) in many users.
• The greater the extent to which antidepressants reduce IGF-1 – the stronger the height reduction effect.

Even antidepressants don’t significantly throw GH and/or IGF-1 out of one’s “normal reference range” does not necessarily mean that levels were not reduced from the antidepressant.

For this reason, I would personally track levels before treatment and then again during treatment to gauge the average/approximate drop – then use exogenous somatropin to optimize levels.

3. Antidepressant specifics

The specifics of antidepressant therapy will likely influence the degree to which a growth stunting effect is likely to occur.

Dosage (potency)

• The higher the dosage of an antidepressant used – the greater the potential it has to disrupt puberty.
• Why? Higher doses exert a stronger physiological modulatory effect and thus should be expected to stunt growth more substantially than lower doses in most cases (particularly for SSRIs).

Specific medication

• Fluoxetine has been suggested by some researchers have a more significant growth stunting effect than other SSRIs.
• (Whether this is actually true remains unclear due to lack of quality head-to-head studies in pediatrics.)

Mechanism of action

• The specific mechanism of action exerted by the antidepressant that’s being used will determine whether growth stunting occurs.
• Medications that inhibit the reuptake of serotonin (SSRIs & SNRIs) as a primary mechanism of action probably have greater growth stunting potential than other agents.

4. Use of other substances

Various hormones, prescription medications, OTC medications, illicit substances, alcohol/nicotine, dietary supplements, etc. – may: (1) potentiate the effect of antidepressants on stunting growth; (2) offset the effect of antidepressants on stunting growth; or (3) have no potentiation/attenuation effect.

Potentiators: Certain substances might amplify the growth suppression effect of antidepressants during puberty.

This could be due to induction of independent growth suppression separate from the antidepressant or some synergistic effect.

For example: Nicotine may stunt growth if done during puberty via acting directly on growth plate chondrocytes (a mechanism that’s independent of SSRIs). (R)

Therefore, someone that ingests nicotine regularly and takes an SSRI may end up smaller than simply using either agent as a standalone.

Attenuators: Certain substances might attenuate the growth suppression effect of antidepressants during puberty.

This would be due to offsetting (i.e. cancelling out) the mechanisms by which antidepressants stunt growth OR by overriding (i.e. overpowering) the stunting effect induced by SSRIs.

Administration of growth hormone (GH), gonadotropin-releasing hormone (GnRH), and/or selective aromatase inhibitors – may increase or optimize pubertal growth such that any stunting of growth by antidepressants is overridden. (R)

Note: Other substances that induce growth may not necessarily attenuate the growth stunting mechanisms of antidepressants – but may simply override it via independent mechanisms.

5. Individual user

The effect of antidepressants on growth may vary between users – such that one person may end up with a significant “growth stunting” effect and another may end up with zero stunted growth despite being on the same drug at the same dosage for the same duration of puberty.

• Genetics: Genetics may dictate the degree to which growth ends up stunted during puberty as a result of antidepressant use. Additionally, genes that influence CYP450 enzyme metabolism of various antidepressants could determine the potency of antidepressant action and subsequent effect on hormones.
• Diet & nutrition: Diet and nutrition can play a role in influencing puberty. Someone with a suboptimal diet and/or malnutrition may experience greater height stunting than a person with nutritional adequacy.
• Hormones: Concentrations of certain hormones (mediated by genetics, environment, diet, sleep, and antidepressant use) can influence whether height ends up altered significantly as a result of antidepressants.
• Body size/composition: Being underweight, skinny fat, and/or overweight/obese may compromise final height development in puberty for some individuals for a variety of reasons. It may also influence the effect of antidepressants on physiology when considering dose to size/weight ratio.
• Sex: Antidepressants seem to have sex-specific effects on neuroendocrinology (e.g. hormones). It’s possible that females are less affected than males by antidepressants during puberty (or vice-versa).
• Lifestyle: A person’s lifestyle including: stress levels, stress management, sleep quality/quantity, exercise habits, social life, etc. – may all influence puberty to some extent. Lifestyle could somehow influence the degree to which antidepressants stunt growth.
• Medical conditions: Certain medical conditions might amplify or attenuate the effect of antidepressants on height. Why? Various medical conditions can alter aspects of physiology (e.g. hormones) and influence puberty.
• General health: A person’s general health (usually determined by lifestyle, environment, & genetics) can influence pubertal development and possibly how one’s physiology reacts to antidepressants during puberty.

Untreated psychiatric disorders may stunt growth?

Any untreated neuropsychiatric disorders have the potential to affect puberty via: (1) abnormal physiology and/or (2) downstream behavioral effects (e.g. undereating & malnutrition).

It’s theoretically possible that antidepressants help “normalize” abnormal physiology resulting from excessive anxiety and/or depression that would’ve otherwise significantly altered pubertal growth.

That said, in pediatrics treated with SSRIs for OCD – it seems as though height gains were significantly greater off of the SSRI (with abnormal OCD physiology) than on the SSRIs.

Anxiety & psychological stress

High anxiety and/or stress may interfere with puberty to some extent and alter: neurotransmitters, hormones, and epigenetics – all of which could reduce adult height.

Stress can cause chronic activation of the HPA axis and result in hyposecretion of growth hormone (i.e. low GH) and elevated glucocorticoids (which inhibit the effect of GH on tissues). (R)

Excess stress may also cause a person to: (A) undereat such that they develop malnutrition and low BMI (both of which can compromise pubertal height development) and/or (B) get poor sleep quality/quantity (which could also affect hormones and pubertal outcomes).

Sheppard et al. (2015) state that early childhood familial disruption (a significant stressor) is associated with shorter adult height for men. (R)

Major depressive disorder

There hasn’t been any significant research examining the relationship between major depressive disorder (MDD) and pubertal growth outcomes.

It’s theoretically possible that pathophysiological underpinnings of depressive disorders somehow interfere with optimal growth & development during puberty.

For example, if one’s depression is associated with high psychological stress and overactivation of the HPA axis – this could yield: suboptimal levels of GH secretion and subsequent interaction between GH and bodily tissue.

Depression is understood to cause some individuals to chronically undereat (such that they become malnourished or have a low BMI/body fat %) – and this could certainly compromise pubertal development. (R)

Depression may also result in suboptimal sleep quality/quantity – such as undersleeping, broken sleep, and/or oversleeping – all of which might affect hormones, epigenetics, and other aspects of physiology in ways that stunt growth during puberty.

Untreated psychiatric disorders may result in suicide…

There is some research suggesting that antidepressants may actually increase suicide rates in young people (age 10-19). (R)

However, many adolescents who use antidepressants find them beneficial – as most do not tend to use medications that aren’t providing any significant benefit (or that are doing harm).

For this reason, I think we can all agree on the fact that if: (1) antidepressants are legitimately helping treat one’s neuropsychiatric condition – then: (2) any moderate stunting of growth is preferable to potential suicide.

Suicide is the second-leading cause of death in young adults (10-24) accounting for 16.8% of all deaths. (R)

Additionally, untreated neuropsychiatric disorders may result in unnecessary suffering & productivity losses – particularly if antidepressants prove to be an effective intervention.

How to avoid growth suppression from antidepressants during puberty…

There is relatively convincing evidence that serotonergic antidepressants (SSRIs) inhibit the secretion of growth hormone (GH) which subsequently lowers IGF-1.

If you’re concerned about “stunted growth” from antidepressant therapy during puberty – talk to a medical doctor and determine potential alternative interventions and/or workarounds (e.g. somatropin).

Avoid antidepressants if possible (during puberty)

Antidepressants should be avoided whenever possible during critical growth years.

When I say “whenever possible” I mean that if safe alternative interventions can manage underlying neuropsychiatric disorders – these should be utilized.

Explore all non-pharmacological treatments for neuropsychiatric disorders such as CBT (cognitive behavioral therapy), physical exercise, circadian rhythm management, nutrient-dense diet, exposure therapy, mindfulness-based stress reduction, etc.

Consider trying various low-risk dietary supplements that may help with neuropsychiatric disorders such as:

• High-dose omega-3 fatty acids
• Creatine monohydrate
• Taurine
• L-Theanine
• Ashwagandha
• Magnesium threonate
• Glutathione (or NAC)
• L-methylfolate
• Lithium orotate
• Chamomile extract
• Alpha lipoic acid
• SAM-e
• Vitamin D
• Physiologic dose melatonin
• Multivitamin
• Probiotics

Do not assume that natural supplements won’t affect pubertal growth in some way – it’s possible that some of these could also stunt growth.

Never use any dietary supplement without first confirming safety and appropriate dosing with a medical doctor and/or pharmacist.

Keep in mind that certain supplements may be better for depression, others may be better for anxiety, and others may be better for less common conditions like OCD, etc.

Note: The above supplements contain affiliate links wherein I earn a commission. The cost is the same either way and you can help support the site if you benefitted from the content.

Lowest effective antidepressant dosage

If antidepressants are necessary (which they will be in a subset of patients) – medical doctors should be using the minimal effective dose of these agents to manage the neuropsychiatric condition(s) being treated.

Specifically, medical doctors may want to start patients on an atypically low dose – gauge responsiveness and gradually titrate upwards until the patient reports an “effect” (positive or negative).

Assuming a positive effect (i.e. adequate symptom reduction) is reported from a dose – the dosage should remain locked and not increase.

By using the lowest necessary dose of an antidepressant – this reduces overall physiologic impact of antidepressants and will likely have a less significant effect on puberty than higher doses.

Unnecessarily high doses of antidepressants elicit a more pronounced effect on physiology wherein concentrations of growth hormone (GH) and IGF-1 may decrease more substantially to yield a greater growth stunting effect.

Evidence suggests that higher doses of antidepressants are associated with more significant growth stunting.

Don’t use antidepressants for longer than needed

The duration of antidepressant usage during puberty is associated with magnitude of growth reduction.

Individuals who use antidepressants for a longer-term during puberty may end up with more significant stunting of growth relative to those who use antidepressants for only a short-term during puberty.

If a medical doctor and/or patient believes it is prudent to stop antidepressants because they aren’t providing significant benefit and/or alternative management strategies for a specific neuropsychiatric condition are proving effective – then they should be discontinued.

Discontinuation of antidepressants should be done with extreme caution and under the supervision/guidance of a psychiatrist.

Evaluate hormone levels

It is recommended to evaluate: growth hormone (GH) and insulin-like growth factor-1 (IGF-1) before and during antidepressant therapy (i.e. at baseline).

Medical doctors may want to determine whether a specific antidepressant and/or antidepressant dosage is reducing GH and/or IGF-1 significantly enough to potentially affect puberty in a patient.

If GH and/or IGF-1 levels plummet substantially after antidepressant therapy – it may be wise to switch to a different treatment option (one that might not affect these hormones at all OR one that affects these hormones to a lesser extent).

Additionally, if GH and/or IGF-1 levels plummet too significantly such that they are way below average reference range in one’s particular stage of pubertal development – then perhaps antidepressant therapy might be considered too harmful for the patient.

HGH treatment (Somatropin)

Assuming that an individual needs an antidepressant during critical stages of pubertal development to maintain normative neuropsychiatric health, it may be useful to prescribe exogenous GH (e.g. Somatropin) and/or IGF-1.

The aim when prescribing exogenous GH and/or IGF-1 should be to increase GH and/or IGF-1 to “normal levels” from an antidepressant-mediated deficiency.

A study by Lundberg et al. (2015) reported that giving high GH doses during puberty was associated with an increase in IGF-1 and a dose-dependent gain in height.

Knowing this, one might hypothesize that simply supplementing with exogenous GH during puberty (to get GH within a healthy reference range) should theoretically boost deficient IGF-1 (resulting from antidepressants) to counteract any potential growth stunting. (R)

Healthy habits

Diet: It is recommended to consume a macronutrient and micronutrient adequate diet during puberty. Lack of calories, deficiencies in key macronutrients, and/or deficits in critical macronutrients – could potentially stunt growth.

Sleep: Teens should strive to get adequate quality sleep on a regular basis during puberty. Poor sleep quality and/or insufficient sleep duration could hinder pubertal growth/development.

Stress management: Excessive stress may interfere with sleep, hormone concentrations, and could ultimately impair pubertal growth/development.

Exercise: Regular physical exercise can help treat neuropsychiatric disorders but also improve sleep, hormone profiles, body composition, etc. Therefore, it should be recommended to exercise regularly during puberty (both cardio & resistance training).

BMI & body fat management: Low BMI & body fat % could interfere with normal pubertal development and height growth. High BMI & body fat % could also possibly interfere with aspects of pubertal development and height growth. It is recommended to maintain a normal/healthy BMI and body fat % during antidepressant treatment for optimizing growth in puberty.

Do I think antidepressants stunted my growth?

Probably to a small degree. As a teenager I had high anxiety with mild OCD – and still have high anxiety at times.

I was initially put on an SSRI medication that worked very well, but it stopped working ~6-8 months after treatment initiation and no other medication(s) worked thereafter.

I was kept on this medication despite its loss of effect – and eventually quit it after ~1 year.

A psychiatrist had me try other medications for ~1 year before I decided to stop seeking psychiatric help – as it caused significantly more harm than benefit (I was in a far worse position mentally than pre-medication).

Alprazolam helped to some extent with anxiety – but it caused significant cognitive impairment and dependence such that I needed to eventually discontinue.

Despite using SSRI antidepressants from age ~14-16 – I ended up slightly taller than both of my parents and above the national average height.

Would I use antidepressants again during my teens knowing what I know about them?

Probably not – but I was between a rock (not trying anything and feeling miserable) and a hard place (trying meds and potentially benefitting – but also potentially feeling even worse).

None of my siblings used antidepressants and all ended up taller than myself – so this may be some evidence to support the general idea (even though we’d technically need an identical twin of myself to accurately confirm this “stunting” effect).

I suspect I may have grown 1-2 inches taller than I currently am (had I not used antidepressants), but I have no way of confirming this.

Moreover, at the time, no psychiatrists/doctors were aware of a possible growth stunting effect from antidepressants (such that somatropin could’ve been used to mitigate risk).

Did you take antidepressants during puberty?

If you took antidepressants during puberty, below are some questions you could answer for the sake of conversation/discussion in the comments section.

Keep in mind that comments are anecdotes and do NOT prove whether antidepressants significantly affected pubertal height in any way.

Also understand that even among those who used antidepressants and grew to be taller than average or the “tallest” in the family – it’s possible antidepressants still stunted height relative to maximum height potential for these individuals.

• What specific antidepressant(s) did you use during puberty? (Did you take any other medications in addition to these antidepressants?)
• If you took antidepressants during puberty – how many years of puberty did you use them and what were the respective dosages?
• Do you think antidepressants affected your overall height?
• If any of your siblings did NOT use antidepressants during puberty – did they end up taller than you?
• Are you as tall as either of your parents? (Both of your parents?)