Testosterone and Aggression in Dogs - Separating Facts from Myths

1. Testosterone: A Brief Neuroendocrine Primer

1.1 Two Pathways of Action

Testosterone is a steroid hormone produced mainly in the Leydig cells of the testes, with smaller amounts from the adrenal glands in both sexes and the ovaries in females. It acts through two routes: a genomic pathway, binding androgen receptors to change gene expression over hours to days; and a non-genomic pathway, acting rapidly on cell membranes or – importantly – being converted to estradiol by the enzyme aromatase, altering neuronal excitability and neurotransmitter release (part of the wider neurochemistry shaping behavior). That aromatase route matters, because some of testosterone's behavioral effects may actually be estrogen effects.

1.2 Organizational versus Activational Effects

Testosterone rises during sexual maturation, but the timing, magnitude, and behavioral significance of that rise vary considerably across individuals, breeds, and developmental trajectories. A two-stage organizational–activational framework explains why castration cannot fully control sexually dimorphic behavior: prenatal testosterone has already organized certain brain structures, and removing circulating testosterone later cannot reverse that established wiring – it can only remove the ongoing activational signal (much of this laid down during early development).

2. Testosterone and Aggression: A Modulatory, Not Causal, Role

2.1 A Weak Baseline Association

Studies comparing baseline testosterone in aggressive versus non-aggressive dogs yield mixed results. Dominant or aggressive individuals tend to show somewhat higher plasma testosterone, but the association is far from universal (Knol, 1989) (and the "dominance" framing itself is scientifically unsound). Crucially, correlation is not causation: higher testosterone in aggressive dogs could be a consequence rather than a cause, since aggressive encounters acutely elevate testosterone – a feedback loop easily mistaken for a stable trait difference.

2.2 Testosterone as a Behavioral Amplifier

A more accurate framework treats testosterone as a modulator that can help bring about or escalate an aggressive state rather than cause it. Compared with a neutered dog, an intact dog may react more readily, escalate faster, plateau at a higher level of reactivity, return to baseline more slowly, and possibly sit at a higher baseline overall (lowering the threshold of an already-aroused nervous system). This reframes testosterone from "cause" to "amplifier" – it lowers the threshold for aggression without being necessary or sufficient for it.

2.3 Non-Genomic Mechanisms and the Amygdala

A dog-specific study examined androgen receptors in the basolateral amygdala of pathologically aggressive dogs, finding significantly more AR-positive neurons in aggressive dogs – yet concluding that genomic androgen-receptor actions are of minor importance, and that the aromatase pathway (testosterone → estradiol) is likely a major route by which testosterone acts within the amygdala (Jacobs et al., 2006). The implication is significant: if much of testosterone's effect works through conversion to estradiol, models focused solely on androgen-receptor blockade or testosterone removal may miss the mark, and estrogen deserves more attention in aggression than it has received. This is a single, small canine study, so its aromatase conclusion is suggestive rather than definitive – but it points clearly away from a simple "testosterone → androgen receptor → aggression" story.

3. Acute versus Chronic Effects: Timing Matters

3.1 Acute Testosterone Fluctuations

Testosterone can shift rapidly with social challenge: a male meeting a rival may show a transient rise that facilitates escalated responding in that moment – adaptive, in that it prepares for conflict without requiring chronically high levels. Clinically, transient flare-ups after GnRH-agonist (e.g., deslorelin) implantation have been reported, with short-term testosterone increases sometimes associated with a temporary worsening of intraspecific aggression, particularly in dogs with pre-existing aggressive tendencies.

3.2 Chronic Exposure

Chronic elevation may have different, more organizational effects, but in dogs the correlation between baseline testosterone and aggression is relatively weak – so chronic levels alone are poor predictors of aggressive behavior. Hormonal status appears to influence how a dog responds to frustration – a key trigger for many forms of aggression – more than it dictates aggression directly.

4. Proactive versus Reactive Aggression: Differential Involvement

Not all aggression is alike. Behavioral neuroscience distinguishes proactive (instrumental, goal-directed, low-arousal) from reactive (affective, fear-driven, high-arousal) aggression, and these have different neurobiology and different relationships to testosterone.

4.1 Proactive Aggression: Testosterone-Associated

Proactive aggression – resource guarding, territorial defense, inter-male conflict – is more likely to be testosterone-influenced, consistent with castration reducing inter-male aggression in roughly 60–75% of cases. A foundational survey found inter-male aggression reduced by neutering in about 60% of dogs, with rapid reduction in 25% and gradual reduction in 35% (Hart & Eckstein, 1997), and a companion study found roughly a quarter of dogs aggressive toward people or other household dogs showed 50–90% improvement after gonadectomy (Neilson et al., 1997). Even here, though, testosterone is not the whole story: marking, mounting, and fighting are complex behaviors with a substantial learning component that castration will not undo.

4.2 Reactive Aggression: Minimal Testosterone Involvement

Reactive aggression – impulsive, emotional, triggered by perceived threat or frustration, and marked by high arousal, fear, and anxiety – appears far less testosterone-dependent, and may even increase after castration in some individuals (the neurological picture of the reactive dog). Some evidence suggests neutering raises the risk of fear, anxiety, and panic responses in certain dogs and contexts, including increased fearfulness toward unfamiliar people and dogs and higher rates of sound phobias (the neurobiology of which castration does not address).

4.3 Implications for Clinical Practice

The upshot is directional: castration is more likely to help with proactive aggression (inter-male, territorial, sexually motivated) and less likely to help – or may be counterproductive – with reactive, fear-based aggression. Even for the responsive types, fewer than a third of dogs can be expected to show marked improvement (Neilson et al., 1997).

5. The Behavioral Effects of Castration: A Complex Picture

A 2025 review concluded that the existing research on neutering, in both behavior and health, remains inconclusive and sometimes conflicting (Arroube & Pereira, 2025) – a fair summary of the whole field.

5.1 What Castration Consistently Reduces

Castration reliably reduces behaviors tied to sexual dimorphism and male reproduction. In the classic study, roaming fell by about 90%, inter-male aggression by roughly 75%, urine marking by about 60%, and mounting by about 80% (Hopkins et al., 1976). These are the behaviors most directly under hormonal control – though it is worth noting these often-cited figures come from a single, decades-old study.

5.2 What Castration Does Not Consistently Change

Other behaviors respond inconsistently or minimally: aggression toward familiar humans (often no change or minimal improvement), fear-based aggression (may increase), learned aggressive behaviors (persisting through reinforcement history regardless of hormones), and territorial aggression toward strangers. One large questionnaire study found that owner expectation and context shaped perceived outcomes – aggression was reported to decrease in dogs castrated to correct unwanted behavior but to increase in dogs castrated for other reasons (Roulaux et al., 2020), a reminder that perception and biology are entangled in this literature.

5.3 Potential Negative Behavioral Effects

Most concerning for behaviorally challenged dogs, castration has been associated in some studies with increases in fear, anxiety, panic responses, sound phobias, and fearfulness toward strangers and unfamiliar dogs. For dogs with fear-based reactivity, removing testosterone may destabilize rather than settle the nervous system – consistent with the idea that gonadal hormones also have stabilizing effects, so that too little testosterone can leave some dogs more anxious or insecure (and chronic stress compounds this). These findings directly challenge the assumption that castration is universally good for behavior.

6. The Influence of Developmental Timing

The age at castration has emerged as a critical variable. A large study of over 6,000 male dogs found that timing of castration, and lifetime exposure to gonadal hormones, was associated with numerous behavioral differences – with longer hormone exposure linked to reduced reporting of many unwelcome behaviors, including several related to fear and aggression (McGreevy et al., 2018).

6.1 Early Castration (Before 6 Months)

Early castration has been associated with increased behavioral risk: in one breed-specific study, Vizslas gonadectomized before six months showed higher rates of behavioral disorders than intact dogs (Zink et al., 2014). Separately, females neutered at five to ten months responded with significantly greater aggression to approaching strangers and dogs five months later than their intact littermates.

6.2 Castration Between 7 and 12 Months

This window shows a mixed picture: dogs neutered at 7–12 months were slightly more likely to show moderate-to-strong aggression toward strangers in one study, while other analyses found no clear connection between neutering and aggression toward familiar people or dogs once triggering factors were accounted for.

6.3 Castration After 12 Months

Limited evidence suggests later castration may carry fewer negative behavioral outcomes, with dogs neutered at 13–18 months closest to intact dogs in aggression levels. But the evidence base is thin – a 2023 scoping review concluded there is a lack of evidence on how neutering bitches before versus after puberty affects behavior.

6.4 The Two-Phase Testosterone Surge

The timing effects make sense in light of two testosterone surges: a prenatal surge that organizes male-typical brain structures, and an adolescent surge that activates them. Castration before the second surge prevents activation but cannot reverse prenatal organization; castration after it removes circulating testosterone but cannot erase behaviors already learned and practiced. This is why castration works better before sexually dimorphic behaviors are fully expressed, yet never fully eliminates established, rehearsed behaviors.

7. Beyond Testosterone: The Multifactorial Nature of Aggression

The most important conclusion in the literature is that testosterone alone is a poor predictor of aggression, which is a complex, multifactorial phenotype.

7.1 Genetic Contributions

Several genes have been associated with aggression-related traits in dogs, including the dopamine receptor DRD4 (part of the dopaminergic system), the oxytocin receptor OXTR (central to social bonding), and serotonin-related genes (SLC6A4, HTR1A, HTR1B, HTR2A) – influencing impulse control, social behavior, and emotional regulation independently of testosterone (with experience shaping their expression).

7.2 Interactions with Other Hormones and Neurotransmitters

Testosterone does not act alone; its effects are mediated by interaction with cortisol, oxytocin, dopamine, and serotonin (Arroube & Pereira, 2025). The testosterone–serotonin relationship is especially relevant: low serotonin is associated with impulsive aggression across species, and testosterone may modulate aggression partly by influencing serotonergic function rather than by acting on aggressive motivation directly.

7.3 The Role of Learning and Environment

Perhaps the strongest challenge to hormonal determinism is learning. Aggression, like any behavior, is shaped by reinforcement history: a dog that has successfully used aggression to make threats go away or secure resources has had that behavior reinforced. Removing testosterone may lower the threshold, but it does not erase the learned association – so behavioral modification is required regardless of hormonal status.

8. Challenging Oversimplified Explanations

Three popular myths deserve rejection. Testosterone is not the sole driver: it modulates some aggression (especially proactive, inter-male) but is neither necessary nor sufficient, and neutered dogs can be more aggressive depending on type and individual. Castration is not a universal solution: by removing sexual hormones it creates potential for both benefit and harm, and is no substitute for behavioral assessment, management, and training (Arroube & Pereira, 2025). Aggression is not purely hormonal: genetics, early experience, learning, pain, stress, fear, and environment all contribute (and undiagnosed pain is a far more common contributor than testosterone excess), yet pain is routinely overlooked in favor of hormonal explanations (because behavior is treated as a simple readout of a single cause).

9. Practical Recommendations

For proactive, inter-male aggression, castration is more likely to help (≈60–75% show improvement in inter-male aggression). For reactive, fear-based aggression, castration is less likely to help and may be detrimental, so addressing the underlying fear through behavior modification and, when indicated, medication should take priority. On timing, if castration is elected, early castration (before 6 months) carries increased behavioral risk in some studies, while later castration (after 12 months) may carry fewer negative outcomes – though evidence is limited. Address learned behavior regardless: a dog that has practiced aggression needs systematic desensitization and counter-conditioning irrespective of hormonal status. Assess comprehensively first: rule out pain, fear, anxiety, frustration, and poor socialization before deciding, since for many dogs these matter more than hormones. And consider alternatives: vasectomy or hormone-sparing sterilization prevent reproduction while preserving gonadal hormones, for owners wishing to avoid castration's potential behavioral downsides.

10. Summary: Testosterone Influence and Castration Effect by Aggression Type

Aggression type Testosterone influence Effect of castration     Proactive / inter-male Moderate to high (modulator, not sole cause) Reduction in ≈60–75% of cases   Territorial / resource guarding Low to moderate Variable; may decrease, but strongly shaped by learning history   Reactive / fear-based Low (less than proactive forms) Often unchanged; may increase in some individuals/contexts   Predatory Very low No consistent effect   Redirected / frustration-based Low Unlikely to improve; address underlying frustration

Individual responses vary significantly. Castration is not a substitute for thorough behavioral assessment and targeted behavior modification.

11. Research Gaps and Critical Appraisal

The confidence attached to the overall picture is high; confidence in specific numbers is lower.

Most evidence is owner-questionnaire and correlational. Many studies lack control groups, are cross-sectional rather than longitudinal, rely on subjective owner reports, and do not distinguish aggression types (Arroube & Pereira, 2025) (a measurement problem endemic to behavior research).

Some figures rest on single or dated studies. The classic castration percentages come largely from one 1976 dataset (Hopkins et al., 1976), and the aromatase-pathway conclusion from one small neuroanatomical study (Jacobs et al., 2006).

Timing evidence is uneven. Large datasets exist (McGreevy et al., 2018), but breed-specific and female-specific conclusions are limited, and scoping reviews note a lack of evidence on pre- versus post-pubertal neutering.

Confounds abound. Owner expectation shapes perceived outcomes (Roulaux et al., 2020), and breed, sex, age, and reason-for-neutering all interact (with breed itself a weak predictor of individual behavior).

12. Conclusion

Testosterone plays a role in canine aggression, but a far more nuanced one than popular discourse allows. It is best understood as a behavioral modulator that lowers the threshold for aggressive responding in specific contexts – particularly proactive, inter-male aggression – and is neither the sole cause nor a universal treatment target. Castration reliably reduces sexually dimorphic behaviors such as roaming, mounting, and inter-male aggression, but has minimal effect on – and may even worsen – fear-based and reactive aggression, with developmental timing further shaping outcomes. Clinical decisions should never rest on hormonal assumptions alone; they require full behavioral and medical assessment. Aggression cannot be reduced to a single hormone, but reflects the interaction of genetic predisposition, hormonal modulation, learning history, stress physiology, and environment. Managing it well means embracing that complexity rather than reaching for a convenient but inaccurate simplification – and, often, looking first for the pain, fear, or frustration that a scalpel cannot touch.

Key Insights (Takeaways)

• Testosterone modulates rather than causes aggression: it lowers the threshold and amplifies responses, especially proactive inter-male aggression, but is neither necessary nor sufficient. Baseline testosterone correlates only weakly with aggression, and aggression can itself raise testosterone (correlation, not causation).

• Much of testosterone's amygdala effect may run through conversion to estradiol (aromatase), not the androgen receptor (Jacobs et al., 2006) – so "block the androgen" models may miss the target. This rests on one small canine study, so it is suggestive, not settled.

• Castration reliably reduces sexually dimorphic behaviors – roaming (~90%), inter-male aggression (~75%), marking (~60%), mounting (~80%) (Hopkins et al., 1976) – and improves inter-male aggression in ≈60–75% of dogs (Hart & Eckstein, 1997; Neilson et al., 1997). It does little for, and may worsen, reactive/fear-based aggression.

• Timing matters: early castration (before 6 months) is associated with increased behavioral risk in some studies (Zink et al., 2014), and longer lifetime hormone exposure is linked to fewer unwelcome behaviors (McGreevy et al., 2018). Prenatal "organization" cannot be reversed, and learned aggression persists regardless of hormones.

• Aggression is multifactorial – genes, other hormones and neurotransmitters, learning, pain, fear, and environment (Arroube & Pereira, 2025). Undiagnosed pain is a far more common contributor than testosterone excess. Decide on castration case by case, treat learned behavior directly, and rule out pain and fear first.

References

Arroube, A., & Pereira, A. F. (2025). Dog neuter, yes or no? A summary of the motivations, benefits, and harms, with special emphasis on the behavioral aspect. Animals, 15(7), 1063. https://doi.org/10.3390/ani15071063

Hart, B. L., & Eckstein, R. A. (1997). The role of gonadal hormones in the occurrence of objectionable behaviours in dogs and cats. Applied Animal Behaviour Science, 52(3–4), 331–344. https://doi.org/10.1016/S0168-1591(96)01133-1

Hopkins, S. G., Schubert, T. A., & Hart, B. L. (1976). Castration of adult male dogs: Effects on roaming, aggression, urine marking, and mounting. Journal of the American Veterinary Medical Association, 168(12), 1108–1110.

Jacobs, C., Van Den Broeck, W., & Simoens, P. (2006). Increased number of neurons expressing androgen receptor in the basolateral amygdala of pathologically aggressive dogs. Journal of Veterinary Medicine Series A, 53(7), 334–339. https://doi.org/10.1111/j.1439-0442.2006.00840.x

Knol, B. W. (1989). Androgens, progestagens and agonistic behaviour: A review. Veterinary Quarterly, 11(2), 94–101. https://doi.org/10.1080/01652176.1989.9694204

McGreevy, P. D., Wilson, B., Starling, M. J., & Serpell, J. A. (2018). Behavioural risks in male dogs with minimal lifetime exposure to gonadal hormones may complicate population-control benefits of desexing. PLoS ONE, 13(5), e0196284. https://doi.org/10.1371/journal.pone.0196284

Neilson, J. C., Eckstein, R. A., & Hart, B. L. (1997). Effects of castration on problem behaviors in male dogs with reference to age and duration of behavior. Journal of the American Veterinary Medical Association, 211(2), 180–182. https://doi.org/10.2460/javma.1997.211.02.180

O'Heare, J. (2009). Die Neuropsychologie des Hundes. Animal Learn Verlag.

Roulaux, P. E. M., van Herwijnen, I. R., & Beerda, B. (2020). Self-reports of Dutch dog owners on received professional advice, their opinions on castration and behavioural reasons for castrating male dogs. PLoS ONE, 15(6), e0234917. https://doi.org/10.1371/journal.pone.0234917

Zink, M. C., Farhoody, P., Elser, S. E., Ruffini, L. D., Gibbons, T. A., & Rieger, R. H. (2014). Evaluation of the risk and age of onset of cancer and behavioral disorders in gonadectomized Vizslas. Journal of the American Veterinary Medical Association, 244(3), 309–319. https://doi.org/10.2460/javma.244.3.309