DHB & Sodium Valproate

Dihydroboldenone (often abbreviated DHB) is a synthetic anabolic–androgenic steroid derived from boldenone. It is not an approved medical treatment and is typically encountered in underground or experimental contexts. DHB is known for strong androgen receptor (AR) agonism with minimal aromatization to estrogen, and it can significantly suppress the hypothalamic–pituitary–gonadal (HPG) axis. Sodium valproate (valproic acid) is a prescription medication primarily used for epilepsy, bipolar disorder, and migraine prevention. It has broad central nervous system effects, including GABAergic modulation and histone deacetylase (HDAC) inhibition, and it also carries well-established safety concerns (hepatic toxicity, teratogenicity, metabolic effects, and drug interactions).

Because both agents are pharmacologically powerful and act systemically, this combination is not a supplement-level intervention. It represents a high-intensity experimental approach that meaningfully alters endocrine signaling, gene expression, and central nervous system regulation.

In PFS/PSSD/PAS communities, the DHB + sodium valproate combination appears in a small number of recovery anecdotes and protocol discussions. The theoretical rationale described by users combines three proposed targets: (1) strong androgen receptor activation (DHB), (2) epigenetic modulation via HDAC inhibition (valproate), and (3) GABAergic system effects (valproate), which some hypothesize could intersect with pathways implicated in persistent post-drug syndromes. Some write-ups frame this as an attempt to “force a reset” of dysregulated androgen signaling and downstream gene expression. It’s important to emphasize that this rationale is theoretical, extrapolated from known pharmacology rather than validated in controlled studies for PFS/PSSD/PAS.

Anecdotes (Community Reports):

https://youtu.be/v4RxgA9TgEM?si=CuMSzg1Ycp_OLmFM

https://youtu.be/nHn4j6kLfPY?si=4p5uWbKle7hmunLl

https://www.reddit.com/r/PSSD/comments/1hjjirv/remission_story_hormone_protocol_recovery/

https://docs.google.com/document/d/1YWCA7EDjZaYxo8U1YFWii5ISjEOylcAjmxMKiymA5XY/edit?tab=t.0

How to Interpret This Page

This page summarizes community anecdotes and informal observations, not medical evidence. “Improvement” here means a person reported feeling better after trying a substance or protocol; it does not prove causation or predict outcomes for others. Reports are often confounded by multiple simultaneous variables (time, stopping another trigger, dose changes, other medications/supplements, diet/sleep), and reporting bias is common. Some substances mentioned in improvement stories are also linked to severe flares or lasting worsening in other reports. Use this page as a starting point for research and discussion with a licensed clinician—not as medical advice.

Community Reports: Mixed Outcomes & High-Stakes Risk Signal

Within PFS/PSSD/PAS communities, the DHB + sodium valproate protocol appears in a small number of highly visible anecdotes describing major improvement or even “full recovery.” These reports tend to stand out because of their dramatic nature. At the same time, many individuals report no meaningful benefit, and others describe partial, temporary, or unstable improvements that do not persist.

Importantly, there are also reports of significant harm, including severe hormonal suppression, neuropsychiatric destabilization, prolonged crashes, and difficulty returning to baseline after stopping. Because these accounts involve extreme interventions, complex timing, underground sourcing, and multiple uncontrolled variables, they should be interpreted as signals of experimentation rather than evidence of efficacy.

Across reports, outcomes appear highly polarized—ranging from dramatic improvement to serious worsening—with relatively few neutral or predictable responses. This clustering at the extremes has led many community members to describe the protocol as high-risk and high-uncertainty, rather than a reproducible or broadly applicable approach.

Given the pharmacology involved, this volatility is not surprising. DHB can profoundly suppress endogenous hormone production and carries known anabolic-steroid risks (endocrine suppression, cardiovascular strain, lipid changes, fertility effects). Sodium valproate has a well-established risk profile, including liver toxicity, metabolic effects, cognitive dulling, teratogenicity, and clinically significant drug interactions. Combining the two introduces additional uncertainty, and abrupt changes (initiation, cessation, contamination, or dosing errors) are frequently cited in worsening anecdotes.

For these reasons, many in the community explicitly frame this protocol as a last-resort or do-not-attempt category, rather than something to trial casually or without close medical supervision.

Evidence Basis

Established pharmacology and safety literature on anabolic–androgenic steroids and sodium valproate; mechanistic discussions involving androgen receptor signaling, HDAC inhibition, and GABA modulation; anecdotal community reports (online forums, self-reports).
No controlled studies demonstrate safety or efficacy of this protocol for PFS/PSSD/PAS.