Ingredients7-Keto-DHEA, chemically known as 7-oxo-dehydroepiandrosterone or (3β)-3-hydroxy-androst-5-ene-7,17-dione, is a naturally occurring metabolite of dehydroepiandrosterone (DHEA) with the molecular formula C₁₉H₂₆O₃. The compound is sold under a number of synonymous names in scientific and commercial contexts. 7-Ketodehydroepiandrosterone (7-keto-DHEA) is chemically known under the name 3-acetyl-7-oxo-dehydroepiandrosterone. In supplement labeling and literature, it also appears as 3-desoxy-7-KETO-DHEA, 7-oxo-DHEA, and 7-KETO (a registered trade name). 7-Keto is a registered trade name for the compound 3-acetyl-7-oxo-dehydroepiandrosterone (DHEA), a stabilized form of 7-oxo-DHEA. Once ingested, acetyl-7-oxo-DHEA is cleaved to 7-oxo-DHEA, a DHEA metabolite naturally found in the body.
The compound is a steroidal ketone belonging to the androstane class. Its defining structural feature is a ketone group at the C-7 position of the steroid nucleus — a modification that distinguishes it both from DHEA itself and from sex steroid hormones. The acetylated compound is less susceptible to oxidation during the manufacturing process relative to 7-keto-DHEA and is rapidly converted to 7-keto-DHEA upon ingestion.
7-keto-DHEA is produced naturally in the body from dehydroepiandrosterone (DHEA), a hormone that comes from the adrenal glands located on top of each of the kidneys. DHEA is one of the most abundant circulating steroid hormones in the body. Although 7-keto-DHEA is endogenously synthesized, it is also found in small amounts distributed across various peripheral tissues. Circulating concentrations of 7-oxo-DHEA in healthy adults are low, with free 7-oxo-DHEA ranging from 0.000 to 0.077 ng/mL and sulfate-conjugated forms from 0.107 to 0.803 ng/mL in serum.
Much like its parent hormone, the endogenous production of 7-Keto DHEA is heavily age-dependent. Human blood levels of both DHEA and 7-Keto DHEA peak during early adulthood, typically around age 20 to 25, and then begin a steep, progressive decline. Levels of 7-Keto seem to follow the same pattern over time as those of DHEA: blood concentrations have almost halved by age 50.
7-keto-DHEA is a naturally occurring metabolite of the steroid hormone dehydroepiandrosterone (DHEA) and is marketed as an anti-obesity dietary supplement. It is commercially available primarily as oral capsules or tablets. The most commonly marketed oral supplement form is the acetylated prodrug 3-acetyl-7-oxo-DHEA, which is more stable during manufacturing. The acetylated version of 7-keto-DHEA, designated as 3-acetyl-7-oxo-dehydroepiandrosterone, or the branded ingredient 7-Keto (licensed by Humanetics Corp.), has been the subject of multiple human randomized, placebo-controlled, double-blind studies. The compound is also available in topical cream formulations. When used on the skin, it has been shown to affect hormone levels in men. Oral doses used in clinical research have most commonly ranged from 100 to 200 mg per day.
Unlike many botanical or herbal ingredients with centuries-long documented traditional use, 7-keto-DHEA has no documented pre-modern traditional use because its molecular identity was not established until the late twentieth century. 3-Desoxy-7-Keto-DHEA is an ingredient commonly found in dietary supplements aimed at supporting metabolism, weight management, and overall vitality.
While DHEA itself has a long history of use in traditional and modern medicine for its potential benefits on vitality, energy, and hormonal balance, the specific metabolite 7-keto-DHEA as a distinct supplement entity emerged from scientific research programs in the latter half of the twentieth century. Historically, DHEA and its metabolites have been researched for their potential to influence energy expenditure and body composition. 7-KETO™ DHEA was the subject of research for over a decade at the University of Wisconsin in Madison. The foundational scientific work on DHEA's 7-oxygenated metabolites was published in 1995 by Lardy and colleagues, which classified these compounds as "ergosteroids" — a term coined to describe naturally occurring steroidal compounds with unique non-sex-hormonal physiological activities. The early scientific interest in DHEA and its metabolites was therefore the proximate historical driver of 7-keto-DHEA's emergence as a supplement ingredient, rather than any ethnobotanical or traditional medicinal tradition.
The synthesis of 7-Keto DHEA in the body is a highly specific, two-step enzymatic process. First, DHEA is acted upon by an enzyme called cytochrome P450 7B1 (CYP7B1), and then further processed by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) to produce the 7-Keto metabolite. More precisely, the synthesis of 7-keto-DHEA begins with an irreversible hydroxylation of DHEA at the position C7 by cytochrome P450 7B1 (CYP7B1) under the formation of 7α-hydroxy-dehydroepiandrosterone (7α-OH-DHEA). 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) then catalyzes the interconversion of 7α-OH-DHEA and 7β-hydroxy-dehydroepiandrosterone (7β-OH-DHEA) through a 7-keto-DHEA intermediary.
The initial step involves irreversible 7α-hydroxylation of DHEA catalyzed by cytochrome P450 7B1 (CYP7B1), an enzyme expressed in various tissues including the liver, brain, skin, and intestines. The process is reversible, allowing interconversion with 7β-hydroxy-DHEA via the same enzyme, enabling dynamic equilibrium among these 7-oxygenated DHEA derivatives in target tissues.
Because its molecular structure has already been altered by these enzymes, 7-Keto DHEA cannot be converted back into DHEA, nor can it be metabolized into testosterone or estrogen. This metabolic dead-end is a key pharmacological distinguishing feature compared with DHEA itself. The analysis by isotope ratio mass spectrometry (IRMS) confirmed that there is no formation of DHEA from 7-keto-DHEA.
Unlike DHEA, 7-keto-DHEA is not converted to steroid hormones such as androgen and estrogen. Taking 7-keto-DHEA by mouth or applying it to the skin does not increase the level of steroid hormones in the blood (oral route; as noted above, topical application may affect hormone levels in men). This property has been cited as a theoretical advantage over supplemental DHEA for individuals concerned about androgenic or estrogenic side effects.
The principal biochemical mechanism underlying 7-keto-DHEA's proposed metabolic effects was characterized in a foundational 1995 study by Lardy and colleagues published in the Proceedings of the National Academy of Sciences. Dehydroepiandrosterone (DHEA), an intermediate in the biosynthesis of testosterone and estrogens, exerts several physiological effects not involving the sex hormones. When fed to rats it induces the thermogenic enzymes mitochondrial sn-glycerol-3-phosphate dehydrogenase and cytosolic malic enzyme in their livers. The 7-oxygenated derivatives are active inducers of these thermogenic enzymes in rats, and the 7-oxo derivatives are more active than the parent steroids.
Research at the University of Wisconsin characterized the relative potency of 7-keto-DHEA versus DHEA in stimulating thermogenic enzyme activity. Researchers reported that 7-keto DHEA was 2.5 times more active at increasing fatty acyl CoA oxidase, malic enzyme, and glycerol-3 phosphate dehydrogenase — liver thermogenic enzymes that regulate how well liver cells direct cells to burn fatty acids for energy. Studies have indicated that 7-keto DHEA can increase the thermogenic activity of fatty acyl CoA by 128 percent, malic enzyme by 86 percent, and glycerol-3-phosphate dehydrogenase by 138 percent. (These figures are derived from preclinical/animal studies and have not been replicated directly in human tissue.)
A second proposed mechanism involves competitive inhibition of the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). The primary mechanism through which 7-Keto DHEA exerts its therapeutic effects is its interaction with 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). In human tissues, particularly in the liver, fat cells, and the brain, 11β-HSD1 acts as a reductase. Its main job is to convert inactive cortisone into active cortisol, thereby amplifying glucocorticoid (stress) signaling at the local cellular level. It is proposed that 7-Keto-DHEA may regulate cortisol activity by competitively inhibiting 11β-HSD1, thereby promoting the production of 7β-OH-DHEA instead of active glucocorticoids. This action might counteract the glucocorticoids' effect of reducing uncoupling proteins — proteins that allow protons to flow into the mitochondrial matrix without generating ATP, thus converting energy into heat and enhancing thermogenesis. Additionally, 7-Keto-DHEA could directly increase the levels of these uncoupling proteins, further supporting its role in promoting thermogenesis.
Beyond direct thermogenic enzyme induction, 7-keto-DHEA promotes fat burning by stimulating the fatty acyl CoA oxidase, which is the major enzyme in the oxidation of fatty acids. Fatty acid oxidation may also be enhanced by 7-keto-DHEA, as suggested by an increase in fatty acyl-CoA oxidase activities in animals after ingesting 7-keto-DHEA. These effects have been demonstrated primarily in animal models and in vitro, and their direct translation to humans remains an area of active inquiry.
Preclinical studies highlight immunomodulatory properties of DHEA derivatives, such as 7-oxo-DHEA (7-OD), which restore Th1 responses, limit Treg expansion, and enhance macrophage antimicrobial activity. At the cellular level, immunomodulatory effects include stimulating interleukin-2 production by human lymphocytes in vitro. Researchers think that it may also stimulate the activity and effectiveness of T-lymphocytes. Research indicates that 7-Keto DHEA enhances Th1 immune responses, crucial for fighting tuberculosis. In studies, 7-Keto DHEA treatment improved the function of CD4+ T cells by increasing their proliferation and boosting the production of key cytokines like IFN-γ and TNF-α, which are vital for controlling mycobacterial infection. These immunological findings are largely from preclinical and in vitro models.
7-Keto-DHEA has been commercially advertised as a dietary supplement to support weight loss. The objective of a 2022 systematic review was to summarize the evidence supporting the use of 7-keto-DHEA in overweight and obese populations. The systematic search was conducted in Medline, Embase, Cochrane Library, CINAHL, Web of Science, Scopus, ICTRP, and ClinicalTrials.gov. Reference lists of eligible studies were considered, and authors of relevant studies were contacted. Two authors independently screened the studies against the inclusion criteria and assessed their risk of bias. In total, 4 out of 686 studies were included in the review, and they all held a low risk of bias.
Half of the included studies showed a significant reduction in body weight. One study found a decrease in body fat percentage, and another one reported a decrease in BMI. Two studies stated an increase in resting metabolic rate. Various possible mechanisms in favor of weight loss are discussed; however, with the evidence currently available, no clear answer can be given regarding 7-keto-DHEA and weight loss. Further studies need to be conducted to clarify the efficacy and safety of this drug before it can be recommended for therapeutic use.
The most cited individual human study by Kalman et al. (2000) used a randomized, double-blind, placebo-controlled design. Researchers randomized people who were overweight to receive a supplement containing 100 mg of 7-Keto or a placebo for eight weeks. While the group receiving the 7-Keto supplement lost significantly more weight than those given a placebo, there was no difference in basal metabolic rate (BMR) between the two groups.
A second trial examined a multi-ingredient formula. A natural metabolite of dehydroepiandrosterone (DHEA), 3-acetyl-7-oxo-dehydroepiandrosterone (7-oxo-DHEA), has been shown to be effective in enhancing weight loss when combined with a diet and exercise program. One study assessed the effects of a formula containing 7-oxo-DHEA combined with l-tyrosine, asparagus root extract, choline bitartrate, inositol, copper gluconate, manganese, and potassium iodide (7-Keto Naturalean™) on weight loss, body composition, and basal metabolic rate (BMR) in overweight patients following a weight-reduction diet and exercise regimen. In this prospective, randomized, double-blind, placebo-controlled trial, healthy, overweight adults were given 7-Keto Naturalean (200 mg/d) or a placebo of maltodextrin and followed a calorie-restricted diet (105 kJ/kg) and an exercise program for 8 weeks. Body weight, body composition (by bioelectric impedance), and BMR (by indirect calorimetry) were measured at baseline, week 4, and week 8. While all participants adhered to a reduced-calorie diet and exercised three days per week, those who received the supplement lost significantly more weight (4.8 pounds or 2.2 kg) than people in the placebo group (1.6 pounds or 0.72 kg). Yet, it is unclear whether this effect can be attributed to 7-Keto alone.
A separate short-term study found that 7-Keto increased resting metabolic rate by about 96 calories a day. The catch is that the study only lasted seven days.
Evidence strength assessment: The current evidence is mixed and limited by factors such as small sample sizes, short study durations, and a lack of diversity in the study populations. Research indicated that optimal weight loss results without a decrease in metabolic rate occur in conjunction with exercise and calorie restriction, particularly in overweight or obese individuals. Humanetics Corp., or companies who have established licensing rights with Humanetics Corp., have sponsored most of the published human clinical trials on the ingredient, which is a relevant limitation for assessing independence of the evidence base.
Research has indicated that DHEA administration might be beneficial in terms of neuroprotection against age-related loss of brain functions like learning and memory. Other research suggests that 7-keto-DHEA improves chemically-induced and age-related memory impairment. The foundational data come from a preclinical study: 7-OxoDHEA is far more effective in enhancing memory in old mice than is DHEA. Scientists observed the potential of 7-Keto to improve memory in both young and old mice with memory impairment. The effect was much stronger in young mice, in which 7-Keto completely reversed memory loss.
The DHEA metabolite, 3-acetyl-7-oxo-dehydroepiandrosterone, also known as 7-keto DHEA, is a neuroprotective compound which appears to have benefits as a natural antiglucocorticoid and to improve symptoms of depression, anxiety, trauma, and improve memory and cognitive functioning. However, this characterization is derived largely from patent claims based on case reports, not from placebo-controlled clinical trials.
Evidence strength assessment: Memory and cognitive effects of 7-keto-DHEA are supported primarily by animal (rodent) models and in vitro research. These findings suggest that 7-Keto DHEA could be a valuable agent for investigating human memory enhancement, particularly because it does not convert to sex hormones and thus avoids the hormonal side effects associated with DHEA. No large-scale randomized controlled clinical trials in humans have been published confirming cognitive benefits. Evidence is preliminary and insufficient to draw conclusions in humans.
A published series of five case reports describes 5 women with severe chronic PTSD resulting from severe early abuse who continued to be highly symptomatic despite receiving extensive psychotherapy and years of psychopharmacologic treatment. All 5 of these treatment-resistant patients experienced a rapid and substantial reduction in their trauma and affective symptoms after starting on treatment with 7-keto DHEA. The improvements in these symptoms were both subjective and objective, and also manifested in significant and rapid benefits in vocational and interpersonal functioning.
In a study on post-traumatic stress disorder (PTSD), benefits were observed when patients received 7-keto DHEA at doses ranging from 25 to 150 mg per day. This treatment, given in an open-label trial, was effective for those with PTSD who had resisted multiple previous treatments. The choice of 7-keto DHEA over DHEA was due to its non-aromatizable nature and potentially superior anti-glucocorticoid properties. On the basis of this 2006 open-label case series, a Phase 2, randomized, double-blind, crossover design study with a placebo control was registered to investigate the possible effect of 7-Keto DHEA on decreasing PTSD symptoms in a Veteran population, proposing that the drug would show significant reduction in overall PTSD symptoms, a decrease in physiological stress response, and higher patient-reported quality of life compared to placebo.
Evidence strength assessment: The psychiatric evidence base consists entirely of open-label case reports and patent filings as of the available published literature. This form of DHEA provided rapid, noticeable improvements in PTSD symptoms, suggesting its potential for larger, more rigorous clinical trials. No peer-reviewed randomized controlled trial results for PTSD have been published to date. Evidence is very preliminary.
Clinical studies on 7-keto DHEA have identified three major areas of potential benefit, including weight loss, cognitive function, and immune function. In vitro, immunomodulatory effects include stimulating interleukin-2 production by human lymphocytes. One human study examined elderly subjects: in elderly subjects, 100 mg of 7-Keto taken twice daily improved immune function. Animal studies confirm that it significantly boosts immune response capacity.
Research indicates that 7-Keto DHEA enhances Th1 immune responses, crucial for fighting tuberculosis. In studies, 7-Keto DHEA treatment improved the function of CD4+ T cells by increasing their proliferation and boosting the production of key cytokines like IFN-γ and TNF-α, which are vital for controlling mycobacterial infection.
Evidence strength assessment: The available studies are few, often small in scale, and primarily address metabolic outcomes rather than direct hormonal or immune changes. The immune data are predominantly from in vitro experiments and animal models. Clinical human evidence for immune modulation is limited and based on small studies.
Supplementing with 7-Keto DHEA may help optimize metabolism and improve T3 levels without influencing TSH or T4 levels, improving overall energy and well-being for those with thyroid disorders. Animal research has indicated a role for 7-keto-DHEA in modulating the thermogenic effects of thyroid hormones, but human clinical data specific to thyroid function remain sparse. Most research focuses on its potential to enhance thermogenesis and metabolic rate rather than to influence hormone levels such as testosterone, estrogen, or cortisol.
Evidence strength assessment: Thyroid-related effects of 7-keto-DHEA in humans are a secondary endpoint in small metabolic studies at best, and no dedicated clinical trials have investigated thyroid outcomes. Evidence is insufficient.
Two preclinical animal studies have examined the effect of 7-keto-DHEA on voluntary ethanol intake. Administration of DHEA, a neurosteroid that can negatively modulate the GABA-A receptor, has been shown to decrease voluntary intake of ethanol in rats. In vivo, DHEA can be metabolized to a variety of metabolites, including 7-keto DHEA, a metabolite without the prohormonal effects of DHEA. One study compared the effectiveness of 7-keto DHEA to DHEA for reducing ethanol intake in the same group of rats. Both 10 and 56 mg/kg of 7-keto DHEA significantly reduced the dose of ethanol consumed. The 56-mg/kg dose of 7-keto DHEA was significantly more effective at decreasing the dose of ethanol consumed than the same dose of DHEA. The fact that 7-ketoDHEA is comparable to DHEA in reducing voluntary ethanol intake has two important implications: 7-ketoDHEA (or related compounds) may have a therapeutic advantage over DHEA for clinical treatment of alcohol abuse and dependence, because it is free of the adverse effects associated with increased production of testosterone and estradiol; and DHEA may exert effects on ethanol intake independently of its role as a hormone precursor.
Evidence strength assessment: These findings are from rodent studies only. No human clinical data are available on 7-keto-DHEA for alcohol use disorder. Evidence is preclinical and exploratory.
The following dosages are those reported directly in the cited scientific studies and trials. No independent dosage recommendations are made here.
The appropriate dose of 7-keto-DHEA for use as treatment depends on several factors such as the user's age, health, and several other conditions. At this time there is not enough scientific information to determine an appropriate range of doses for 7-keto-DHEA.
The safety profile of 7-keto-DHEA appears to be generally well-tolerated with a low side-effect profile, but changes in blood hormone parameters have been reported. In the escalating-dose human study, no adverse treatment-related effects were seen in adult men given 200 mg/day (100 mg twice daily) of 7-Keto for 28 days. Safety parameters evaluated at each dose level included measurement of total testosterone, free testosterone, dihydrotestosterone, estradiol, cortisol, thyroxin, and insulin levels, and no clinically significant alterations in these parameters were observed at studied doses. Mild adverse effects that have been reported in some subjects include heartburn, nausea, or a metallic taste.
Several small studies have shown that 7-keto DHEA does not convert to sex hormones, which differentiates it from DHEA itself, and may make it a safer alternative for those concerned about hormonal side effects. This is a meaningful safety consideration for populations where exogenous sex hormone exposure carries risk (e.g., hormone-sensitive cancers). However, the potential benefits and safety of 7-keto-DHEA, particularly with long-term use, are not established.
The US Food and Drug Administration (FDA) has not added 7-keto-DHEA to the list of bulk drug substances due to a lack of clinical evidence regarding its safety and efficacy. The FDA has not reviewed 7-keto-DHEA for safety and effectiveness. It is sold as an over-the-counter dietary supplement in the United States, where dietary supplements are not required to demonstrate efficacy or safety prior to marketing.
7-keto-DHEA (3β-hydroxy-androst-5-ene-7,17-dione) is included in section S1 of the World Anti-Doping Agency (WADA) List of Prohibited Substances. The detection of its misuse in sports needs special attention, since it is naturally present in urine samples. 7-Keto-DHEA may trigger positive tests for performance-enhancing drugs. The World Anti-Doping Agency (WADA) lists 7-keto-DHEA as a prohibited anabolic agent. Consequently, competitive athletes subject to WADA testing should avoid this supplement.
An additional analytical complication has been identified: some deoxidation reactions, including arimistane formation, were found in metabolic studies and most probably can be linked to the sample preparation or instrumental analysis. This is important when interpreting the results after the application of procedures to detect steroids in urine currently used in antidoping laboratories. Arimistane (androst-3,5-diene-7,17-dione) is itself a distinct prohibited substance, meaning that 7-keto-DHEA use could potentially produce positive tests for more than one banned compound depending on laboratory methods used.
Not enough is known about the use of 7-keto-DHEA during pregnancy and breast-feeding. The conservative recommendation is to avoid use in these populations.
No pharmacokinetic drug-drug interactions for 7-keto-DHEA have been established in peer-reviewed human studies at the time of this writing. While 7-keto DHEA is marketed for adrenal support and claims relating to hormone balance, clinical evidence supporting these claims is sparse and not robust. Given the compound's proposed action on 11β-HSD1 — an enzyme involved in glucocorticoid interconversion — theoretical interactions with corticosteroid medications are plausible but unconfirmed in clinical research. 7-keto DHEA added to selective serotonin reuptake inhibitors (SSRIs) may help compensate for the relative hypogonadism or lower levels of circulating gonadal steroids in premenopausal and postmenopausal women, though this claim is from a patent application and is not supported by a controlled clinical trial.
The FDA has not tested 7-keto-DHEA products to confirm that they contain the ingredients stated on their labels. Some dietary supplements have been tested by third-party organizations to confirm that they contain the ingredients listed on their labels and do not contain any harmful chemicals.
The overall scientific evidence base for 7-keto-DHEA / 3-desoxy-7-KETO-DHEA remains limited. Additional human intervention trials involving 7-keto-DHEA (particularly as a monotherapy) are warranted to substantiate the efficacy of this ingredient for weight management in humans, as well as provide larger understanding of its vast effects in the body. The current research, however, does support a thermogenic effect of 7-keto-DHEA. The body of human clinical evidence consists of a small number of randomized controlled trials (totaling only four studies in the most comprehensive systematic review), with small sample sizes, short durations, and a high degree of industry sponsorship. For cognitive function, immune modulation, PTSD, thyroid effects, and alcohol modulation, evidence remains at the preclinical or very early clinical stage.
Health conditions that 3-desoxy-7-KETO-DHEA may help support.
Body systems that 3-desoxy-7-KETO-DHEA may help support.
Go back