Turkesterone

Ingredient Overview

Turkesterone is a naturally occurring plant-derived steroid belonging to the class of phytoecdysteroids. These compounds are analogues of the molting hormones (ecdysteroids) found in insects, but in plants they act as defensive molecules against herbivores¹. Turkesterone was first isolated in 1975 from the Eurasian herb Ajuga turkestanica (Regel) Briq., a plant rich in ecdysteroid compounds². Chemically, turkesterone is a polyhydroxylated cholesterol derivative, sharing a common four-ring steroid backbone with other ecdysteroids³. It gained scientific attention in the 1970s and 1980s when Soviet researchers explored extracts of A. turkestanica for their potential to improve physical performance, although turkesterone itself is not an anabolic-androgenic steroid². Today, turkesterone is marketed as a dietary supplement ingredient, valued in sports nutrition for its purported effects on muscle protein synthesis (despite a lack of official health claims or approvals)¹. Importantly, it is not classified as an essential vitamin or nutrient in humans, but rather as a novel bioactive food compound.

Chemical Classification and Structure

Figure: Chemical structure of turkesterone, a polyhydroxylated steroid (C₂₇H₄₄O₈) with a cyclopentanoperhydrophenanthrene core. This structure features multiple hydroxyl (–OH) groups attached to the steroid backbone, distinguishing turkesterone and related ecdysteroids from the less-hydroxylated animal steroid hormones. Turkesterone is classified as a phytoecdysteroid, meaning it is a plant-produced ecdysteroid. Like other ecdysteroids, its structure is based on a cholestane skeleton (27 carbon atoms) with a β-oriented side chain at C-17³. The IUPAC chemical name of turkesterone illustrates its complexity; in simplified form it can be described as 2,3,11,14,20,22,25-heptahydroxycholest-7-en-6-one (with specific stereochemistry at multiple chiral centers)³. In essence, turkesterone’s structure is similar to the insect molting hormone 20-hydroxyecdysone, except turkesterone contains an additional hydroxyl group at the C-11 position on the steroid nucleus. This high degree of hydroxylation confers a relatively polar character compared to human steroids like testosterone. Turkesterone and its analogues (e.g. 20-hydroxyecdysone, ajugasterone C) all share this general steroidal framework, and collectively over 500 ecdysteroid compounds have been identified in nature⁴⁵. Such compounds are classified separately from mammalian steroids due to their unique structural features and occurrence in non-animal sources.

Dietary Sources

Turkesterone is not synthesized by the human body; it is obtained from natural sources, primarily certain plants. Ajuga turkestanica (also known as Turkestan mint) is the most cited source, as it contains turkesterone as a major constituent in its leaves and stems⁵. Studies indicate that A. turkestanica has a remarkably high concentration of turkesterone – on the order of ten times higher than its content of 20-hydroxyecdysone (another ecdysteroid)⁵. Other plants in the same family and beyond also provide turkesterone or related ecdysteroids. For example, Rhaponticum carthamoides (Maral root) and Cyanotis arachnoidea (a member of the Commelinaceae) are known to produce both 20-hydroxyecdysone and turkesterone as dominant secondary metabolites¹. These species, along with A. turkestanica, have long been used in traditional herbal practices as tonics and adaptogens (i.e. to support physical adaptation and strength), which correlates with their phytoecdysteroid content⁸. Trace amounts of ecdysteroids have even been identified in common foods like spinach (Spinacia oleracea) and quinoa (Chenopodium quinoa), though those foods predominantly contain 20-hydroxyecdysone rather than turkesterone¹. In summary, the natural dietary occurrence of turkesterone is limited to certain herbs and botanical extracts; it does not naturally occur in appreciable quantities in typical food crops aside from these specific ecdysteroid-rich plants. For consumers, turkesterone is usually obtained via supplements standardized to extracts of A. turkestanica or similar botanical sources.

Biochemical Role and Presence in the Body

Turkesterone has no confirmed endogenous role in human or animal physiology – it is not produced by human metabolic processes. In insects, by contrast, ecdysteroids (like ecdysone) serve as hormones controlling molting and development⁹. Humans lack a dedicated “ecdysteroid receptor”; the insect ecdysteroid receptor complex (EcR–USP) is specific to invertebrates⁹. As a result, when turkesterone is ingested by humans, it does not engage any known hormone receptor system in the body in the way that testosterone or estrogen would. Nevertheless, research has explored how turkesterone and related ecdysteroids might exert biological activity in mammals through non-androgen pathways. Notably, experiments indicate that ecdysteroids do not bind to the androgen receptor in muscle tissue, yet they may still enhance protein synthesis via alternative signaling mechanisms⁹. One proposed mechanism is activation of the phosphatidylinositol 3-kinase (PI3K)–Akt signaling pathway in muscle cells, which can upregulate protein synthesis independent of androgen signaling. Some studies have also suggested ecdysteroids could interact with estrogen receptor beta or other nuclear receptors in a modulatory way⁴.

After oral intake, turkesterone is thought to be absorbed from the gut in its intact form (being a moderately polar steroid, it may absorb less efficiently than lipophilic steroids). It can transiently circulate in the bloodstream, but because there is no specific binding protein or receptor for it, turkesterone’s presence in the body is short-lived. Instead, it is treated as a foreign plant-derived compound, subject to metabolic breakdown and excretion (as described below). Importantly, turkesterone is not stored or incorporated into tissues in any significant manner, and there is no physiological requirement for it in the human diet. Its biochemical “role,” insofar as it has one in humans, is limited to the potential modulatory effects on cellular pathways that researchers are currently studying (in contexts like muscle protein synthesis, glucose metabolism, and stress response), with no definitive endogenous function.

Metabolism and Excretion

The metabolism of turkesterone in humans has not been characterized in full detail, but it is presumed to follow pathways similar to other steroidal molecules. Upon ingestion, turkesterone likely undergoes first-pass metabolism in the liver. Phase I metabolic reactions (such as reduction or dehydroxylation) may modify its numerous hydroxyl groups. In fact, analysis of human urine after consumption of ecdysteroid-containing supplements has identified several de-hydroxylated metabolites of ecdysteroids. For example, after 20-hydroxyecdysone intake, researchers reported the appearance of 2-deoxyecdysterone and 14-deoxyecdysone in urine, among other metabolites⁹. By analogy, turkesterone is expected to be metabolized into analogous “deoxy” forms as the body breaks it down. Conjugation reactions (Phase II), such as glucuronidation, could further increase the compound’s water solubility to facilitate excretion.

The primary route of elimination for turkesterone and its metabolites is presumed to be renal (urinary) excretion, as has been observed for related ecdysteroids in metabolism studies⁹. Minor elimination through bile/feces is possible given turkesterone’s sterol-like structure, but data are lacking. Due to rapid metabolism, the half-life of turkesterone in the body is believed to be relatively short—on the order of hours—meaning that most of an ingested dose is metabolized and cleared within a day or two⁹. There is currently no evidence of turkesterone accumulating in tissues or bioactivating into any hormone-like compound. It is effectively treated by the body as a xenobiotic (foreign substance) and eliminated accordingly. This rapid clearance is one reason why turkesterone’s physiological effects in humans, if any, are transient and require continual supplementation to maintain purported activity. It also underpins why turkesterone has not been found to cause long-term changes in hormone levels.

Industrial Production Methods

Turkesterone used in supplements is obtained either by extracting it from natural plant sources or by semi-synthetic production. The most common method is extraction from Ajuga turkestanica or other turkesterone-rich plant material. Industrial extraction typically involves drying the plant and using solvents (such as ethanol or methanol) to dissolve the steroid constituents, followed by filtration and concentration of the extract. Because A. turkestanica yields a mixture of phytoecdysteroids (turkesterone, 20-hydroxyecdysone, etc.), further purification is often done using chromatographic techniques (e.g. high-performance liquid chromatography, HPLC) to isolate turkesterone at high purity⁴. An HPLC method has been validated to simultaneously identify and quantify turkesterone and ecdysterone in dietary supplement products, underscoring the industry’s effort to ensure quality and accurate labeling. In terms of yield, A. turkestanica is prized because turkesterone constitutes a significant fraction of its extractable content – an advantage since many other plants contain only trace amounts.

Nevertheless, extracting pure turkesterone is more challenging and costly than obtaining some more abundant ecdysteroids (like 20-hydroxyecdysone from sources such as Cyanotis or quinoa). This has led to interest in semi-synthesis: for instance, starting with abundant 20-hydroxyecdysone and chemically modifying it to add the C-11 hydroxyl group, thus producing turkesterone. While feasible in laboratory settings, such chemical synthesis is complex due to the molecule’s many chiral centers and functional groups. There are reports of synthesizing various turkesterone derivatives (e.g. 2-acetate or 22-acetate forms) for research purposes. However, a full industrial synthetic route for turkesterone is not widely employed. Instead, cultivation of A. turkestanica and advanced extraction techniques remain the primary production strategy. Producers often standardize the extracts to a certain percentage of turkesterone (for example, 10% turkesterone by weight in an extract), blending it into capsules or powders for supplementation. Throughout production, the emphasis is on maintaining the stability of this relatively heat- and light-sensitive steroid and preventing contamination with other steroids or impurities. The end product is typically a refined plant extract containing turkesterone as the key active ingredient, with purity and content verified by analytical methods.

Regulatory and Historical Background

The discovery of turkesterone in 1975 is credited to Soviet-era scientists who isolated it from Ajuga turkestanica during a search for bioactive compounds in traditional medicinal plants². In the following decades, Eastern European research examined turkesterone and related ecdysteroids for potential uses in agriculture and medicine. By the late 20th century, turkesterone-containing extracts were being used in parts of Asia and Eastern Europe as tonics or “adaptogens.” However, formal regulatory acknowledgment of turkesterone as a dietary ingredient came much later.

Safety and Recommended Dosages

Because turkesterone is not an essential nutrient, there is no recommended daily allowance or dietary requirement. Any “dosage” refers to supplemental use. Supplement manufacturers typically offer turkesterone in doses ranging from about 250 mg to 500 mg per day, often standardized from plant extracts. These dosing practices have been informed by preliminary research and traditional usage, although robust clinical data are sparse. A recent human trial illustrated a typical regimen: healthy adults took 500 mg of turkesterone (as Ajuga extract) daily for 4 weeks, which was reported to be well-tolerated and caused no significant adverse effects or biochemical abnormalities⁷. Notably, in that controlled study, turkesterone supplementation showed no significant difference from placebo in altering body composition over the one-month period⁷, indicating a need for further research on efficacy.

In terms of safety, the available evidence suggests turkesterone has a wide safety margin. Compounds in its class are considered to have low toxicity in mammals. For example, the related ecdysteroid 20-hydroxyecdysone has an oral LD₅₀ in mice exceeding 9 g/kg body weight, indicating extremely low acute toxicity¹⁰. Turkesterone is presumed to share this benign acute toxicity profile. So far, no serious side effects have been documented in animal or human studies using turkesterone at supplement doses. Unlike anabolic-androgenic steroids, it does not seem to cause hormonal disturbances or organ stress at typical doses – one review noted turkesterone’s use has “no reported adverse side effects” in the literature compared to traditional anabolic agents. That said, absence of evidence is not evidence of absolute safety. Users have occasionally reported mild transient effects (e.g. headache or gastrointestinal upset), though it’s unclear if these are attributable to turkesterone or other components of the extracts.

Toxicological studies specifically on turkesterone are limited; therefore, conservative usage is advised. Official agencies have not set any tolerable upper intake level, but some national authorities have issued precautions against its use pending further safety evaluation (as reflected by the EU novel food status). As a prudent measure, many supplement labels recommend not exceeding 1,000 mg per day, and advise discontinuing use if any adverse symptoms occur. In summary, current data indicate that turkesterone at common supplemental doses is likely safe for short-term use in healthy individuals, with a very high lethal dose in animal models and no observed toxicity red flags. However, long-term safety and effects in special populations (such as those with medical conditions, or pregnant/lactating women) remain undocumented. Consumers are therefore urged to use turkesterone responsibly and within suggested limits, pending more comprehensive safety research.

Conclusion

Turkesterone is a distinctive dietary supplement ingredient characterized by its origin in certain exotic plants and its identity as a plant analog of insect steroid hormones. Chemically, it is a heavily hydroxylated sterol that sets it apart from human hormones. This overview has outlined how turkesterone is sourced (primarily from Ajuga herbs), how it behaves in the body (without engaging typical steroid receptors, and being rapidly metabolized and excreted), and how it is currently produced and regulated. While scientific interest in turkesterone’s potential biological activities (such as supporting muscle protein synthesis or stress adaptation) is ongoing, no health claims are established or permitted for this compound under EU law. Turkesterone’s regulatory status as a novel, unapproved food ingredient in Europe highlights the cautious approach taken until safety and efficacy are confirmed.

In practical terms, turkesterone appears to be well-tolerated at usual supplement doses, and its historical use in folk medicine and recent experimental use have not revealed major safety concerns. However, consumers should remain aware that turkesterone is a non-essential, pharmacologically active compound still awaiting comprehensive evaluation. Its role in supplementation should be considered supplementary and experimental, rather than essential to health.

This scientific overview has presented chemical, biochemical, and regulatory context without any health claims. The European Food Safety Authority (EFSA) has not approved any health or physiological claims associated with Turkesterone. Consumers should not interpret this educational information as medical advice or a basis for health decisions. Always consult a healthcare professional before starting dietary supplements or making significant dietary changes. Supplements should complement, not replace, a varied and balanced diet or a healthy lifestyle.

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