IngredientesChromic chloride, the dietary-supplement form of chromium, is the inorganic trivalent salt of chromium. Its formal systematic name is chromium(III) chloride (also written chromium trichloride). The compound has the CAS number 10025-73-7, the EC number 233-038-3, a molar mass of 158.35 g/mol, and the molecular formula CrCl₃. The hexahydrated form — chromic chloride hexahydrate — is the biologically relevant preparation used in nutritional applications and intravenous solutions. Related terms encountered on dietary supplement labels include "Chr. chloride," "chromic chloride," and "chromic chloride hexahydrate."
In its anhydrous state, chromic chloride is a highly corrosive, blue or greenish to black crystalline solid with a molecular weight of 158.35 g/mol, a melting point of 1,152 °C, and a boiling point (with decomposition) of approximately 1,300 °C. The anhydrous form has very low solubility in pure water, but it dissolves readily in the presence of Cr²⁺ ions. By contrast, the hexahydrate has a density of 1.76 g/cm³, a melting point of 83 °C, and is soluble in water and alcohol.
Chromium is a metallic element whose oxidation states range broadly, but two predominate in nature and commerce. Chromium is a metallic element with oxidation states ranging from chromium(−II) to chromium(+VI), with the trivalent (III) and hexavalent (VI) states being the most predominant. The most stable forms are trivalent chromium [Cr(III)] and hexavalent chromium [Cr(VI)]. These two valence states differ dramatically in toxicology: Cr(VI) is more soluble in water than Cr(III) and 100 times more toxic. Hexavalent chromium is a toxic by-product of stainless steel and the manufacturing industry, harmful to humans, whereas trivalent chromium is the form available in foods and supplements.
Chromium compounds are most stable in the trivalent state under environmental conditions and occur in nature in ores, such as ferrochromite (FeCr₂O₄). The most stable oxidation state of chromium in biological systems is trivalent chromium (Cr³⁺), which forms relatively inert complexes with proteins and nucleic acids.
Dietary supplements contain many forms of chromium, including chromium picolinate, chromium nicotinate, chromium polynicotinate, chromium chloride, and chromium histidinate. Chromic chloride — specifically its hexahydrate — is one of the earliest and most widely used inorganic supplement forms, and it is also used in intravenous (IV) nutritional preparations. Chromium chloride, the form used in many multivitamins, is less well absorbed than organic complexes. Chromium supplements are most frequently available as Cr-III in the chloride or picolinate salt form.
Chromium is an essential mineral that the body needs in trace amounts. It is naturally present in a wide variety of foods, though only in small amounts, and is also available as a supplement. The most concentrated sources are brewer's yeast (not nutritional or torula yeast) and calf liver; two ounces of brewer's yeast or four ounces of calf liver supply between 50 and 60 micrograms (mcg) of chromium. Other good sources include whole grains, beer, and cheese.
Chromium is present in many foods, including meats, grain products, fruits, vegetables, nuts, spices, brewer's yeast, beer, and wine; however, chromium amounts vary widely depending on soil conditions, growing methods, and manufacturing processes. Chromium is also found in drinking water, especially hard water, but concentrations vary widely. Many good sources of chromium, such as whole wheat, are depleted of this mineral during processing. Stainless steel equipment can also transfer chromium to food during processing and cooking.
Dietary intake of chromium cannot be determined reliably because the content of the mineral in foods is affected substantially by agricultural and manufacturing processes and perhaps by contamination when foods are analyzed. Food-composition databases generally provide only approximate values.
The element chromium itself was first isolated in 1798 by the French chemist Nicolas-Louis Vauquelin, who received crystals of crocoite and in 1798 obtained pure chromium metal by heating chromic acid with carbon in a graphite crucible. Its nutritional importance, however, was not recognized until the mid-twentieth century.
In 1957, Schwarz and Mertz observed impaired glucose tolerance in rats fed certain diets and postulated that the condition was due to a deficiency of a new dietary agent, designated the glucose tolerance factor (GTF). The discovery that chromium affected glucose metabolism was formally reported by K. Schwarz and W. Mertz in 1959. Schwarz and Mertz (1959) identified chromium as the element that restored glucose tolerance in rats.
As originally defined, glucose tolerance factor (GTF) is a material absent from Torula yeast that, when fed to rats on a Torula yeast diet, reverses apparent glucose intolerance in those rats. Later, it was shown that chromium is an integral and active part of GTF, the exact structure of which is not well understood, but is believed to contain two nicotinic acid molecules per chromium atom and possibly contains cysteine, glycine, and glutamic acid residues.
However, the GTF concept subsequently became scientifically controversial. Early study equated the term GTF with the chromic ion; later the term was applied to a material extracted and partially purified from brewer's yeast. Those original studies were shown to be methodologically flawed, and the brewer's yeast material was shown to be an artifact. Given the considerable confusion over this name and its history, the terms "glucose tolerance factor" and "GTF" should no longer be used in chromium nutritional and biochemical research.
Impaired glucose tolerance of malnourished infants responded to an oral dose of chromium chloride (Hopkins and Majaj, 1967; Hopkins et al., 1968); subsequently, benefits of chromium chloride were reported in a patient receiving total parenteral nutrition (TPN) (Jeejeebhoy et al., 1977). These early case reports — chromium deficiency states reversed by chromium chloride supplementation — formed the initial clinical basis for interest in chromium as an essential trace mineral.
Chromium is a nutritionally essential trace element; the necessity of dietary chromium was established in 1959 by Schwartz. Chromium depletion is characterized by the disturbance of glucose, lipid and protein metabolism and by a shortened lifespan. Chromium is essential for optimal insulin activity in all known insulin-dependent systems.
Whether trivalent chromium is truly an essential nutrient remains one of the more significant unresolved questions in trace mineral nutrition. The question of whether chromium is truly "essential" is more contested than for most trace minerals. In 2001, the Food and Nutrition Board (FNB) of the National Academies considered chromium essential based on its effects on insulin action and established Adequate Intake (AI) levels; however, subsequent research has challenged this classification.
The essentiality of trivalent chromium is questioned, and its proposed function in the body remains poorly understood. In 2014 the European Food Safety Authority (EFSA) concluded that a dietary requirement — or even an adequate intake — cannot be set for trivalent chromium as no conclusive evidence exists that chromium is essential at any dietary intake. Trivalent chromium appears to have health effects only at pharmacological doses, and a dietary deficiency of the mineral has not been observed.
The US FNB considers it essential (2001), but EFSA concluded in 2014 that there is no convincing evidence of essentiality.
The leading molecular model for how Cr(III) functions in the body centers on a chromium-binding oligopeptide. Chromodulin (also known as low-molecular-weight chromium-binding substance, LMWCr) is a chromium-binding oligopeptide proposed to play a role in insulin signaling and chromium transport in mammals. The LMWCr molecules are aspartate- and glutamate-rich oligopeptides which possess multinuclear chromium assemblies.
The proposed mechanism operates as an autoamplification loop for insulin signaling: based on available evidence, apochromodulin is stored in insulin-sensitive cells. In response to increases in blood insulin concentrations, insulin binds to its receptor, bringing about a conformational change that results in autophosphorylation of tyrosine residues on the internal side of the receptor, transforming the receptor into an active tyrosine kinase. In response to insulin, chromium is moved from the blood to insulin-sensitive cells. The chromium flux results in the loading of apochromodulin with chromium; the holochromodulin then binds to the receptor, presumably assisting in maintaining the receptor in its active conformation and amplifying its kinase activity.
LMWCr does not affect the tyrosine protein kinase activity of rat adipocytic membrane fragments in the absence of insulin; however, insulin-stimulated kinase activity is increased up to 8-fold by the oligopeptide. Using isolated rat insulin receptor, LMWCr has been shown to bind to insulin-activated insulin receptor with a dissociation constant of approximately 250 pM, resulting in an increase in its tyrosine protein kinase activity. This ability is dependent on LMWCr's chromium content.
Importantly, this mechanism has significant limitations: while this model is supported by in vitro studies, this mode of action for chromodulin has not been confirmed to date by in vivo studies. Furthermore, the precise composition and structure of the biologically active form of chromium is not known. One model postulates that trivalent chromium might be the cofactor of LMWCr or chromodulin, which has been shown to play a role in the transport of chromium from the tissues to the bloodstream for ultimate elimination in the urine.
Chromium potentiates the action of insulin both in vivo and in vitro. When chromium is consumed at high levels, such as from dietary supplements, levels of chromodulin in tissues rise; at these high levels, chromodulin is proposed to enhance the cascade of signaling events induced by the binding of insulin to the extracellular α-subunit of the insulin receptor. Upon insulin binding, the tyrosine kinase domain of the intracellular β-subunit becomes activated and causes phosphorylation of tyrosine residues in the β-subunit itself, triggering a series of rapid phosphorylation reactions that activate many downstream effectors, eventually resulting in increased glucose uptake and storage.
In the gastrointestinal tract, chromium acts very much like iron. Different chromium salts as well as different forms of chromium have diverse solubilities that potentially affect absorption. In addition, the amount of chromium in a dose affects absorption, with a lower percentage being absorbed from higher doses.
Chromium has fairly low bioavailability; only 0.4–2.5% of the chromium ingested is absorbed in the intestinal tract, yet the human body contains about 4–6 mg of this trace mineral. The vast majority of chromium is excreted in the urine and feces, up to 0.4 μg/day, with increased excretion in those with diets high in simple carbohydrates.
Chromic chloride is specifically one of the least bioavailable supplement forms. Research suggests that the proportion of chromium absorbed from chromium picolinate is about 1.2%, whereas that from chromium chloride is about 0.4%. Organic forms are better absorbed than inorganic forms. Chromium picolinate and chromium polynicotinate are both better absorbed than chromium chloride; however, the absolute absorption of all forms remains low (generally 0.4–2.5%). Trivalent chromium chloride is not well absorbed, and in vivo toxicity has not been observed.
Several dietary and pharmacological factors modulate chromium absorption: consumption of vitamin C and niacin and intake of insulin and anti-inflammatory drugs appear to increase chromium absorption, whereas intake of antacids and proton pump inhibitors may block chromium absorption or increase excretion. High-sugar diets increase urinary chromium excretion, potentially worsening chromium status.
There was not sufficient evidence to set an Estimated Average Requirement (EAR) for chromium; therefore, an Adequate Intake (AI) was set based on estimated mean intakes. The AI is 35 μg/day and 25 μg/day for young men and women, respectively. Men and women older than 50 years require slightly less, at 30 and 20 micrograms daily respectively; for pregnancy and lactation, the AI is 30 and 45 micrograms daily.
Few serious adverse effects have been associated with excess intake of chromium from food; therefore, a Tolerable Upper Intake Level (UL) was not established.
This is the most extensively studied application of chromium supplementation in humans. Most clinical trials have used chromium picolinate, with chromium chloride used less frequently. Evidence is mixed and clinical significance remains uncertain.
A 2019 review of chromium and glycemic control included eight meta-analyses and systematic reviews of a total of 58 clinical trials. The trials lasted from 3 weeks to 6 months and administered 1.28 to 1,000 mcg chromium daily. The most frequently used form was chromium picolinate, followed by yeasts containing chromium and chromium chloride. Overall, when used as an adjuvant treatment, chromium lowered fasting plasma glucose and HbA1c levels slightly in people with diabetes. However, the clinical significance of these findings is unclear.
A 2007 systematic review in Diabetes Care analyzing 41 randomized controlled trials reported a statistically significant but modest effect: among participants with type 2 diabetes, chromium supplementation improved glycosylated hemoglobin levels by −0.6% (95% CI −0.9 to −0.2) and fasting glucose by −1.0 mmol/L. Almost half of the 41 eligible trials were of poor quality.
A 2016 review examining 20 RCTs in type 2 diabetes patients applied clinically meaningful treatment thresholds: using systematic search criteria, 20 randomized controlled trials of chromium supplementation in T2DM patients were identified. Clinically meaningful treatment goals were defined as an FPG of ≤7.2 mmol/dL, a decline in HbA1c to ≤7%, or a decrease of ≥0.5% in HbA1c. In only a few randomized controlled trials did FPG (5 of 20), HbA1c (3 of 14), or both (1 of 14) reach the treatment goals with chromium supplementation. HbA1c declined by ≥0.5% in 5 of 14 studies. On the basis of the low strength of existing evidence, chromium supplements have limited effectiveness, and there is little rationale to recommend their use for glycemic control in patients with existing type 2 diabetes.
A 2020 meta-analysis of 28 RCTs examining glycemic control showed statistically significant but highly heterogeneous results: twenty-eight studies reported fasting plasma glucose (FPG), insulin, hemoglobin A1C (HbA1C) and HOMA-IR as outcome measures. Results revealed a significant reduction in FPG (weighted mean difference: −19.00 mg/dl, 95% CI: −36.15, −1.85, P = 0.030; I²: 99.8%). The extremely high heterogeneity (I² = 99.8%) substantially limits the interpretability of this finding.
The current position of major diabetes authorities is clear: the position of the American Diabetes Association (ADA) in 2024 is "there is insufficient evidence to support the routine use of herbal supplements and micronutrients, such as chromium, to improve glycemia in people with diabetes." A 2016 review similarly concluded there is insufficient rationale to recommend chromium supplements for people with type 2 diabetes, and that chromium supplements do not help moderate glucose levels in healthy individuals.
Regarding healthy, non-diabetic populations: a meta-analysis showed no association between chromium and glucose or insulin concentrations among nondiabetic subjects. Supplementation in healthy individuals without insulin dysregulation appears to provide no benefit and may be counterproductive at high doses.
Dietary supplementation of chromium to normal individuals has been reported to lead to improvements in glucose tolerance, serum lipid concentrations including high-density lipoprotein cholesterol, insulin, and insulin binding. However, the clinical evidence for meaningful lipid-lowering effects from chromic chloride specifically remains limited.
A systematic review and meta-analysis found that chromium supplementation may significantly improve lipid profile in patients with T2DM by decreasing triglycerides (TG) and total cholesterol (TC) and increasing HDL; however, chromium failed to affect LDL, and the lipid-lowering properties were small and may not reach clinical importance.
An early study cited in the research literature — Riales and Albrink (1981) — specifically examined chromium chloride: it investigated the effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein in adult men (Am J Clin Nutr 34(12):2670-2678, 1981). The overall evidence base for cardiovascular lipid outcomes from chromium is preliminary, with most data deriving from chromium picolinate rather than chromic chloride.
Chromium supplements are promoted to suppress appetite, break down fat, and stimulate thermogenesis causing a mild increase in calorie usage; however, chromium supplements have not been found to produce significant weight loss. Most clinical trials available are of short duration (six months or less) and do not control for confounders such as dietary intake and physical activity.
A 2023 systematic review and meta-analysis of 14 RCTs specifically in type 2 diabetes patients examined body composition: the results showed that chromium supplementation did not have any significant effect on fat mass (WMD = −0.43%; 95% CI −0.94, 0.09) or BMI (WMD: 0.09 kg/m², 95% CI: −0.03, 0.2).
The overall evidence for chromium as a standalone weight management intervention is weak. The evidence for chromium as a standalone weight loss tool is modest — studies show small but consistent reductions in body weight, with more meaningful effects seen on insulin and metabolic markers.
PCOS involves insulin resistance as a central feature, providing a theoretical rationale for chromium supplementation. However, the clinical evidence from RCTs and meta-analyses is inconsistent and generally negative.
A 2017 meta-analysis of 6 RCTs involving 351 women with PCOS found mixed results: no significant difference was found in indexes of insulin metabolism (body mass index, fasting insulin, fasting blood sugar, and quantitative insulin sensitivity check index), hormone status (luteinizing hormone, follicle-stimulating hormone, and prolactin), or lipid profiles (cholesterol and triglycerides) between chromium and placebo groups. The conclusion was that supplementation with chromium may not have significant benefits for women with PCOS, and more RCTs with low heterogeneity are required.
A 2018 systematic review reached similar conclusions: chromium supplementation has limited effects on weight reduction, glucose control, lipid profile, and hormonal disturbance of women with PCOS; however, more studies are needed due to the clinical changes observed in some patients with PCOS after chromium supplementation.
A 2025 meta-analysis of 10 RCTs involving 683 women with PCOS found that chromium picolinate supplementation at a dosage of 200 μg may provide benefits similar to metformin with regard to fasting blood glucose, fasting blood insulin, ovulation, and pregnancy incidence, with fewer side effects in patients with PCOS. However, this evidence derives from chromium picolinate, not chromic chloride specifically, and evidence that supplemental chromium can help treat metabolic syndrome or polycystic ovary syndrome is largely lacking.
The most solidly documented clinical application of chromic chloride specifically is its use as an additive in total parenteral nutrition (TPN) solutions. This use is based on documented cases of chromium deficiency-induced glucose intolerance in patients receiving long-term IV nutrition without chromium. Benefits of chromium chloride were reported in a patient receiving total parenteral nutrition (TPN) who developed chromium deficiency-associated glucose intolerance (Jeejeebhoy et al., 1977). The hexahydrate form (chromic chloride 6H₂O) is a pharmaceutical-grade preparation used in IV admixtures for this purpose.
The primary locus of chromium's proposed biological activity is the endocrine-metabolic axis. A number of the signs and symptoms of diabetes are shared with chromium deficiency; these include impaired glucose tolerance, fasting hyperglycemia, glucosuria, hypoglycemia, elevated circulating insulin, decreased insulin receptor number, and peripheral neuropathy. Chromium depletion is characterized by the disturbance of glucose, lipid and protein metabolism and by a shortened lifespan.
Supplemental chromium in the trivalent form, e.g. chromic chloride, has been associated with improvements of risk factors associated with adult-onset (Type 2) diabetes and cardiovascular disease. These associations are based on improvements in lipid profiles and insulin sensitivity, both of which are established cardiovascular risk factors. The evidence remains indirect and preliminary.
As discussed above, chromium's influence on insulin signaling has theoretical relevance for PCOS, where hyperinsulinemia drives ovarian androgen production. However, clinical trial data to date show limited efficacy of chromium supplementation on the hormonal and reproductive parameters of PCOS.
The dosage of chromium used in studies ranges from 200 to 1,000 mcg daily, mostly in the form of chromium picolinate. These and all other dosages cite the amount of the actual chromium ion in the supplement ("elemental chromium"), discounting the weight of the substances attached to it.
In the 2019 review of 58 clinical trials: the trials lasted from 3 weeks to 6 months and administered 1.28 to 1,000 mcg chromium daily.
In the 2016 meta-analysis of 13 RCTs: total doses of chromium supplementation ranged from 42 to 1,000 μg/day, and duration of supplementation ranged from 30 to 120 days.
Most people meet the Adequate Intake through diet alone. The AI for young adult men is 35 μg/day and for young adult women is 25 μg/day. Supplement doses used in clinical research are far above dietary AI values, typically in the 200–1,000 mcg/day range.
In PCOS-focused studies, chromium picolinate at a dosage of 200 μg has been examined in direct comparison with metformin.
Chromic chloride hexahydrate is also used as a pharmaceutical additive in intravenous TPN formulations; the doses in this context are determined by clinical need and calculated to replace demonstrated deficiencies rather than to achieve pharmacological effects.
Due to its low bioavailability, acute Cr(III) toxicity by ingestion is unlikely. No significant toxic effects of chromium chloride have been reported. Few serious adverse effects have been associated with excess intake of chromium from food. The Food and Nutrition Board reviewed the evidence and concluded that high intakes of the nutritional form of chromium (trivalent chromium, or chromium III) have not been linked to adverse effects, so no Tolerable Upper Intake Level was established.
Despite the absence of an established UL, adverse events have been documented at higher supplement doses. At large doses, Cr(III) may reduce iron absorption and cause symptoms of anemia and rhabdomyolysis. Hepatotoxicity from ingestion may present as jaundice, hyperbilirubinemia, elevated lactate dehydrogenase, and transaminitis, and nephrotoxicity may demonstrate acute renal failure, proteinuria, hematuria, and anuria with both Cr(III) and Cr(VI) toxicity, as the kidneys are the primary organs of excretion for chromium compounds.
In animal studies: the ingestion of 1,000 μg/mL of chromium as chromium chloride in drinking water for 12 weeks led to significant reductions in the weight of the rat's testes and seminal vesicles. Other adverse effects observed after high chromium intakes include rhabdomyolysis.
Antidiabetic medications and insulin: Taking chromium together with insulin might cause low blood sugar levels. If taking antidiabetes medicine, taking chromium dietary supplements might also cause low blood sugar levels.
Levothyroxine: Levothyroxine is a medication used to treat hypothyroidism. Taking chromium dietary supplements together with levothyroxine might reduce the amount of levothyroxine the body absorbs, so the full effect of the medication may not be obtained. This interaction is supported by clinical pharmacokinetic data: one study in seven healthy volunteers testing the effect of concomitant use of l-T4 (1,000 μg) and chromium picolinate (1 mg) revealed that chromium supplementation decreases l-T4 bioavailability by 17%.
NSAIDs and aspirin: Intake of insulin and anti-inflammatory drugs appears to increase chromium absorption. The proposed mechanism involves inhibition of cyclooxygenase and lowering of intestinal pH.
Antacids and proton pump inhibitors: Intake of antacids and proton pump inhibitors may block chromium absorption or increase excretion.
Calcium carbonate: Calcium carbonate interferes with the absorption of chromium.
Vitamin C: Vitamin C enhances chromium absorption. While generally beneficial, this could theoretically increase chromium exposure when both supplements are taken together.
Chromium deficiency is rare, and the recent EFSA report calls into question whether low intake in humans results in physiological consequences. Those potentially at risk are those who may excrete higher levels of chromium or are unable to absorb chromium from the diet. This category includes patients on long-term total parenteral nutrition without chromium supplementation.
One study found high-dose chromium (1,000 mcg/day) worsened insulin sensitivity in healthy adults. This finding emphasizes that the absence of a formal UL should not be interpreted as evidence of safety at any dose.
Chromic chloride as a dietary supplement ingredient is listed in the NIH Office of Dietary Supplements' Dietary Supplement Label Database. Dietary supplement use is widespread in the United States; over one-half the adult US population consumes nutritional supplements, and over one-quarter consumes supplemental chromium. Patients who use chromium supplements typically report doing so for weight loss or glucose regulation; these preparations contain chromium picolinate or chromium chloride, forms of trivalent chromium.
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Chromium supplementation has been specifically studied for carbohydrate cravings in both clinical trials of atypical depression and food intake studies in overweight adults. Two published RCTs demonstrate reductions in carbohydrate cravings and carbohydrate-driven eating behavior with chromium. The mechanism is linked to insulin sensitization and serotonin/dopamine pathway modulation.
Clinical research suggests chromium may modestly suppress appetite and reduce food intake, particularly in individuals with carbohydrate cravings. A double-blind RCT found chromium picolinate reduced food intake, hunger, and fat cravings in overweight women. The proposed mechanism involves sensitization of brain glucoreceptors and effects on serotonin and dopamine pathways.
Chromic chloride (trivalent chromium) has been studied in multiple clinical trials for glycemic control. Meta-analyses show inconsistent but sometimes significant reductions in fasting glucose and HbA1c, primarily in people with type 2 diabetes. Effects in healthy individuals are minimal. Chromium chloride specifically showed a non-significant effect on fasting glucose in subgroup analyses compared to other forms.
Several meta-analyses have examined chromium's effects on total cholesterol, LDL, and HDL with inconsistent results. A meta-analysis of 24 RCTs in T2DM found significant reductions in total cholesterol and increases in HDL. An umbrella meta-analysis of eight prior meta-analyses found no significant overall lipid effects. The early literature includes a specific study on chromium chloride supplementation and serum lipids in adult men.
Several clinical trials have investigated chromium picolinate specifically in atypical depression, a subtype characterized by mood reactivity, carbohydrate craving, and hypersomnia. A pilot RCT at Duke University (n=15) and a multicenter 8-week RCT (n=113) both found improvements in atypical depression symptoms, particularly in patients with high carbohydrate cravings. Proposed mechanisms include 5-HT2A receptor downregulation and enhanced insulin sensitivity.
Multiple meta-analyses and a Cochrane review have examined chromium supplementation for weight management in overweight and obese adults. Results consistently show a small but statistically significant reduction in body weight and body fat percentage, though the magnitude is considered clinically negligible. The Cochrane Review characterized the effect as of 'debatable clinical relevance' with low overall evidence quality.
Chromic chloride and other trivalent chromium forms have been investigated for improving insulin sensitivity, primarily in insulin-resistant populations. The proposed mechanism involves chromodulin-mediated activation of insulin receptor tyrosine kinase and enhanced GLUT-4 trafficking. Results are mixed: some studies show benefit in insulin-resistant subjects while others, including a rigorous clamp study in healthy subjects, found no improvement.
Chromium supplementation has been studied in metabolic syndrome given that insulin resistance is a shared feature. A prospective cohort study found lower toenail chromium concentrations were associated with higher incidence of metabolic syndrome. However, a controlled trial in 65 metabolic syndrome patients found no benefit on glucose, insulin, or lipid parameters, and both the NIH ODS and Linus Pauling Institute conclude current evidence does not support chromium for treating metabolic syndrome.
Several RCTs and meta-analyses have examined chromium supplementation in women with PCOS, given the central role of insulin resistance in this condition. A systematic review of five RCTs found chromium significantly lowered a measure of insulin resistance and one trial showed improved beta-cell function, though effects on fasting insulin and insulin sensitivity per se were not significant. Overall evidence is mixed and of uncertain clinical relevance.
Chromium supplementation has been evaluated for effects on serum triglycerides in multiple meta-analyses with conflicting results. A 2021 meta-analysis of 24 RCTs in T2DM patients found a small but statistically significant reduction in triglycerides, while an umbrella meta-analysis of eight prior meta-analyses (2022) found no significant overall effect. Examine.com concludes chromium does not appear to affect triglycerides.
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