Chromium (Cr)


Mineral Health Connection

Chromium is an essential trace mineral. In its trivalent state, it is critical for carbohydrate, lipid and nucleic acid metabolism. Chromium enhances the effects of insulin. Chromium activates phosphoglucosonetase and other enzymes.

Mechanism of action:

Chromium plays an important role in carbohydrate, fat and protein metabolism and has an impact on the expression of genes and nucleic acid synthesis.  
Insulin binding to cells seems to be increased by the presence of chromium as well as the number of insulin receptors. It activates insulin receptor kinase which increases insulin sensitivity (source). Trivalent chromium is an essential component of glucose tolerance factor. Glucose tolerance factor is believed to aid glucose transport across the cell surface as well as mediate the effects of insulin. Glucose tolerance factor also consists of two nicotinic acid molecules and a small oligopeptide, chromodulin. Chromodulin is believed to play a role in the auto-amplification of insulin signalling (source).

Food sources:

Chromium is found in various foods in quantities that correlate to the presence in the soil. It can be found in brewers yeast, cheese, molasses, wheat germ and whole grains, sugar beets, eggs, meat and seafood. Some recommend barley as a good source for chromium. Absorption of chromium is about 10%.


A safe and adequate daily intake of chromium is between 50-200mcg. However, the therapeutic dose ranges from 200-2000mcg/day.

Clinical Uses:

Dietary sugar loads increase the natural rate of urinary chromium loss by 300% for 12 hours (source). Those with glucose intolerance such as type-1, type-2, gestational, and steroid-induced diabetes have all shown improved glucose metabolism with supplemental chromium (source). Chromium picolinate at 1,000mcg/day has had notable beneficial effects on hemoglobin A1C, glucose, insulin and cholesterol levels in those with type-2 diabetes in a clinical trial (source). It should be noted that the beneficial effects of chromium appear to only be relevant at levels which are five-fold higher than the upper limit which is supposed to be the estimated safe and adequate daily intake without any documented side-effects.

The overall requirement of chromium is relative to the degree of glucose intolerance, and while a higher intake is more effective, 200mcg of supplemental chromium is adequate to improve mild glucose intolerance in individuals. Daily intake of 8mcg/kg body weight of chromium is more effective than 4mcg/kg in women with gestational diabetes (source) and steroid-induced diabetes can be reversed with doses of 600mcg/day (source). Corticosteroids deplete chromium. A double-blind, crossover trial has confirmed that chromium supplementation improves glucose and lipid levels while decreasing medication dosage in type 2-diabetes. The results found that brewers yeast (consisting of 23.3mcg/day) was more marginally more effective than chromium chloride (200mcg/day) (source).  Preliminary observations suggest that those with a dysthymic disorder may experience symptomatic improvement within three days of treatment with chromium supplementation once or twice daily and it may enhance antidepressant therapy (source). Chromium supplementation may also be helpful for refractory mood disorders with mild side-effects (enhanced dreaming and mild psychomotor activation). The antidepressant effects of chromium have been accounted for due to the enhancement of insulin utilization and the related increases in tryptophan availability in the central nervous system, and/or by the effect of chromiums norepinephrine release (source).

Caloric restriction in athletes seeking to maintain low bodyweight compromises chromium status. Chromium has been praised as a trace element that maintains lean body mass and decreasing body fat (source), though it appears that supplementation does not promote muscle growth, strength or fat-loss in young men and women (source). Sweating from acute yet intense activity induces a short-term loss of chromium in both urine and sweat which may affect recovery days after exercise.

Significant decreases of chromium concentrations of hair, sweat and blood have been reported in age-related diseases (source).

Hair Test Notes:

Chromium concentrations in human hair is ten times greater than that found in blood. For this reason, hair tissue mineral analysis is a much more accurate representation of chromium stores in the human (there is an average of 1.5 mg in the human body under optimal conditions).

Toxicity/ Drug interactions:

At present, there is little information regarding the long-term toxicity of chromium supplements.

Not much chromium is stored in the human body; once chromium is absorbed, it is almost entirely excreted in the urine (and for this reason, urine chromium levels can be used to approximate dietary chromium status). The estimated safe and adequate daily allowance level appears to be safe and non-harmful (source). Trivalent chromium appears to have a broad safety range and no toxic effects have been reported at doses upwards of 1mg/day (source). Chromium intake excess of 100mg/day may lead to retardation of growth, cardiomyopathy, and perhaps hepatic and renal damage.

Iron and chromium compete for binding on transferrin and supplemental chromium picolinate decreases transferrin (but not chromium chloride). Chromium nicotinate or chromium picolinate has a high bioavailability. Oral hypoglycemic agents may be enhanced by chromium while reducing insulin requirements. Those that are consuming hypoglycemic agents may need to modify their dosage (source)

Vitamin C and the B vitamin niacin increase chromium absorption.  

Antacids, corticosteroids, H2 blockers (such as cimetidine, famotidine, nizatidine, and rantidine), Proton-pump inhibitors (such as omeprazole, lansoprazole, rabeprazole, pantoprazole, and esomeprazole) may inhibit chromium absorption due to alterations in stomach acidity. Whereas Beta-blockers (such as atenolol or propanolol), corticosteroids, insulin, nicotinic acid, nonsteroidal anti-inflammatory drugs (NSAIDS), or prostaglandin inhibitors (such as ibuprofen, indomethacin, naproxen, piroxicam, and aspirin) may have their effects enhanced when taken in conjunction with chromium, or increase chromium absorption (source, source, source, source)

Clinical Caution:

Assessment of dietary chromium is often problematic and suboptimal due to the absence of a reliable indicator for chromium status. Suboptimal intake of chromium is associated with risk factors for diabetes and cardiovascular diseases such as impaired glucose tolerance and metabolism, elevated circulating insulin levels, glucosuria and hyperlipidemia. The lowest normal intake of chromium has deleterious effects on glucose tolerance, insulin and glucagon levels in those with mildly impaired glucose tolerance (source). 200 mcg of chromium increased the number of insulin receptors in people with hyperglycemia. Diabetes may intensify chromium deficiency. People with type-2 diabetes lose more chromium in their urine than those who don't have diabetes. Diets with low chromium intake may have negative effects on those with borderline diabetes (source).

Diseases and Symptoms of Chromium Deficiency:

  • Low blood sugar

  • Reactive hypoglycemia

  • Bedwetting

  • Pre-diabetes

  • Diabetes (Type 2)

  • Hyperinsulinemia

  • Hyperactivity

  • Learning disability


  • Hyperirritability

  • Depression

  • Manic depression

  • “Bi-polar” disease

  • Dr Jekyll/Mr. Hyde rages (“Bad Seeds”)

  • Impaired growth

  • Peripheral neuropathy

  • Negative nitrogen balance (protein/muscle loss)

  • Elevated blood triglycerides (> 200)

  • Elevated blood cholesterol (> 270)

  • Coronary artery disease

  • Aortic cholesterol plaque

  • Infertility (anovulation and low sperm count)

  • Shortened life span

  • Elevated CRP

Practice Tips:

  • Long-term chromium supplements are generally not recommended in excessive doses because the effects are unknown.

  • People who consume a diet of refined foods and high dietary sugar over prolonged periods are at risk for a chromium deficiency.

Additional Reading:

Manganese (Mn)


Mineral Health Connection

Manganese is an essential trace element to all known living organisms. It is an activator of several metalloenzymes, including arginase, pyruvate carboxylase, glutamine synthetase, and one form of superoxide dismutase (SOD). Manganese also functions as a non-specific enzyme activator and facilitates the synthesis of mucopolysaccharides (such as chondroitin sulfate), lipids and thyroxine. It helps prevent tissue damage caused by lipid oxidation and is an antioxidative transition metal. Manganese is part of the developmental process and the structure of the fragile ear bones.

Deficiency of this element has been induced in several animal species by feeding diets low in manganese. Signs of deficiency in animals include impaired growth, skeletal defects, depressed reproductive functions, ataxia in newborns, and defects in metabolism.

Mechanism of Action:

Manganese is an essential nutrient involved in the formation of bone and in amino acid, cholesterol, and carbohydrate metabolism. It is an enzyme activator and is a component of many metalloenzymes and may play a prominent role in calcium mobilisation. Manganese is part of the enzyme manganese superoxide dismutase and reduces the exposure to free radicals. It generates oxaloacetate, a substrate in the tricarboxylic acid (Krebs) cycle, as a constituent of pyruvate carboxylase and may play a role in glucose homeostasis. Manganese also activates enzymes that are involved in the synthesis of cartilage, facilitate the formation of urea, and activates various kinases, decarboxylases, hydroxylases and transferases.

Food sources:

Sources of manganese include; nuts, seeds and vegetables. It’s found in hazelnut, blackberries, pineapple, lentils, beans and whole grains. Due to milling, manganese content is much lower in milled whole grains. Absorption of manganese varies from 10-40%. The average body content is 0.012 g.


Biliary secretion is the main pathway for manganese excretion (source, source). In the liver, Manganese is extracted from the blood, conjugated with bile and excreted into the intestine. A small amount of manganese in the intestine is reabsorbed, establishing an enterohepatic circulation (source) which is critical for maintaining manganese levels. The recommended intake ranges from 2.5-3mg (source). The therapeutic dose range is between 2-50mg/day.

Clinical Uses:

The control of blood sugar in diabetes and a reduction of inflammation in arthritis has been speculated of manganese.

As a component of superoxide dismutase, manganese may be useful to define therapeutic strategies for the clinical management of glioblastomas. High levels of manganese superoxide dismutase is found in patients with glioblastomas have a median survival time lower (6.11months) whereas those with low levels of this enzyme have a median survival time of 12.17 months (source). Two distinct groups of glioblastomas can be distinguished based on the content of manganese superoxide dismutase.

Toxicity/ Drug Interactions:

Oral consumption of manganese is generally non-toxic. Excessive levels of manganese found in certain community water supplies and in some industrial processes can produce a Parkinsonian syndrome or a psychiatric disorder (“locura manganica”) that resembles schizophrenia.

The clinical syndrome associated with excessive manganese and its neurodegenerative effects of manganese toxicity is known as 'Manganism' (source). However, mild inhalation of manganese could impair memory and coordination, weakness, anorexia, fatigue, depression, apathy and disturbed sleep have all been reported, irritability, hallucinations, and poor coordination have all been reported in those with manganism. Manganese in excess amounts can irreversibly damage the nervous system (source). Several clinical neurological disorders of manganism have been described as extrapyramidal motor system dysfunction and in particular idiopathic Parkinson’s disease and dystonia (source). Tremors are a critical sign of excess manganese. Despite having similar effects as the symptoms described in Parkinson's disease, the dopamine transporter activity (source).

Manganese deposits have been found in patients with biliary atresia. Possibly caused by an increase in portsystemic shunt, and latent or subclinical encephalopathy (source).

Clinical Caution:

The signs and effect of human deficiency of manganese have not been clearly established, but some potential cases in adults have shown failure in normal hair pigmentation, dermatitis, and hypocholesterolemia (source). Deficiency may cause growth impairment, tendon and bone disorders in animals but not necessarily in humans. Multiple sclerosis and Amyotrophic lateral sclerosis may have dysfunctional manganese metabolism.

Mineral Relationships

Manganese, iron, vitamin C and/or molybdenum deficiency can lead to an accumulation of copper.

Synergistic Nutrients

  • Zinc, choline, vitamin K

Antagonistic Nutrients


  • Calcium, phosphorus, iron, soy protein.


  • Copper, magnesium, iron, vanadium

Practice Tips:

  • The only known reliable indicator of manganese at this time is hair tissue mineral analysis.

  • Deficiency diseases of manganese ranges from severe congenital birth defects (such as congenital ataxia, deafness, chondrodystrophy, Ehlers-danlos Syndrome etc.), allergies, asthma, convulsions, retarded growth, skeletal defects, disruption of fat and carbohydrate metabolism to joint problems (tendon and ligament degeneration, TMJ, repetitive motion syndrome, carpal tunnel syndrome, etc.), hypoglycemia, diabetes myasthenia gravis, dizziness, ringing in the ears, fatigue, muscular weakness, bone fractures or osteoporosis, weak ligaments and tendons.

Additional Reading: