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Does B6 Help Feelings of Sadness?

Vitamin B6 is one of the very important B vitamins. It is essential for a number of metabolic and physiological processes, and preliminary studies suggest that it may be useful in the treatment of depression. Is vitamin B6 effective in the treatment of depression? How does it help improve mood? Read on to find out.
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What is Vitamin B6?

Vitamin B6 is a member of the B vitamins. It is needed in the body for various functions such as the production of red blood cells, protein metabolism and regulation of the nervous system function.

Dietary sources of vitamin B6 include meat, fish, vegetables, bananas, nuts, whole grain products, potatoes, beef liver, spinach and  fruits (other than citrus fruits).

The different forms of Vitamin B6 include pyridoxal, pyridoxine, pyridoxamine, pyridoxal phosphate, pyridoxamine phosphate and pyridoxine phosphate. As a supplement, it is commonly sold as pyridoxine hydrochloride in oral dosage forms (capsules and tablets) and liquid form. 

The body can obtain vitamin B6 easily from dietary and supplementary sources. Though the body absorbs large quantities of vitamin B6, the metabolites of the vitamin are excreted in the urine. Therefore, vitamin B6 toxicity is rare.

Storage, cooking and processing led to the loss of vitamin B6 from foods. The extent of the vitamin lost to food processing techniques depend on the form of vitamin present in them. Plant foods lose the least amount during processing because they contain pyridoxine, which is more stable than the pyridoxal or pyridoxamine found in animals.

The metabolically active form of vitamin B6 is pyridoxal phosphate. It is usually synthesized from pyridoxal by the enzyme pyridoxal kinase and then metabolized in the liver.

This is the bioactive from of vitamin B6 and the form in which the human body utilize the vitamin.

Pyridoxal phosphate is a versatile biological catalyst that can act as a co-enzyme in many biochemical reactions such as decarboxylation, racemization, deamination, transamination and beta-group interconversion reactions.

It is usually found in the body tissues and is mainly excreted in the urine as pyridoxic acid, along with minute amounts of pyridoxal and pyridoxamine.

The absorption of vitamin B6 takes place in the small intestine especially in the jejunum and ileum from which it is taken into the blood by passive diffusion. Due to its great capacity for absorption, animals are able to absorb more than the needed amount of vitamin B6 on a daily basis.

The absorption of pyridoxamine phosphate and pyridoxal phosphate involve a process known as dephosphorylation, which is normally catalyzed by a membrane-bound alkaline phosphatase. Dephosphorylation is a reaction which involves the removal of phosphate groups from an organic compound by hydrolysis.

Vitamin B6 majorly functions in the following metabolic processes:

Major Metabolic Functions of Vitamin B6
  • Neurotransmitter synthesis
  • Histamine synthesis
  • Amino acid, glucose and lipid metabolism
  • Hemoglobin synthesis
  • Gene expression

Pyridoxine deficiency also known as vitamin B6 deficiency rarely occurs even in developing countries but it is common among infants.

Some of the causes of vitamin B6 deficiency are regular intake of alcohol, poor diets, genetic disorders, starvation and drug interactions. It is also common in individuals with poor renal functions and autoimmune disorders.

In the body, alcohol produces acetaldehyde, a chemical product that reduces the formation of pyridoxal phosphate and competes with it in protein metabolism.  This results in the loss of pyridoxine and finally vitamin B6 deficiency.  Alcoholics are therefore liable to have pyridoxine deficiency.

The levels of pyridoxine can also be affected by certain drugs such as anticonvulsants, corticosteroids, isoniazid, cycloserine and penicillamine. These drugs can reduce vitamin B6 levels by

  • impairing vitamin B6 metabolism
  • displacing pyridoxal phosphate from enzyme sites
  • blocking the action of pyridoxal kinase.

The symptoms of vitamin B6 deficiency include seizures, conjunctivitis, insomnia, irritability, depression, weakness, cracked skin at the corner of the mouth, sore or inflamed tongue, paranoia, neurologic symptoms of confusion, somnolence and neuropathy.

This deficiency can be treated with vitamin B6 supplements or by consuming more foods rich in the vitamin.

Although the Institute of Medicine states that no adverse effect has been associated with vitamin B6 from foods, vitamin B6 supplements may cause adverse effects. For example, prolonged use of high doses of the supplemental form is associated with peripheral sensory neuropathy.

Therefore to prevent vitamin B6 deficiency or negative effects associated with high vitamin B6 intake, experts provide daily intake recommendations that vary with age.

For adults (18 years and above) the recommended daily intake of vitamin B6 is 1.4 mg. While pregnant and breastfeeding women need 1.9 mg and 2.0 mg daily respectively support infant growth and development.

The upper limit for daily vitamin B6 intake is 100 mg for adults, pregnant and lactating women above 18 years of age.

How Vitamin B6 Affects Depression

To understand the importance of B6 to depression, a basic knowledge of how the brain establishes mood is required.

All neuronal communication in the brain goes through neurons or nerve cells. This communication flows in the form of signals which are transmitted in the form of electrical impulses across a synapse to a target cell by endogenous chemicals known as neurotransmitters. A synapse is the gap between two nerve cells.

These neurotransmitters carry impulses that are important for a balanced emotional state as well as form the messengers responsible for the brain’s ability to control other processes in the body.

Pyridoxal phosphate, its active form of vitamin B6 can easily cross into the brain. In the brain, it is a coenzyme that plays an important role in the biosynthesis of the following neurotransmitters: serotonin, dopamine, epinephrine, norepinephrine and gamma-aminobutyric acid (GABA).

In the synthesis of GABA, pyridoxal phosphate acts as a cofactor for the enzyme glutamic acid decarboxylase which catalyzes the decarboxylation of glutamate to gamma-aminobutyric acid and CO2.

The synthesis of the amino acid, tryptophan to serotonin also depends on the actions of pyridoxal phosphate.

Of the neurotransmitters listed above, three monoamine neurotransmitters largely control mood in the brain. The neurotransmitters that are required in optimal concentrations to improve mood are serotonin, dopamine and norepinephrine.

Pyridoxal phosphate is also essential in the metabolism of homocysteine, a non-protein amino acid that is biosynthesized from methionine by the removal of its terminal methyl group.

Homocysteine is a toxic intermediate of amino acid syntheses. It is meant as a stopgap between two essential amino acids. However, the body requires vitamin B6 to convert homocysteine to the next amino acid or to recycle it back to methionine.

Therefore, high levels of homocysteine can result from pyridoxine deficiency. The accumulation of this toxic intermediate has been shown to cause damage to the brain and the heart. In addition, the accumulation of homocysteine in the brain has been linked to depression.

In summary, low levels of pyridoxal phosphate in the brain can cause depression by

  • reducing the amount of serotonin, dopamine and norepinephrine synthesized  
  • increasing the concentration of homocysteine which can cause neurological disorders such as depression

Studies on Vitamin B6 and Depression

In a 1995 study published in the Journal of Neural Transmission, the effect of pyridoxine on the rate of synthesis of serotonin in the brains of monkeys was explored.

For this study, the subjects were rhesus monkeys and the effect of the co-factor pyridoxine on the activity of aromatic amino decarboxylase enzyme was studied using positron emission tomography, PET.

For the first PET study, the rate constant for the formation of serotonin was measured using a two tissue section model with reference area in the brain. Then a pre-treatment with intravenous pyridoxine hydrochloride was carried out before doing a second PET study. The second study showed that the rate constant increased by an average of 20%.

The increase varied significantly among different monkeys starting from no effect to more than 60%.

The study supports the belief that pyridoxine is essential in the synthesis of serotonin and that it can also be used in the treatment of diseases linked with neurotransmitter deficiencies.

In another study published in the Journal of Steroid Biochemistry in 1975, the effect of pyridoxine hydrochloride on oral contraceptive-induced depression was studied in a double blind crossover trial.

The participants consisted of a group of 39 depressed women whose depressive symptoms were judged to be the effects of oral contraceptive. 19 of these women were diagnosed with true vitamin B6 deficiency while the other 20 were non-B6 deficient. All the women were given pyridoxine hydrochloride (vitamin B6).

The group of women with vitamin B6 deficiency responded well to the administration of pyridoxine hydrochloride while the remaining 20 showed no response.

The results showed that oral contraceptive-induced depression is solely due to the effect of vitamin B6 deficiency. Oral contraceptives are known to reduce brain decarboxylase activity and amine synthesis. The depressive symptoms in the other women without B6 deficiency may have also been a result of the diversion of substrate from amine synthesis.

In 2001, a research at Felsenstein Medical Research Center showed the anti-depressive effect of pyridoxine in neuroleptic–treated patients who also suffered from minor depression.

The research involved nine schizophrenic patients with co-morbid minor depression. All the patients had an unchanged clinical state, when they were evaluated using the Brief Psychiatric Rating Scale (BPRS).

They were all kept on the anti-psychotic drugs they were taking for at least 4 consecutive weeks prior to the commencement of the study. After this, the patients received 150 mg of pyridoxine daily in addition to their anti-psychotic drugs for 4 consecutive weeks.

The patients’ mental statuses were evaluated before, during and at the end of 4 weeks of pyridoxine treatment using the Scale for the Assessment of Positive Symptoms (SAPS), Scale for the Assessment of Negative Symptoms (SANS), The Hamilton Rating Scale for Depression (HAM-D) and BPRS.

Two of the patients that had high initial SANS and HAM-D scores experienced significant improvements in depressive symptoms following 4 weeks of pyridoxine administration. In one of these two patients, the improvement in depressive symptoms was followed by a great decrease in SANS score.

The study concluded that a subgroup of schizophrenic patients with co-morbid minor depression may benefit from the addition of pyridoxine to their anti-psychotic treatment.





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