Vitamin B12 inhibits an enzyme that is involved in Parkinson’s disease
Parkinson’s disease, also known as shaking palsy, is one of the most common chronic disorders among older people. There is no effective cure at this point, and the only way to address the disease is to suppress the symptoms but that does not treat the underlying cause. Even though most cases of Parkinson’s disease are sporadic, it turns out that the hereditary variants of the disease are linked to mutations in a particular gene. A team of scientists from University of the Basque Country in Spain has discovered that vitamin B12 blocks the enzyme that is involved in these mutations. An earlier study has also shown that in newly diagnosed Parkinson’s patients who have low levels of vitamin B12 the disease develops faster than in patients with higher levels of the nutrient.
The scientists therefore recommend supplementing with vitamin B12 to prevent or at least delay the disease. Earlier studies also show that vitamin B3 and Q10 may have a positive effect. So the reason that Parkinson’s disease is especially likely to affect old people is that they are at increased risk of lacking these essential nutrients.
Parkinson’s disease typically occurs in the ages between 50 and 70 years and is caused by damaged nerve cells and lack of dopamine, a neurotransmitter that the brain uses to control various movements. The symptoms are typically uncontrollable trembling, stiff muscles, slow movements, poor balance, fatigue, and impaired facial mimicry. The disease may also lead to depression and los of cognitive skills.
In 1990, it was proved that Parkinson’s disease may be caused by changes to our genetic material (DNA), and science has now identified 13 genes and genetic areas that are involved in the condition. Still, even if a person is genetically prone to Parkinson’s disease, the condition may not develop in all cases. There can be different reasons why Parkinson’s disease develops, including environmental factors such as poisoning, lack of nutrients, and ageing processes.
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Vitamin B12 as a new therapeutic potential
Hereditary versions of Parkinson’s disease are mainly linked to mutations in the gene that codes the LRRK2 enzyme and the accompanying kinase activity. This was what a team of scientists from University of the Basque Country in Spain discovered in 2004. The enzyme has been given the international name “dardarina”, which is the Basque name for shaking.
Consequently, the LRRK2 enzyme is the therapeutic target for the development of new drugs for treating hereditary forms of Parkinson’s disease. There are currently drugs that work as powerful inhibitors of the LRRK2 enzyme but these drugs have undesirable side effects and have not shown convincing clinical results. Therefore, the team of Basque scientists wanted to look closer at the problem. They discovered that vitamin B12 also inhibits the LRRK2 enzyme in cell cultures and in rodent brain tissue.
Their research shows that vitamin B12 supplements may be a whole new angle to controlling the LRRK2 enzyme and the accompanying kinase activity that is involved in the onset of hereditary Parkinson’s disease. The scientists see a huge therapeutic potential in vitamin B12 and there are not even any side effects. Their study results are published in the science journal Cell Research.
Vitamin B12 deficiency speeds up the development of Parkinson’s disease
An earlier study that is published in Movement Disorders, a science journal, shows that Parkinson’s patients with lower levels of vitamin B12 in their blood have more problems with keeping their balance and walking safely. The scientists behind this study assume that it is the vitamin B12 deficiency that affects the central and peripheral nervous systems.
A blood test can reveal vitamin B12 deficiency |
Widespread lack of vitamin B12 has several causes
Vitamin B12 is found primarily in animal food sources like liver, meat, fish, and dairy products. The vitamin is taken up by the small intestine with help from a carrier compound called intrinsic factor. Although the coli bacteria in the colon are able to produce small quantities of vitamin B12, we are unable to absorb it from here. Around one in four Americans older than 60 years of age lacks vitamin B12, and a similar pattern can be expected in other western countries. This is because the ability to absorb the vitamin from food or from supplements decreases with age. In fact, it may be as little as one percent of the nutrient that is absorbed. So, it appears there is a clear link between ageing, lack of vitamin B12, and an increased risk of developing Parkinson’s disease.
Too little gastric juice, overconsumption of alcohol, plus regular use of hormone pills and sleeping pills may also reduce your ability to absorb vitamin B12. Other studies show that around 20 percent of people who take metformin against type 2 diabetes are deficient or borderline-deficient of vitamin B12.
Supplements and effective absorptionMany vitamin B12 supplements contain large quantities of the nutrient because it is so difficult for the body to absorb it |
Vitamin B3 also has a positive effect on Parkinson’s disease
A study of patients with early stages of Parkinson’s disease shows that it pays off to increase your intake of vitamin B3 from food or supplements. This is because the vitamin is actively involved in the cellular energy turnover and in the repair of damaged nerve cell DNA. Vitamin B3 is mainly found in high-protein foods such as meat, fish, poultry, nuts, kernels, and seeds
Deficiencies and poor utilization of vitamin B3 may be a result of unhealthy eating habits, alcohol abuse, ageing processes, and prolonged used of diuretics.
Diuretics, which many older people take, inhibit the utilization of vitamin B12 and vitamin B3 |
Q10 can relieve Parkinson’s symptoms
Q10 is a coenzyme that is found in two forms. One form, ubiquinone, is involved in cellular energy turnover that takes place inside the mitochondria. The other firm, ubiquinol, works as an antioxidant and protects cells and their mitochondria against free radicals and oxidative stress. With Parkinson’s disease, there are signs of defect mitochondria in the brain, which is why it made perfect sense to look at the effect of taking Q10 as a supplement.
A Japanese study shows that daily supplementation with Q10 (300 mg) relieves the symptoms in some Parkinson’s patients, which means that Q10 could be used as an adjuvant in therapy. We humans make most of our own Q10 but the endogenous synthesis of the compound gradually decreases from the age of 20 years, and many people can feel their vitality go down once they are in their fifties.
Cholesterol-lowering drugs (statins) also block the body’s Q10 synthesis. It is possible to compensate for the loss of Q10 by taking a supplement, preferably one with good documentation. Q10 is a compound that is very difficult for the body to absorb. One has to use a technique that involves mixing Q10 with special oils and exposing it to a particular heating process before the small intestine can absorb the compound. This way, the Q10 crystals dissolve completely so they are able to pass through the intestinal wall and reach the bloodstream.
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References:
Adam Schaffner et al. Vitamin B12 modulates Parkinson´s disease LRRK2 kinase activity through allosteric regulation and confers neuroprotection. Cell Research, 2019
University of the Basque Country. Vitamin B12 is identified as the inhibitor of a key enzyme in hereditary Parkinson´s disease. ScienceDaily, April 4, 2019
Vitamin B12 supplementation could postpone disease progression in Parkinson´s patients. News Medical Life Sciences, March 19, 2018
University of Leicester. People with forms of early-onset Parkinson’s disease may benefit from boosting niacin in diet, research suggest. ScienceDaily. 2017
Yoritaka A et al. Randomized, double-blind, placebo-controlled pilot trial of reduces coenzyme Q10 for Parkinson´s disease. PubMed 2015
https://www.parkinson.dk/fakta-om-parkinson/hvad-er-parkinsons-sygdom/arvelighed
https://www.sundhed.dk/borger/patienthaandbogen/hjerne-og-nerver/om-hjerne-og-nerver/nervesystemet/
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