Possible Neuroprotective Mechanisms Of Vitamin B3 In Pd
Firstly, numerous studies have demonstrated that mitochondrial dysfunction and cellular energy failure are pathophysiological features of PD. Nicotinamide participates in the biosynthesis of nicotinamide adenine dinucleotide via various metabolic pathways . NADH is an essential cofactor assisting the tetrahydrobiopterin functioning in tyrosine hydroxylase, which can hydroxylate tyrosine and produce dopamine NADH deficiency is common in PD .
Secondly, NADH is indispensable for the physiological function of mitochondrial complex I in ATP synthesis, and the corresponding dysfunction is involved in PD patients and animal models . Nicotinamide mononucleotide constitutes one of the key precursors of NAD+. In previous in vitro studies, the scholars have established a cellular model of PD using rotenone-treated PC12 cells, and they found the NMN treatment was associated with a significantly higher survival rate in the rotenone-treated PC12 cells. NMN is assumed to enhance the intracellular levels of NAD+ and ATP in the cellular model of PD .
Followed For 18 Years
For the study, researchers followed 41,058 adults in Sweden for an average of 18 years. None had Parkinsons at the start of the study.
Every participant completed a questionnaire at the start of the study about their medical history and lifestyle factors like diet and exercise, including height, weight and physical activity. Researchers calculated body mass index for each participant and activity levels.
Participants were asked to report how often they consumed various foods and beverages during the past year, including portion sizes. Vitamin and mineral supplements were not considered due to inadequate information on brands, dosing and how often supplements were taken.
Vitamin E The Crucial Molecule Of Our Diet
Vitamin E is an essential component of our diet. Apart from its many other functions in the body, vitamin E is involved in the proper development and function of the brain. Its deficiency has been associated with many brain diseases including Alzheimers and Parkinsons .
Therefore, one must consume enough vitamin E in order to protect from brain diseases. Dry fruits like walnuts, almonds, hazelnuts, and leafy vegetables like spinach and broccoli are the rich sources of vitamin E. Other sources include plums, sesame seeds, wheat germ, vegetable oils, soy, and avocado .
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Adequate Selenium Levels For Preventing Diseases
Studies that investigated the effect of Se on various parameters related to health or disease in humans have used various approaches. These studies used food questionnaires , measured mineral levels in plasma and breast-milk , and incorporated supplements . Regarding the use of Se supplements in research with adult humans, additional doses up to 200 g of Se/day may be appropriate. This value represents an amount of mineral approximately 4 times higher than the recommended value but much less than the amount that could pose a risk to health . Clinically, Se supplementation may be important for individuals from populations that live in geographical areas where the mineral is not easily consumed through diet or have genetic variations that alter the metabolism of the mineral . Methodological approaches using various animal models or cell cultures are useful for answering questions related to the effects of Se on health/disease but cannot be investigated by testing in humans due to ethical and methodological reasons.
Clinical Studies Regarding Vitamin E In Pd
The DATATOP experiment is a multicentre-controlled clinical trial to investigate the long-term efficacy of treatment with deprenyl and/or copherol and to explore whether it is possible to extend the time before the application of levodopa treatment. At 28 US and Canadian sites, 800 eligible patients with untreated early-stage PD were enrolled in DATATOP and randomized to four groups: deprenyl 10mg/d, copherol 2000IU/d, placebo-controlled, and deprenyl 10mg/d and copherol 2000IU/d. Deprenyl can delay the development of functional disorders, delay the application of levodopa, and improve motor symptoms, but vitamin E is disappointing . Similarly, another two population-based studies also did not find the association between vitamin E intake and risk of PD .
However, a large community-based study showed that high intake of dietary vitamin E may reduce the occurrence of PD . Another pilot trail suggests that long-term treatment with vitamin E may delay the use of levodopa in patients with PD . Further research is needed to verify these results.
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Ascertainment Of Pd Cases
Identification of PD cases among cohort participants was previously described., In brief, potential cases were identified from three independent sources. Three follow-up interviews were conducted on all surviving cohort participants in 1999â2004 , 2006â2010 , and 2014â2016 . Participants were asked whether they had ever been diagnosed by a physician to have PD and, if yes, age at which the diagnosis was ascertained. Record linkage of the cohort database with the government-established nationwide hospital discharge database was carried out with computer assistance. All diagnoses with the International Classification of Diseases, Ninth Revision code 332 from 1990 to 2018 in public and private hospitals were identified. Record linkage of the cohort database with three hospital-based PD registries in Singapore through 31 July 2018 was carried out by database linkage. These PD registries listed patients with a diagnosis of PD and who were followed up primarily as outpatients in PD centers housed in the three largest public hospitals in Singapore.
Vitamin E May Protect Brain
In the study, researchers reviewed studies on vitamin C, vitamin E, and beta-carotene and Parkinson’s disease risk published between 1996 and March 2005. The results appear in the May 19 online edition of Lancet Neurology.
Overall, seven studies showed that diets that contained a moderate amount of vitamin E reduced the risk of developing Parkinson’s disease by 19%.
Moderate vitamin E diets were those that fell in the middle range of intake of the vitamin in each of the studies included. According to the federal government, the recommended dietary allowance for vitamin E is 15 milligrams of the alpha-tocopherol form of vitamin E. Alpha-tocopherol is the form of the vitamin that the body uses.
Although eating larger amounts of vitamin E appeared to further reduce Parkinson’s risk, researchers say too few studies contained data on this to draw any firm conclusions.
But seven studies on vitamin C and four on beta-carotene did not indicate that diets rich in these nutrients had a protective effect against Parkinson’s disease.
The American Dietetic Association gives the following examples of how much vitamin E is in a variety of foods:
- 24 almonds. About a handful has 7.4 milligrams
- Hazelnuts. 20 nuts has 4.3 grams
- Broccoli. 1 cup cooked has 2.9 milligrams
- Wheat germ. 1 tablespoon has 1.3 milligrams
- Avocado. 1 ounce has 0.4 milligrams
Show Sources
Lancet Neurology
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Vitamin E In Foods Prevents Parkinsons
But Pills Dont Pack Anti-Parkinsons Punch
Oct. 21, 2002 Say nuts to Parkinsons disease. Nuts and other foods rich in vitamin E lower the risk of this debilitating illness, a dietary study suggests.
These foods must have more good stuff than just the vitamin, however. People who took vitamin E pills did not lower their risk of Parkinsons. Only those whose diets were heavy on vitamin-E-rich foods particularly nuts got the benefit.
We found no evidence that use of vitamin E or C supplements or multivitamins reduced the risk of Parkinsons, study author Shumin Zhang, MD, ScD, said in a news release. Zhang and colleagues at Harvard Medical School reported the findings in the Oct. 22 issue of Neurology.
Zhangs team gathered detailed information on the diets of 76,890 women and 47,331 men enrolled in two huge studies of diet and health. Both studies enrolled healthcare workers. People who sign up for this kind of study tend to have healthier lifestyles than those who dont. That means there may be other healthy things, in addition to a diet rich in vitamin E, that help lower the risk of Parkinsons disease.
Compared with those who ate the fewest servings of vitamin E-filled food, those who ate the most had 32% fewer cases of Parkinsons disease after 12 to 14 years.
Foods rich in vitamin E include:
Vitamin Therapy For Parkinsons Disease
Parkinsons disease also termed as paralysis agitans, is a degenerative disorder of the nervous system, marked by gradual loss of the ability to control physical movements. It results from the destruction of brain cells that are primarily responsible for the production of a neurotransmitter called dopamine and most often affects people over the age of 50.
Insufficient production of dopamine prevents the execution of smooth and controlled movements, thus leading to symptoms like trembling, slurred speech, loss of flexibility of muscles, slowness of movement and gait, difficulty while walking and cognitive decline.
Even though, there is no cure for Parkinsons disease, a multidisciplinary approach involving lifestyle changes, healthy eating habits, regular physical activity and medications can work in concert to help you manage the symptoms of the disease in a better way, thus enabling you to enhance the quality of your life.
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Diagnosis And Biological Markers Of Parkinsons Disease
There is no specific biochemical test to indicate the presence of PD. The diagnosis is made primarily from signs and clinical features presented by the patient and can only be confirmed at postmortem examination . Recently it was demonstrated that quantify the expression of -synuclein in skin biopsies have the potential to be used as an additional tool for the diagnosis of PD . Some of the clinical signs used to establish the diagnosis of PD are tremor at rest, postural instability, muscular rigidity, and difficulty in initiating movements or continuing them , among others that affect movement .
The involvement of genetic factors in the onset of PD is quite relevant. In a recent meta-analysis conducted by Nalls et al. , six new risk loci for PD were described: SIPA1L2, INPP5F, MIR4697, GCH1, VPS13C and DDRGK1. In meta-analysis studies, Dai et al. reported that TNF-1031 polymorphism is a possible risk factor for PD, and Wang et al. concluded that the null genotype of GSTT1 is also related to increased risk of the development of PD, at least in Caucasians. The roles of the genes parkin, DJ-1 and PINK-1 in the susceptibility to PD should be highlighted, as well as the LRRK2 gene . Genetic mutations affecting the PINK1 and LRRK2 proteins are related to mitochondrial dysfunction and the formation of reactive oxygen species , which are events involved in PD pathophysiology.
Oxidative Stress and Other Molecular Dysfunctions in Parkinson´s Disease
Vitamins C And E Linked To Reduced Risk For Parkinson’s Disease
Erik Greb
Higher intake of vitamins C and E was associated with a reduced risk for Parkinson’s disease in an analysis of a national cohort study. Higher intake of both vitamins, as opposed to one, strengthened the association with lower PD risk.
In addition, body mass index and coffee consumption appeared to influence the magnitude of these vitamins’ effect on PD risk. Dietary beta-carotene and dietary nonenzymatic antioxidant capacity had no effect on this risk, however.
Dr Essi Hantikainen
“Our findings suggest that the protective effect of dietary vitamins on Parkinson’s disease risk might be limited to specific vitamins, such as vitamin E and C,” Essi Hantikainen, PhD, a postdoctoral researcher at the University of Milano-Bicocca, Milan, Italy, told Medscape Medical News. “Therefore, implementing foods in the diet that are rich in vitamin E and C might help to prevent the development of Parkinson’s disease,” she said.
More research is needed to confirm these findings, she added. “In addition, it is not yet clear what are the most beneficial amounts of vitamin E and C intake to reduce the risk of Parkinson’s disease.”
The research was January 6 in Neurology.
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Dietary Sources And Nutritional Recommendations
Se is an essential nutrient, and the human diet is a natural source for obtaining it in relevant amounts. The dietary sources of Se are quite diverse, including meat, milk, eggs and vegetables . The amount of Se present in most vegetables depends on the amount of the mineral present in the soil in which the plant was cultivated. Therefore, plants grown in soils rich in Se have high mineral levels, whereas the opposite is also true . It was recently demonstrated that in monsoonal China, precipitation has an important effect on the distribution of Se in soil . This fact demonstrates that populations living in specific regions of the world are susceptible to high or low consumption of Se, and the amounts vary according to environmental conditions that modify the mineral content of the soil where they live. This influence is greatest where the importation of food from various locations is lower, because it makes the consumption of local foods greater, to the detriment of food from various geographical and environmental origins.
Biological Roles Of Selenium
Se deficiency has been associated with some diseases such as Keshan disease . Se deficiencies are also related to genomic instability . Additionally, Se is able to perform epigenetic changes through DNA methylation and histone modifications . Complex pathological situations such as infection by human immunodeficiency virus and cancer also appear to be influenced by body levels of Se. In this context, the antioxidant function of Se involves protecting from and slowing the development of diseases that involve oxidative damage to cellular components.
Figure 1Figure 2
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A Higher Consumption Of Vitamin E Also Reduced Patients’ Risk Of Parkinson’s By 32 Percent
The study’s results showed a higher intake of vitamin E and vitamin C yielded very similar results. “Researchers found a rate of 67 cases of Parkinson’s disease per 100,000 person-years in the group that consumed the highest amounts compared to a rate of 110 cases in the group that consumed the lowest amounts,” the study authors stated. “After adjusting for the same factors, people in the highest consumption group had a 32 percent lower risk of Parkinson’s disease than those in the lowest group.”
Meanwhile, a 2005 meta-analysis published in the journal Lancet Neurology also found that an increased amount of vitamin E reduces your risk of developing Parkinson’s by 19 percent.
Similar to vitamin C, vitamin E is also an antioxidant that’s used to boost your body’s immune system. The fat-soluble nutrient, which can be found in vegetable oils, nuts, and green vegetables, also protects your cells from free radical damage, according to NIH.
And to see if you’re lacking another common nutrient, here are 20 Symptoms of Vitamin D Deficiency, According to Medical Experts.
How Can Vitamins Help With Parkinson Disease
How Can Vitamins Help with Parkinson Disease?By: Dr. George Obikoya
Parkinson’s disease is a common neurodegenerative movement disorder that is associated with significant medical disability, reduction in quality of life, and, in advanced stages, caregiver burden. Approximately half a million to one million individuals in the United States have been diagnosed with PD, most falling within the age range of 55 to 60 years at time of diagnosis.
With the increase in the senior population of the United States, the prevalence of PD is expected to rise. In response to this anticipated increase in the prevalence of PD, the search for agents that may delay or arrest its pathologic progression has become a high priority among researchers.
Neuroprotection is defined as protecting neurons from cellular damage induced by various biochemical insults associated with the pathogenesis of PD. There is no known cure for Parkinson’s disease.
Parkinson’s disease is caused by deterioration of nerve cells in the basal ganglia, the part of the brain responsible for muscle movement. As less dopamine is produced, muscle function is lost. Symptoms of Parkinson’s include unstable balance, slow movement, difficulty walking, muscle stiffness or rigidity, difficulty initiating movement, muscle tremors, muscle ache, and speech changes.
Other supplements at earlier stages of investigation in the laboratory include nicotinamide, riboflavin, acetyl-l-carnitine and alpha lipoic acid.
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Electrophysiology In Pd Mouse Model
According to our previous findings , HFS protocol performed on parasagittal slice preparation induced a robust LTD in MSNs recorded from WT mice , whereas it failed to elicit LTD in PINK1/ mice . After removal of magnesium from the bathing medium, HFS induced LTP in WT mice . In PINK1/ mice, HFS also increased EPSPs compared to pre HFS , but the magnitude was significantly lower than WT mice , suggesting the impairment of this form of plasticity.
Trolox fully rescues both forms of altered synaptic plasticity in PINK1/ mice. Time-course of LTD in WT and PINK1/ mice recorded from parasagittal slices. HFS induces LTD in WT mice , but not in PINK1/ mice . The inset shows a representative sample of EPSPs recorded in PINK1/ before and 20 min after HFS. The LTP induction protocol causes LTP in WT mice but not in PINK1/ mice . The magnitude of LTP measured in PINK1/ mice is significantly reduced. The inset shows a representative sample of EPSPs recorded in PINK1/ before and 20 min after HFS. In slices acutely treated with Trolox 100 M or in slices from mice chronically treated with Trolox, both LTD and LTP is rescued. LTD is fully rescued, while LTP increases in magnitude as in normal condition. The insets show two representative samples of EPSPs recorded in PINK1/ before and 20 min after HFS. Each data point represents the mean ± SEM from acute and chronic treatment, respectively.
Potential Noxious Effects Of Selenium Overload
It is important to mention that despite Se influence on the metabolism of various human diseases by its antioxidant action, the role of this mineral cannot always be protective or combat injury inherent to a pathological condition. Se may not often act protectively or even beneficially, as demonstrated by Maraldi et al. in a test performed in vitro using human neuron cells and by Estevez et al. , who showed that a high dose of Se can induce oxidative stress in cholinergic neurons of Caenorhabditis elegans. Recent results indicated that the supplementation of 200 g of Se/day is not recommended for preventing prostate cancer . This information calls attention to the importance of not considering the mineral only as a protective agent when introduced into a research protocol. Depending on the quantities used, type of Se chosen and experimental conditions, Se could have detrimental effects, similar to those mentioned above.
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