This century is a century of medical improvement. all over the world, understanding of the pathology of many diseases has extremely increased, as a result, more effective treatments have been developed. It was a sight near the end of the twentieth century that was at the end, we can develop a drug for any disease in order to completely eliminate the disease from the population. However, this generation began to realize that a drug might not be what we should rely on. Medicine, while it is able to treat symptoms or even cure many diseases, it also often presents bad side effects to patients, as well as extreme financial concerns. One aspect of health care that is slowly attracting more attention is nutrition and lifestyle. Many researchers have researched the relationship between diet and both chronic and acute diseases. The main chronic diseases examined include type 2 diabetes and cardiovascular disease. For these chronic diseases, the diet has consistently been shown to be a major factor in their incidence and prevalence. Another concern that has recently gained much attention is cancer, which has also been strongly associated with dietary behaviours. After knowing the high relationship between dietary patterns and chronic diseases such as these, it is important to study how nutrition can affect the development and development of other types of diseases. Specifically, the effect of nutrition on neurological diseases should be particularly important. However, many diseases have a significant impact on the nutrition and nutritional status of infected patients. In addition to paralysis, immobility, abnormal motor function and various neuropsychiatric disorders, it is dysphagia swallowing and swallowing vessels and the deepest effect on dietary intake.
Brain’s health and nutrition:
there are links between nutrition and lifestyle and the brain’s health in general. The efficiency of the brain tends to decrease with age as part of the natural process of aging, which can lead to a decline in cognitive functioning, development of dementia or Alzheimer’s, or other neurological disorders. However, diet and lifestyle factors have been shown to prevent or reduce this neurodegeneration that occurs with age. This correlation can be explained by what is known about how the vascular system is affected by diet, which is important in the functioning of the brain because the brain consumes over twenty percent of the body’s oxygen and nutrients even though it only makes up approximately two percent of the body’s weight (Kalaria, 2010). This relationship between thevascular system’s health and neurological health can be explained because pathological changes in the smooth muscle of the walls of the cerebral resistance arteries change the brain’s autoregulatory responses. For example, changes in circulation due to dilation or constriction of cerebral resistance arteries often results in hypertensive encephalopathy or cerebral hypoperfusion. Many links such as these exist between the cardiovascular system and the brain’s functioning. For example, hypertension is correlated with an increased risk of dementia, particularly Alzheimer’s disease, and adult onset type 2 diabetes mellitus leads to a 2 to 2.5 fold increased risk of dementia with aging (Kalaria, 2010). Further, the nutritional interventions that prevent neuronal degeneration are very similar to those that improve cardiovascular functioning.
Multiple sclerosis and saturated fat:
Multiple sclerosis is one of the neurological diseases that can be greatly affected by nutrition. This interaction has suggested epidemiological studies indicating that the prevalence of multiple sclerosis is higher in areas where saturated fat intake is higher than trans fats (Payne, 2001). In the case of the united states of the World Health Council, the number of people living with HIV/AIDS is estimated at 100 million. The type of fat that is consumed is also something that has been investigated. Essential fatty acids (EFAs) are currently recommended for patients with multiple sclerosis. The effect of a low fat diet on multiple sclerosis can be enhanced, while wonderful, by an antioxidant supplement. Mores and others conducted a 42-day randomized randomized trial of long-term residents with multiple sclerosis to investigate the effect of this supplementation on cell metabolism and multi-sclerosis inflammatory processes (2013). In this study, five participants were assigned to the experimental group, which was given a low-fat diet and antioxidant supplements, while four participants were placed in the control group, receiving only a low-fat diet and placebo instead of antioxidant supplements. Biomarkers were measured at the baseline, then after 42 days of experimentation. In the end, participants in the intervention group reduced the reactive proteins C and inflammatory markers isoprostane 8-iso-PGF2α and interleukine IL-6 compared to the controlled group (Mauriz et al., 2013). Therefore, when treating multiple sclerosis through dietary interventions for a low-fat diet, it will be useful to include antioxidant supplements.
One of the nutritional interventions that has been used as a primary treatment is details to reduce the prevalence of seizures in epilepsy patients. Unlike the recommended diet for MS, the recommended diets for the treatment of epilepsy have promoted high-fat diets, particularly the importance of medium-chain triglycerides. Ketone is the first of these suggested diets, indicating that epileptic patients consume a diet consisting of 90% fat and 10% protein and carbohydrates combined. This led to the development of the average diet of the modified triglyceride series, which recommended a slightly lower fat content, in a total of 71-75% of the diet consisting of fat, 10% protein, and 15-19% carbohydrates. Furthermore, this diet explained that 30-60% of the diet should be specifically from medium-chain triglycerides, while 11-45% should come from long-chain triglycerides, regardless of anything, this breakdown should add to at least 71% of the fat diet. Newer, less
Diets often used include low blood sugar treatment, which breaks the composition of a healthy diet down to 60% fat, 20-30% protein, and only 10-20% of carbohydrates, and the modified Atkins diet, which strongly encourages eating high-fat and high-protein foods with a reduction in carbohydrate intake to 10 to 15 grams per day (Neil and Cross, 2010).
Neil and Cross (2010) conducted a literary review of several studies examining the effectiveness of these diets. The ketone diet and the medium-ketone tri-chain diet have shown to be the most effective. The government's ability to provide as much as a large number of staff is also needed to provide a clear and comprehensive account of the financial and financial needs of the public and the public. Furthermore, 30% to 100% of the participants, based on a specific study, experienced a 50% or more reduction in the frequency of seizures. While these diets may be effective in reducing the prevalence of seizures, other health aspects should be considered in such a severe diet. These diets revealed negative effects on children's biomarkers. One study examined children's biomarkers after six months of dietary adherence. These effects included a significant increase in blood plasma in LDL, VLDL, and non-HDL cholesterol as well as a significant decrease in HDL cholesterol. In addition, levels of triglycerides and polypoprotein B have increased dramatically in the blood plasma of these children (Kwiterovich et al., 2003). In response, Johns Hopkins stated that children should adhere to the diet for only two years, after which their seizures may not return and their biological markers should return to normal (Lawson, 2003).
Whole of Diet Approaches and Alzheimer`s Disease:
There is some evidence that adherence to diets based on health policy guidelines may be associated with improved cognitive function through population studies that have examined regiments from several countries including the United States, the Netherlands, Finland, Italy, Canada and France. Literature has begun to reinforce the importance of studying dietary patterns or the entire diet approach rather than individual foods or nutrients because of the likely synergistic effects of nutrient compositions. For example, a diet that is high in saturated fatty acids and also high in monounsaturated fatty acids may have conflicting effects on the risk of creation and there is an overall null effect. Thus, the study of dietary patterns and the evaluation of food compositions may provide insights into the synergistic effects of some nutrient formulations in relation to delaying the onset of a thousand. Food/clinical trials with multi-nutrition interventions (treatment of neurological protection, cardiovascular and inflammatory responses should be over a sufficient period of time (minimum 12 months, 18 months or more, better), which control the confusion of food and lifestyle factors, and with study designs that allow for the identification of synergistic or multifactor effects of nutritional interventions being evaluated, to demonstrate the clinically relevant effects of dietary interventions on delaying the onset of control.
Western diet and impaired hippocampal-dependent learning and memory:
The Western diet is a diet with fruits, vegetables, whole grains, legumes, fish, low-fat dairy products, excessive amounts of refined and processed foods, alcohol, salt, red meat, sugary drinks, snacks, eggs and butter. The Western diet, which suffers from low potassium, high sodium, fat scinfected and simple carbohydrates, has been implicated in many diseases, including atherosclerosis, type 2 diabetes, high blood pressure, and obesity. However, this diet negatively affects memory and learning:
- The Western diet is associated with learning deficits that depend on hippopotamus and memory over age.
- Hippothal dysfunction is associated with increased BBB permeability
- Western diets disrupt nerve signals that affect the formation of hippopotamus nerves and plasticity.
- Eating the Western diet may lead to a vicious cycle of obesity and cognitive decline.
- Gontism and cognitive dementia may have common nutritional origins.
Vitamin E in neurological health:
The critical needs of vitamin E have been recognized in the NHS for more than 50 years, when 'prominent ataxia'' and neuromuscular disability were first described in vitamin E vitamin e-deficient mice. Similarly, humans who have mutations in the TTPA gene are primarily present with ataxia with vitamin E deficiency, characterized by ataxia and extremely low vitamin E levels (3 micrometers). Improving AVED patients with vitamin E supplementation emphasizes an indispensable condition of vitamin E for optimal neuromuscular health. Due to the vital need to maintain the optimal status of vitamin E, CNS has developed unique mechanisms to maintain vitamin E balance. The turnover rate of vitamin E in the brain is up to 10 times slower than that in other tissues. In addition to progressive ataxia, other neurological manifestations of vitamin E deficiency include the loss of proprep, areflexia, the removal of the sensory myela in the spine, and purkinje neuron degeneration, accompanied by atrophy of neurons and axis spheroids. Neuromodifications that accelerate the atxphenic phenotype are the atrophy and decrease of the dural arboretise of purkinje neurons, which are responsible for the only motor output of the cerebellum cortex.
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