Parkinson’s disease is a chronic progressive neurodegenerative disease, the exact cause of which has not been fully elucidated, and may be influenced by a combination of genetic and environmental factors, among which diet may also play an important role. In addition, due to the unique pathological characteristics, clinical manifestations and treatment options of Parkinson’s disease, proper diet and balanced nutrition are crucial in measuring and evaluating the overall treatment effect and quality of life of the patients throughout the course of the disease from the onset of the disease. Therefore, appropriate dietary and nutritional management of patients with Parkinson’s disease should be carried out at an early stage: dietary status assessment should be part of the routine examination of patients with Parkinson’s disease, dietary education should be one of the therapeutic measures to improve the overall condition of the patients, and nutritional interventions should be a part of the treatment strategy of Parkinson’s disease. This article describes the relevance of diet and nutrition to Parkinson’s disease in terms of prevention and treatment, respectively. I. Prevention Although most studies have not found an exact correlation between dietary nutrition or its components and Parkinson’s disease, a large number of related studies have shown that poor diet may be a risk factor for Parkinson’s disease, and the evidence is relatively strong. 1. Caffeine and nicotine: Caffeine and nicotine are the more studied risk factors. In 2 authoritative meta-analyses, 44 case-control studies and 4 cohort studies on the association between smoking and Parkinson’s disease were statistically analyzed. In 8 case-control studies and cohort studies on the association between coffee and Parkinson’s disease, it was concluded that long-term coffee drinkers or smokers had a lower risk of developing Parkinson’s disease. This research suggests that smoking may inhibit free radical damage to nigrostriatal cells through nicotine stimulation of dopamine release and upregulation of nicotinic receptors, inhibition of monoamine oxidase B or competitive inhibition of neurotoxins preventing neuronal damage; caffeine directly downregulates adenosine A2 receptors, counteracts adenosine inhibition of dopaminergic transport in the brain, and inhibits 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity. However, studies have shown that long-term coffee consumption significantly reduces the risk of Parkinson’s disease only in men, but in women the risk is U-shaped with respect to intake, with the risk being lowest when 1-3 cups of coffee are consumed per day. In addition, a large prospective study found that the use of estrogen therapy is not used in menopausal women, caffeine intake can reduce their risk of disease, but for those who have been taking estrogen therapy, the risk is increased, which may be related to estrogen changes the effect of caffeine. Alcohol: The correlation between alcohol consumption and the risk of Parkinson’s disease is not clear. A case-control study (interspersed in a large prospective cohort study) containing 395 patients with Parkinson’s disease showed that alcoholics had a significantly lower risk of developing Parkinson’s disease (OR=0,77, 95% CI 0,58-1,03 for those who drank at least 2 drinks per day). However, a recent large prospective study including 605 patients with Parkinson’s disease did not support the association of alcoholic beverages (beer, wine, spirits) with the development of Parkinson’s disease: relative to non-drinkers, men who ingested 30 g or more (the highest amount) of alcoholic beverages per day had an RR value of 1,29 (95% CI 0,9-1,86), and women who ingested 15 g or more (the highest amount) per day had an RR value of 1,29 (95% CI 0,9-1,86). ) of women, the RR value of 0, 77 (95% CI 0, 41 ~ 1, 45). 3, tea: tea is rich in tea polyphenols, caffeine, flavonoids and other substances, these substances exist in certain antioxidant, neuroprotective and anti-inflammatory effects. A meta-analysis containing 1,418 cases and 4,250 controls pointed out that long-term tea consumption can reduce the risk of Parkinson’s disease, but did not find a significant dose relationship. In addition, a prospective cohort study in Singapore that included 63,257 Chinese showed that black tea consumption reduced the risk of Parkinson’s disease, whereas no correlation was drawn for green tea. Presumably, in addition to the nature of the tea polyphenols contained in the two are significantly different, may also be related to different manufacturing processes, raw materials, production areas caused by changes in the content of bioactive compounds in the tea, but the exact mechanism needs to be further studied. 4, fat and cholesterol: unsaturated fatty acids are substrates for lipid peroxidation, which can generate free radicals and cause oxidative stress. Oxidative stress is an important link in the pathogenesis of Parkinson’s disease. Regarding the link, animal fats were shown to increase the risk of Parkinson’s disease in an early investigative study. A recent Japanese case-control study including 249 patients with Parkinson’s disease suggested that arachidonic acid intake significantly increased the risk of Parkinson’s disease, but did not find any differences in the risk of the disease by intake of total fat, saturated fatty acids, monounsaturated fatty acids, omega-3 polyunsaturated fatty acids, alpha-linolenic acid, eicosapentaenoic acid, docosahexaenoic acid, omega-6 polyunsaturated fatty acids, or linoleic acid. Differences. In addition, the association between cholesterol intake and Parkinson’s disease is inconclusive. 5, dairy products: a large sample cohort study in the United States showed that a high intake of dairy products can significantly increase the risk of Parkinson’s disease in women, presumably the possible mechanism is that dairy products reduce the concentration of circulating uric acid, uric acid, as a natural antioxidant, can reduce oxidative stress damage in order to protect the nerves, but does not rule out the possibility that dairy products are contaminated with pesticides that have neurotoxins. However, a Japanese case-control study showed no significant correlation between the amount of total dairy products, milk, yogurt, cheese, ice cream, calcium, or vitamin D intake and the risk of developing Parkinson’s disease, and no gender differences. The results of the two different studies may be related to the origin of dairy products, quality and research methods. 6. Vitamins: A recent meta-analysis showed that moderate intake of vitamin E has a protective effect against Parkinson’s disease and reduces the risk of developing Parkinson’s disease, and no association was found between vitamin C and the prevalence of Parkinson’s disease. Based on current evidence, the neuroprotective effects of the antioxidants vitamin A and vitamin C are unclear, so some scholars do not advocate routine oral supplementation. 7, turmeric: as a spice, used in traditional Indian cuisine and traditional Chinese medicine, with antioxidant, anti-inflammatory and neuroprotective effects, a recent animal study showed that slowly supplying turmeric through food to MPTP-intervened mice can protect against MPTP-induced protein damage, protection of mitochondrial activity and nigral neuron degeneration, so further study of its active ingredients, to guide the prevention and development of Parkinson’s disease has an important role. 8. Mediterranean diet: While emphasizing the role of individual nutrients, the overall diet type and habits are equally important. The Mediterranean diet, a type of diet rich in fruits, vegetables, legumes, whole grains, poultry and fish, low in saturated fatty acids, and moderate in alcohol, reduces the risk of Parkinson’s disease, a finding that has been confirmed in a large prospective cohort study. This may be related to factors such as the high availability of antioxidant foods in the diet, but the mechanism of the protective effect of this fish-inclusive, vegetarian-based diet against Parkinson’s disease requires further study. Second, treatment Both the symptoms of Parkinson’s disease itself and the adverse effects of anti-Parkinson’s disease medications can affect the nutritional status of patients. For example, myotonia and tremor can increase the energy consumption of the body, and the different degrees of adverse effects of anti-Parkinson’s disease drugs on the digestive system, coupled with the emergence of psychiatric disorders, autonomic dysfunction, sleep disorders and other non-motor symptoms, all of which are prone to cause weight loss and malnutrition of the patients, which further accelerates the progression of the disease and aggravates the extent of the disease. Therefore, the principle of combining prevention and treatment should be actively adopted to co-manage patients’ diet and nutrition, so as to improve patients’ therapeutic effect and survival quality. 1, Improvement of motor symptoms related to dietary regulation: food-based Parkinson’s disease treatment research is not much, one of the food is the prickly sallow bean, whose dried seed powder contains 0, 2% ~ 2, 0% levodopa, and the latter is one of the main drugs for Parkinson’s disease treatment. Two studies have reported that people with Parkinson’s disease may benefit from its extract, but large clinical trials to confirm this are lacking. Alternatively, patients with Parkinson’s disease who have mild symptoms may experience improvement from long-term consumption of fava beans.84 g of fresh or canned fava beans may contain 50 to 100 mg of naturally occurring levodopa. It should be noted that the amount of levodopa in beans is not consistent, and its effective and toxic doses are not yet known, so taking natural beans freely is also not recommended. There is also a ketogenic diet rich in fatty acids that may protect motor function. An animal study showed that hydroxybutyric acid protects against MPTP-induced dopamine neuron degeneration and Parkinson-like symptom deficits. In a feasibility study conducted by Vanitallie et al. that included 7 patients with Parkinson’s disease, 5 patients adhered to a ketogenic diet for 28 d and had improved Unified Parkinson’s Disease Scale scores (but did not exclude a placebo effect). 2, Dietary regulation of symptom fluctuations: in clinical work, doctors often tell patients to take their medication 30 min before meals to ensure maximum absorption of the drug. This is because a large number of neutral amino acids in the diet (isoleucine, leucine, valine, phenylalanine, tryptophan, tyrosine) can competitively inhibit the absorption and transport of levodopa in the intestinal tract, so levodopa and protein with the same dose can reduce its bioavailability, thus slowing down or attenuating the “open” period. Dietary management related to different disease stages can focus on protein intake. In early Parkinson’s disease, a normal protein diet of about 15% of total energy is advocated, whereas the principles of a low-protein and protein-redistributive diet (about 10% of total energy) are more appropriate for patients with advanced Parkinson’s disease with fluctuating comorbid symptoms. The latter is based on the principle that protein intake needs to be restricted during the day (i.e., breakfast and lunch) while a high-quality, high-protein diet can be consumed at night so as not to interfere with the absorption of oral medications during the day. The daytime low-protein diet is effective in improving symptom fluctuations and has been shown in a randomized, single-blind clinical trial to significantly shorten the “off” period with only slight weight loss relative to a balanced diet. However, in a systematic review, there was insufficient evidence to support the use of a low-protein diet. Protein redistribution diets may improve motor function, but they are poorly flavored, difficult to adhere to, and may lead to complications as patients age, such as deficiencies in various micronutrients (calcium, iron, vitamins, etc.), osteoporosis, myopathy, fractures, and increased risk of falls (there is now a large body of evidence to support that small increases in protein intake in older adults are better at minimizing the incidence of these complications). Given the changes in levodopa dosage forms and the introduction of complementary medications such as levodopa degradation inhibitors and/or dopamine agonists, the long-term nutritional impact of low-protein and protein-redistributive diets and their real effectiveness in clinical practice deserve to be reassessed. Dietary modification of non-motor complications: Dysphagia is most common in patients with advanced disease, and motor retardation and dystonia of the digestive tract muscles can cause dysphagia and affect food intake. In order to improve this situation, the following points are worthy of attention: in the control of Parkinson’s disease on the basis of nutritional supportive therapy, try to use fluid diet. If adequate nutritional intake is not possible for a long time, an indwelling gastric tube or gastrostomy or endoscopic cricopharyngeal myotomy may be considered to ensure nutritional and medication intake. Constipation often exacerbates motor symptoms and can be the primary symptom in many patients, and an increased fiber diet (at least 30-35 g/d) and fluid intake (at least 1500-2000 ml/d), as well as appropriate exercise, are recommended. Of these, emphasis should be placed on vegetarian fiber intake. Results of an open study including 19 patients with Parkinson’s disease showed that a diet rich in soluble fiber not only improved constipation, but also increased levodopa bioavailability and improved overall motor symptoms in patients with Parkinson’s disease. A recent study reported that regular intake of fermented milk containing probiotics significantly improved chronic constipation symptoms in Parkinson’s disease patients. Delayed gastric emptying and gastroesophageal reflux are one of the symptoms that often occur in early and late stage Parkinson’s disease patients, which may be related to autonomic dysfunction and long-term medication-induced slowing of gastrointestinal peristalsis and muscle spasms. Delayed gastric emptying can cause loss of appetite, bloating, etc., and reduce the absorption of medications. Effective methods include eating smaller meals and taking medication 30 minutes before meals. Nausea, vomiting and anorexia mostly occur in the early stage of drug administration, and may slowly improve with later tolerance. To avoid interfering with drug absorption, it is generally recommended to take the drug on an empty stomach or with a small amount of food, such as fruit juice, cookies, fruits and so on. Taking the medication may reduce symptoms. Upright hypotension may have dizziness or no symptoms. It is recommended to increase the amount of sodium in the diet, such as using high-salt foods or sodium-containing tablets; increase the total fluid intake, at least 1,5~2,0 L/d. 4. Dietary modification after surgical operation: weight gain is often caused after surgical operation (pallidocerebellar disfigurement, deep brain electrical stimulation), which may be related to the condition getting better, the slowing down of the dopaminergic side effects (such as dyskinesia) and the gradual recovery of neuroendocrine function (such as insulin and growth hormone) gradually returning. Weight gain can slow down the improvement of motor function, lead to metabolic disorders, and increase the occurrence of diabetes, cardiovascular disease and other co-morbidities, thus reducing the outcome and prognosis of the surgery. Therefore, postoperative weight control is necessary. However, for patients with functional deficits in Parkinson’s disease, conventional weight loss is undesirable, and weight control can only be achieved through individualized modification of dietary habits and appropriate control of food intake. In one study, 57 Parkinson’s disease patients who underwent bilateral thalamus nucleus stimulation were evaluated nutritionally, and under the same nutritional status, caloric requirements were calculated and redistributed over 1 d (15% protein, 20% fat and 65% carbohydrates), and the results showed that patients’ weight gain or weight loss was controlled. 5. General principles of dietary therapy: Disease assessment of Parkinson’s disease patients with long-term follow-up should include all issues including medication and dietary management in order to achieve the combined goals of treating the disease and improving quality of life. Optimizing pharmacological treatment of motor and non-motor symptoms throughout the course of the disease is essential. Although the impact of nutritional management on the course of Parkinson’s disease is not completely clear, the following nutritional counseling and interventions can be used as general principles of dietary treatment for Parkinson’s disease: (1) Eat a balanced diet, paying special attention to fluid and fiber intake, and incorporate the principle of individualization to proactively prevent weight changes. (2) Optimize the pharmacokinetics of levodopa and avoid interactions with nutrients such as dietary protein. A balanced Mediterranean-style dietary pattern may be advocated until levodopa is administered. When the disease has progressed to the point where the addition of levodopa is necessary, protein redistribution dietary regimens may improve its absorption. (3) Improve gastrointestinal dysfunction such as dysphagia, gastroesophageal reflux, and constipation. (4) Actively preventing, monitoring, and supplementing readily available nutritional deficiencies, especially micronutrients and vitamins, such as vitamin D, vitamin B12, coenzyme Q10, vitamin B6, and vitamin E, in appropriate amounts. III. Conclusion It can be seen that diet and nutrition have an important role to play in the occurrence and development of Parkinson’s disease. Good nutritional status should be maintained throughout the entire course of Parkinson’s disease, from the onset of the disease to the end of the disease. Nutritional requirements are individualized and vary from time to time, and should be determined based on a comprehensive assessment of the response to treatment, side effects of medications, and complications of the disease. As patients are more likely to suffer from malnutrition and weight loss due to various reasons, which will definitely worsen the disease, it has become a difficult but important task for nutritionists, medical staff and relatives (or companions) to ensure proper dietary and nutritional management without compromising the anti-Parkinson’s disease drug therapy.