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Basics of Parkinson's disease
Parkinson's disease (PD) is a progressive neurological condition limiting movement. It is one of the most common brain diseases, second only to Alzheimer's, affecting an estimated 1.5% of people over 65 .
Early-onset PD, occurring before 50 years of age, is relatively rare and often hereditary. Most cases after age 50 are sporadic , suggesting that environmental factors probably play an essential role .
Non-motor PD symptoms, including constipation, anxiety disorder, rapid eye movement, sleep behavior disorder (RBD) and anemia, occur long before most patients get a diagnosis . In PD, a preclinical phase spanning 20 or more years often precedes the appearance of overt signs, such as developing a tremor .
In the early stages, the general trend is for patients to develop shoulder stiffness and decreased movement in the shoulder simultaneously with reduced gut function. As other aspects of the brain become affected, patients also develop Lewy body dementia.
Origins of Parkinson's disease
PD occurs due to the inadequate functioning of many dopaminergic neurons in the basal ganglia part of the brain. More specifically, in the locus niger, locus coereleus and the dorsal nucleus of the vagus nerve .
These neurons die or become clogged up through impaired cellular function and cannot emit the signals that activate the striatum neurons that produce the dopamine controlling movement. This event causes a cascade effect whereby other types of neurons that are no longer regulated by dopamine start producing an excess of another neurotransmitter called acetylcholine.
The latter stimulates excessively neurons that produce GABA, resulting in the slowing down of motor neurons of the cerebral cortex. The inhibitory input is eventually relayed to the spinal cord and muscles and is responsible for uncoordinated movement .
Rigidity problems that often accompany movement disorders in PD do not stem from the brain telling muscle to contract; the part of the brain that inhibits muscle contraction is not working.
Role of diet in Parkinson's disease
Dietary and lifestyle changes are instrumental in helping to protect dopamine-producing neurons and stave off complications due to the limitations of current PD therapy.
The primary medication in PD, Levodopa (L-dopa), works by enhancing dopamine production. Still, it has a short half-life and limited and variable reabsorption through the digestive and blood-brain barriers. L-dopa also requires the amino acid decarboxylase to synthesize dopamine, which declines in the striatum with disease progression.
In early PD, someone may take Levodopa once or twice a day, and it works to control symptoms. But as PD progresses, after 5 or 7 years on medication, the doses become closer together and even giving it every hour is not enough . Increasing the efficacy of L-dopa therapy through diet can be a powerful strategy.
Dietary changes alongside standard therapy hold great promise for reducing movement disorders and improving the quality of life of PD patients.
Anecdotal evidence suggests that patients can expect up to a 50% reduction in tremors and decreased muscle stiffness in five to six months following the adoption of healthy eating habits. Dietary interventions can also reduce depressive symptoms that often accompany motor symptoms in PD.
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The main goals of nutrition interventions are to protect healthy dopaminergic neurons and slow the progression of further cell death. One goal is to make sure mitochondria are protected with antioxidants and not attacked by neurotoxic substances in the diet. Improving gut function and restoring microbiome diversity is also paramount to addressing intestinal hyperpermeability in many patients.
A hypotoxic, ancestral-type diet that is much higher in good fats and restricts carbohydrates does not present any risks and is well tolerated in PD. One recommendation is to follow a low-carbohydrate diet (to less than 100 grams a day), based on mounting evidence of a link between metabolic syndrome and PD .
A process similar to insulin resistance might occur in the PD brain, even without metabolic disorders. The consumption of modern diets, high in carbohydrate and animal-derived foods, also promotes the formation of advanced glycation end products (AGEs) and could result in the glycation of alpha-synuclein proteins leading to their aggregation into Lewy bodies .
While the evidence is scarce, interventions that improve insulin resistance, such as adhering to a low-carbohydrate diet, seem to be associated with a reduced risk of developing PD.
This type of high-nourishment diet is also helpful to maintain sufficient caloric intake, as disease progression and L-dopa usage tend to cause significant weight loss .
Let's now explore other recommendations for each food group and micronutrients in detail.
Setting minimum intakes for protein is a balancing act in PD. On the one hand, protein intake should be raised slightly after age sixty-five to seventy in individuals losing weight and muscle. On the other hand, excess protein notoriously interferes with dopamine production .
Dietary proteins compete with L-dopa for intestinal absorption and transport across the blood-brain barrier (BBB), and this competition ultimately limits the effectiveness of the treatment.
The consensus is that PD patients should consume low but sufficient proteins. Limiting protein intake to the RDA of 0,8g for 1kg of total bodyweight per day or 10-15% of calories is a safer strategy. And so is eating a primarily plant-based diet, as plant foods are lower in protein than animal foods.
Estimates suggest that the (omnivore) Mediterranean diet provides about 100 grams of daily protein, 50 grams above PD patients' needs. It also includes red meat, yet excluding red meat improves movement . Heme iron in meat is problematic as it increases superoxide radicals and hydrogen peroxide, two factors contributing to oxidative stress in dopamine-producing neurons.
According to research, those following a plant-based diet can reap a multitude of benefits. One pilot study found that motor function scores were twice as good after one month on this diet than in the regular diet group. The study also found that the reduced protein intake increased the transport of L-dopa and tyrosine into the brain .
Therefore, aiming for a plant- and low-mercury-fish-based shore-type diet may be more suitable. Since PD patients tend to report that protein aggravates symptoms, displacing protein intake in the evening is another consideration.
PD patients may benefit from limiting carbohydrates in the diet. A low-carbohydrate diet generally entails reducing total carbohydrate intake to less than 130 grams per day, including the recommended 30 grams of fiber.
Interestingly, there is evidence that a ketogenic diet (at around 20 to 50 grams of daily carbohydrates) could potentially help prevent or combat PD. In a small, uncontrolled study, PD patients experienced a 43% reduction in symptoms after following a ketogenic diet for 28 days .
Other research suggested that ketones produced on a ketogenic diet may positively affect how the brain responds to dopamine, reducing the condition's symptoms . This effect is, in part, mediated by the ketone beta-hydroxybutyrate (BHB), which limits the death of dopaminergic cells.
Some evidence suggests that the ketogenic diet promotes the creation of new mitochondria. This is an exciting benefit because mitochondria accumulate damage with age (just as cells do), accelerating the aging process and PD progression.
More research will be needed, though, before we can say with any certainty whether ketones and the ketogenic diet can indeed help in PD.
As a general rule, as long as PD patients focus on non-starchy vegetables and high-fiber fruits, there should be no need for strict adherence to a ketogenic diet to see improvements. Carbohydrates should be from natural foods with a carbohydrate density (CD) of less than 25% (25 grams per 100g).
The minimum daily intake for fat should be greater than 40 grams for men and greater than 30 grams for women with no upper limit and no less than 15% of total calorie intake. These figures come from the Food and Agricultural Organization of the United Nations (FAO) guidelines for the general population .
PD patients are likely to require higher dietary fat intakes to compensate for the decrease in carbohydrate and excess protein.
Overall, the diet should be rich in "good" unsaturated fat but very poor in saturated fat, hydrogenated and trans fats. Research suggests that replacing polyunsaturated fat with saturated fat may increase the risks of developing PD in men .
Polyunsaturated fats include omega-6 and omega-3 fatty acids. Keeping a nearly equal balance of omega-3 to omega-6 fatty acids is essential. Higher omega-6s in the diet may increase the risk for PD .
As most people are deficient in omega-3, it is advisable to eat dense sources that are also low in mercury. Higher omega-3 (DHA) is considered neuroprotective against oxidative stress and inflammation. It may protect the brain by increasing glutathione which helps decrease the accumulation of oxidized proteins in the brain .
One study also showed that supplementation with omega-3s reduced depression in PD patients . One caveat is that DHA in the esterified, phospholipid form (fish or fish roe) rather than unesterified, free fatty acid form (fish oil supplements) is better absorbed by the brain .
Compared to fish, which contain between 1% and 1.5% phospholipids, fish roe (from herring, salmon, pollock, and flying fish) have between 38%–75% of their lipids in the form of phospholipids—making them ideal omega-3 sources in PD.
According to Dr. Bruce Ames's triage theory, metabolic processes that mitigate aging in the long term ultimately get neglected through strategic rationing of micronutrients in favor of pathways essential for short-term survival. This evolutionary adaptation accelerates the aging process and can lead to neurodegenerative diseases.
High consumption of calorie-rich, micronutrient-poor unbalanced diets only exacerbates the problem. Many nutrients influence neurotransmitter activity and brain function, but the RDAs are probably set much lower than they need to be.
They are sufficient to quell acute deficiencies but way too low to hit optimum levels. More moderate deficiency levels could be causing insidious changes over time, culminating in diseases of aging like PD .
The gut microbiota also dictates the absorption rate and trafficking of a range of essential nutrients. In addition to healing and inoculating the gut with a mix of different species of microorganisms, PD patients should aim to get a broad spectrum of vitamins, minerals, enzymes and diverse hormetic plant compounds through the diet or by supplementing wisely.
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