Parkinson's disease: most effective dietary supplements

Parkinson's disease is a degenerative disease of the central nervous system that primarily affects people over 50 years old. It is characterized by a progressive loss of dopaminergic neurons in the substantia nigra of the midbrain, a region essential for movement coordination. It is the second most common neurodegenerative disease after Alzheimer’s disease. Chronic, progressive and currently incurable, it leads to a variety of motor and non-motor symptoms that progressively impair patients' quality of life.

Origin and pathophysiology

Parkinson's disease results from the degeneration of dopamine-producing neurons, a key neurotransmitter for movement regulation. These neurons, normally numbering around 500,000 in the substantia nigra (or locus niger), see their population drastically decrease as the disease progresses. When their number falls below the critical threshold of 100,000, dopaminergic transmission is no longer sufficient to suppress the excessive activity of cholinergic neurons. This cholinergic hyperactivity stimulates areas such as the thalamus, the globus pallidus and the cortex, causing the characteristic motor disturbances. The causes of this degeneration include several biological mechanisms: oxidative stress, mitochondrial abnormalities, glutamate excitotoxicity, disruption of trophic factors, and chronic inflammation. In addition, abnormal accumulation of the protein alpha-synuclein in neurons, forming Lewy bodies, is a key marker of the disease. These pathological aggregates disrupt the functioning of dopaminergic neurons and other neuronal systems, such as those involving acetylcholine, serotonin and norepinephrine.

Etiology and risk factors

Parkinson's disease has a multifactorial origin, combining genetic and environmental factors. Mutations in certain genes (notably involved in juvenile or early-onset forms) play a role, as do environmental exposures to pesticides, herbicides or heavy metals. Repeated head traumas, as observed in boxers, are also risk factors. Certain dietary behaviors, such as excessive consumption of iron-rich meats or animal fats, also increase risk. Conversely, studies suggest a protective effect of substances like caffeine, although these results are not yet fully confirmed.

Clinical symptoms

Parkinson's disease manifests with motor and non-motor symptoms that evolve over time. Motor symptoms include: • Resting tremor: Primarily affects the hands and feet, often unilateral at onset. These tremors disappear during voluntary movements and during sleep, but worsen with stress or fatigue. • Muscle rigidity: Muscular stiffness occurs, often described as a "cogwheel" sensation during passive movements. • Bradykinesia: Movements become slow and clumsy, with a loss of dexterity, such as in handwriting. • Akinesia: Difficulty initiating movements, loss of automatic movements (for example, arm swing when walking) and a masked facial expression. The non-motor symptoms include: These symptoms, sometimes present several years before motor manifestations, include: • Olfactory disturbances. • Sleep disorders (insomnia, periodic limb movements). • Gastrointestinal problems (constipation), urinary problems, and orthostatic hypotension. • Cognitive and psychiatric symptoms: depression, anxiety, irritability, and in advanced stages, dementia.

Diagnosis

Diagnosis is essentially based on the clinical exam, relying on the characteristic motor symptoms (resting tremor, bradykinesia, rigidity). Asymmetry of symptoms and a favorable response to levodopa strengthen the diagnosis. Imaging tests, such as dopamine transporter scintigraphy, can be used to resolve doubts. Scales like the UPDRS (Unified Parkinson’s Disease Rating Scale) allow assessment of clinical status and treatment effectiveness.

Treatments

Treatment of Parkinson's disease aims to alleviate symptoms and improve quality of life. Current approaches include: • Levodopa: Converted into dopamine in the brain, it is the reference treatment. • Dopaminergic agonists: Directly stimulate dopamine receptors. • Monoamine oxidase B inhibitors: Prolong the effect of dopamine by reducing its breakdown. • Treatment of non-motor symptoms: Medications for constipation, insomnia, or mood disorders. • Deep brain stimulation: A technique reserved for advanced cases, where electrodes implanted in the brain can reduce tremor and rigidity. There are complementary measures: • Physiotherapy and rehabilitation to improve mobility. • Appropriate physical activity to maintain flexibility and reduce postural problems. • A balanced diet rich in antioxidants to combat oxidative stress.

Prevention and outlook

No effective means of prevention is recognized to date, but certain habits could reduce risk: adopting a diet rich in B vitamins and antioxidants, and avoiding prolonged exposures to pesticides or heavy metals. Current research is exploring new therapeutic avenues, notably inflammatory mechanisms, trophic factors, and gene therapies, offering hope for disease-modifying treatments in the near future.