Hi  – I’m sorry to hear that. Please bear with the long response but I want you to have a thorough reply to give you a better understanding and actions steps that you can also share with him:

Parkinson’s disease (PD) is a neurodegenerative disease involving damage to the part of the brain called the substantia nigra, affecting the brain’s dopamine production. Since dopamine is involved in muscle control and movement, as well as many neurological functions, it can cause a wide range of symptoms, including:
• Tremors that progress to weakness and constant shaking of the head and limbs
• Unstable and rigid gait, shuffling
• Poor balance
• Slowness and muscle stiffness
• Behavioral/mood dysfunction
• GI dysfunction, which may include• Constipation – a key symptom that can precede diagnosis by decades
• Nausea and bloating
• Loss of sense of smell – often precedes the diagnosis
• Loss of volume and clarity of speech
• Difficulty with handwriting
• Orthostatic hypotension

Many risk factors can be involved in the development of PD, including:
• Insulin resistance• People with diabetes are four times more likely to get Parkinson’s disease. Encourage getting a blood sugar panel tested.
• Twice the rate of brain loss with HbA1c of just 5.7 or 5.8
• Toxins• It is well known that various heavy metals can directly impair cellular energy production within the mitochondria.  A poorly fueled cell, over time, becomes a dysfunctional cell.
• Low cellular glutathione levels in the substantia nigra. There is a similar loss of glutathione in the nigra in Incidental Lewy body disease, which is thought to be an early form of PD.  This may interest you.  Studies to increase this were largely ineffective (not surprising given the difficulty of absorbing plain glutathione orally), but intranasal administration is showing promise, and IV glutathione has shown to be effective at increasing levels within tissues. Addressing key nutrients for glutathione production (e.g. cysteine, glycine, glutamine, selenium) and reducing exposure to factors that use up glutathione should be prioritized.
• Pesticides • Organochlorine pesticides – high levels double the risk
• PCBs and organophosphates – damage the enteric nervous system (GI tract nervous system)
• Glyphosate
• Heavy metals, especially:• Mercury – remove dental amalgams biologically, check seafood intake
• Aluminum• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8504163/ 
• Aluminum preferentially accumulates in the mitochondria and nucleus of the cell, where it evades chelation.
• Overnight fasting may help to increase autophagy.
• BPA – higher levels increase the risk of developing alpha-synuclein antibodies (found in Parkinson’s)• Mold (e.g. Ochratoxin A exposure has been shown to decrease dopamine levels in the brains of mice)
• High manganese levels
• Dysbiosis• • Constipation is often the first symptom.
• Constipation reduces the body’s ability to remove toxins.
• High LPS (lipopolysaccharides – bacterial byproducts) has been found in those with PD
• Low Prevolellaceae and high Enterobacteriaceae 
• Inflammation• • Elevated levels of TNF-alpha (TNF-a), inducible nitric oxide synthase (iNOS), and interleukin-1 beta (IL-1b)
• Traumatic Brain Injury• • Microglial activation due to physical trauma
• Brain-gut axis dysfunction due to head injury
• Sleep deprivation• • Those with PD have less REM and deep sleep and take longer to fall asleep
• They also commonly have higher cortisol and lower melatonin levels
• Lectin sensitivity (vegetarianism is more prevalent in those with PD) and aquaporins• This seems to be specific to non-organic lectin consumption.   
• Nutrient deficiencies• • High homocysteine is highly prevalent in those with PD, which increases free radicals (oxidative stress) in the brain, brain inflammation, nerve cell death and protein clumping in the brain. 
• Levels >11 are shown to increase the risk of cognitive decline and dementia. 
• MRI studies show white matter hyperintensities in the brain in those with high homocysteine, and these Parkinson’s individuals had the worst balance and most difficulty walking.
• Investigate:• Vitamins B6, B9, and B12
• Vitamin D 
• Lithium orotate deficiency 
• Viruses may be a contributing factor:• • HSV-1
• EBV
• Cytomegalovirus
• Chlamydia pneumoniae
• Hepatitis C (and the interferon treatment inhibits dopamine transmission in the midbrain)
• Genetics• While the vast majority of cases are not believed to be genetic, there have been some genetic contributors found. Of note are genes that influence one’s ability to detoxify various chemicals and prevent their build-up in the body.
• There may also be genetic issues with regard to overall cellular antioxidant synthesis.  For example, impairment in sulfation-related detoxification pathways has been found in 63% of PD patients vs. 37% of hospitalized controls.
• Others include:• PINK1 kinase
• PRKN ubiquitin ligase
• SOD2 – https://pubmed.ncbi.nlm.nih.gov/15287506/  

 
The challenge in PD is that by the time the disease has been diagnosed, 60-80% of the substantia nigra has already been damaged. Medications are available to reduce symptoms and slow the progression of the disease, but they become less effective over time. In terms of targeted support for this diagnosis, consider the following:
• Here is a comprehensive review of supplements that have shown benefits in PD.
• CoQ10 is a critical coenzyme for mitochondrial function. Low cellular CoQ10 has been shown in PD patients. Study results have been mixed (e.g. here and here), but in some cases, improvements in functioning have been demonstrated. The ability to convert the widely-used ubiquinone form of CoQ10 to its active (reduced) ubiquinol form likely plays a role in study results variability. Test levels if possible, and consider 300-400 mg twice daily of the ubiquinol form of CoQ10. Studies that paired CoQ10 with a high intake of Vitamin E showed less benefit. It is also likely that CoQ10 is more likely to be effective if started as early as possible in the disease progression.
• Vitamin B6 is a critical cofactor for the synthesis of dopamine throughout the body. Research shows improved function and fewer symptoms with Vitamin B6 supplementation (but is contraindicated in those using levodopa medication on its own (vs. in combination with carbidopa), as B6 can increase peripheral (vs. nervous system) synthesis of dopamine). Consider ~30mg daily of the P5P form of Vitamin B6 (pyridoxal-5-phosphate so that the body does not have to convert to this final form). Low intake of Vitamin B6 is independently correlated with a higher risk of PD (for example). This is likely best taken along with a high-quality B-complex at a different meal (e.g. Thorne’s Basic B Complex). • Since high homocysteine is associated with PD progression and increased symptoms, test homocysteine and aim to optimize levels. A urinary organic acids test (OAT) measures xanthurenate and kynurenate levels which can help to gauge cellular B6 status.
• Glutathione and N-acetyl cysteine (NAC). It is encouraged to seek out local clinics for regular intravenous glutathione therapy.  I know Dr. Roze offers IV therapies. Intranasal glutathione has been shown to be effective, but the therapeutic dose is widely disagreed on and still being investigated. Research (here, here, here) also shows NAC to be likely effective in preventing dopaminergic neuron death and raising cellular glutathione (by providing cysteine, one of the critical amino acids needed to synthesize glutathione), 1500mg daily in divided doses (build up to this over a couple of weeks). And this will likely be more effective when combined with adequate glycine (e.g. Pure Encapsulations NAC + Glycine powder). Additionally, glycine can help chelate glyphosate. Oral NAC has been shown to increase brain glutathione. Selenium is also critical for glutathione synthesis. Check to be sure the serum or RBC level is in the upper half of the reference range.
• Reduce exposure to toxins by choosing organic foods (to avoid pesticides, glyphosate, etc.), avoiding pesticide use in or around the home, choosing more natural cleaning products and personal hygiene products, and filtering water and air in the home and work environment. Additionally, consider toxins testing for heavy metals, mycotoxins, and environmental toxins for more targeted investigation and avoidance, as well as to assess needs for detoxification, binders, etc. 
• Antioxidant support.  Because of the role of increased oxidative stress in PD, broad-based antioxidant consumption should be increased via a diverse intake of vegetables, fruits, herbs, and spices. Melatonin sufficiency is especially important for countering inflammatory brain diseases like this. You might also consider alpha lipoic acid (ALA, specifically the “R” isomer form only,  a potent antioxidant that specifically helps to recycle glutathione for ongoing antioxidant use; 200-300mg twice daily (build up to this over a couple of weeks). Replete B vitamins first to ensure adequate methylation. (Monitor homocysteine every few months to ensure ongoing ALA use is not increasing it.)  If additional support is needed, pycnogenol from pine bark is a particularly potent option (200-300mg daily), as is ginkgo biloba extract (300mg daily). 8-OHdG can be measured in the blood as an accurate marker of oxidative stress and should ideally be in the lowest third of the reference range.
• Omega 3s (high DHA formula) to boost antioxidant capability and reduce brain inflammation (~2000 mg combined EPA + DHA per day).  
• S-acetyl-carnitine, a form of l-carnitine that is particularly well absorbed in the gut and taken up in neurons, directly supporting the use of fatty acids for cellular energy production. Consider 1000 mg twice daily for PD. This supplement has been shown to be effective at countering the effects of many different types of neurodegeneration. Cell line and animal studies have shown this to be particularly effective in combination with alpha lipoic acid in countering mitochondrial dysfunction in response to oxidative damage as well.
• Support digestion, especially constipation.  PD affects motor function throughout the body and thus can affect any muscle function, including motility, peristalsis, and – thus – the entire GI tract. The vast majority of PD patients have constipation several years before diagnosis (and having poor stomach function will deplete magnesium and other minerals and thus make this challenge even worse!).  Magnesium citrate supplementation will likely help, as well as probiotics with high Bifidobacteria content (e.g. Renew Life’s Ultimate Flora Adult 50+ formula). Over time, these patients may also benefit from digestive enzyme support with meals. As an additional note, there is new evidence that the microbiome in PD patients differs significantly and consistently from that of healthy controls; this will undoubtedly be a fascinating future area of research.

Additional considerations
1. If a person is using conventional levodopa medication (most commonly today in a combination drug called Sinemet), it has been demonstrated that a “protein redistribution diet” can significantly reduce PD symptoms. This involves minimizing protein during breakfast and lunch meals and focusing it during a dinner meal. To avoid creating insulin resistance, breakfast and lunch meals should focus on healthy fat and unrefined carbohydrate intake. There is some initial evidence that a ketogenic diet could help counter the effects of damaged mitochondria in neurons (and certainly makes sense in light of the pathophysiology of PD), but this has not been thoroughly researched yet.
2. Because it can interfere with the efficacy of medication, iron supplements are contraindicated in these patients.  There is also some evidence that elimination of red meat intake (which would be synergistic with the overall reduction in protein indicated above) can be helpful for this reason as well.

Regular daily, moderate exercise is also powerful in improving insulin sensitivity and managing oxidative stress.