This intrigues me.
Summary: Levodopa, a drug commonly prescribed for the treatment of Parkinson’s disease that increases dopamine in the brain was found to reverse the effects of neuroinflammation on the reward system and improve symptoms associated with depression.
Who do we believe?
ncbi.nlm.nih.gov/pmc/articl....
A relevant quote :
' The literature data indicate that L-dopa therapy of PD patients may induce oxidative stress by different mechanisms [5-7], and increase the levels of inflammatory markers [8], and leads to abnormal biothiols levels [9], and apoptotic [9] or possibly autophagy cell death [10-13]. Moreover, in PD change levels of biochemical parameters may also lead tomicroglial activation [14], DA oxidation [15] and Lewy’s bodies (LB) deposition [16].
In PD the level of homocysteine (Hcy) is increased, which may in these patients augment the risk of this neurodegenerative disease by toxic effects in dopaminergic neurons [17]. High Hcy concentrations in patients with PD may also lead to impaired cognitive and motor skills and the development of depression and progression of the disease [18]. '
Melatonin inhibits the toxicity of homocysteine :
ncbi.nlm.nih.gov/pmc/articl....
On the other hand melatonin may be helpful either way :
A relevant quote :
' Pro-inflammatory systemic conditions that can cause neuroinflammation and subsequent alterations in brain regions involved in emotional regulation have been suggested as an underlying mechanism for the pathophysiology of major depressive disorder (MDD). A prominent feature of MDD is disruption of circadian rhythms, of which melatonin is considered a key moderator, and alterations in the melatonin system have been implicated in MDD. Melatonin is involved in immune system regulation and has been shown to possess anti-inflammatory properties in inflammatory conditions, through both immunological and non-immunological actions. Melatonin has been suggested as a highly cytoprotective and neuroprotective substance and shown to stimulate all stages of neuroplasticity in animal models. The ability of melatonin to suppress inflammatory responses through immunological and non-immunological actions, thus influencing neuroinflammation and neurotoxicity, along with subsequent alterations in brain regions that are implicated in depression, can be demonstrated by the antidepressant-like effects of melatonin. Further studies that investigate the associations between melatonin, immune markers, and alterations in the brain structure and function in patients with depression could identify potential MDD biomarkers. '
Art
One of my many frustrations regarding PD is the frequency of studies which appear to be contradictory. I just know I need carbidopa levodopa to function and high doses of melatonin seem to have helped me, too, despite the criticisms of both.
No criticisms from me on either because they both have the potential to improve quality of life in PwP and melatonin has more than enough studies to support the positive things I have said about it on this forum.
Btw, Jim, what dose of melatonin are you currently at?
Art
120 mg per night.
Are you tolerating that dose well? I'm at 132 mg/day.
Art
I have taken 60 to 200 mg melatonin each night for about 6 years. I think it works. Along with about 20 nutrients for inflammation and mitochondrial enhancement.
regarding CL, interesting it’s antinflammatory given it’s causing an increase in homocysteine. Would you recommend liposomal glutathione and/or NAC to reduce homocysteine?
B-12, B6, Folate, B2, B1, NAC, melatonin, zinc and astaxanthin which like melatonin also works against homocysteine neurotoxicity. Your ability to tolerate and how effective they are for you will help determine which ones are best for you .
Art
The study I quoted described the following which not only sounds inflammatory to me, but also conducive to disease progression unless other steps are taken to mitigate these levodopa effects, so I am not sure what you mean by "antinflammatory"? Here is the study quote:
' The literature data indicate that L-dopa therapy of PD patients may induce oxidative stress by different mechanisms [5-7], and increase the levels of inflammatory markers [8], and leads to abnormal biothiols levels [9], and apoptotic [9] or possibly autophagy cell death [10-13]. Moreover, in PD change levels of biochemical parameters may also lead tomicroglial activation [14], DA oxidation [15] and Lewy’s bodies (LB) deposition [16].
In PD the level of homocysteine (Hcy) is increased, which may in these patients augment the risk of this neurodegenerative disease by toxic effects in dopaminergic neurons [17]. High Hcy concentrations in patients with PD may also lead to impaired cognitive and motor skills and the development of depression and progression of the disease [18]. '
Art
New Levodopa Pump Approved 
Levodopa ER before bed?
Negative levodopa
Avoid levodopa phobia
