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Dr. Mercola's Censored Library (Private Membership)

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Just steve's avatar
Just steve
Mar 17

What does it take? Is this enough? Today's third article exposing while still the Gold Standard for babies, Mom's Milk, research showing how pollutants, plastic residues, chemicals from many sources are health, growth, mental, emotional, gender/reproductive disruptive even in small quantities. Decades of Public Campaigns that the world is over populated and World Leaders, Shakers and Mover's meeting in organizations such as WEF, a giggling Bill Gates expressing we could reduce population with Vaxxx's. Then add in what little Dark Horrors have dripped out from the Epstein Files of unthinkable treatment of not only the public, but to babies, toddlers, and youngsters, what else is needed to wake up and smell the coffee? For a portion of the 1% Humanity isn't even viewed as Human, viewed as less than animals. From cradle to grave the World is being poisoned, and sterilized. Positive, peaceful, health healing, health building is possible but will only come from the Bottom Up. Cash is Freedom, use it Locally, as much as possible or lose both. Figure out what can be done Locally to supply the solid basic needs - Locally! Cities built to fill the 1% current control systems enforcers are even being taken over by Tech. No humans need apply. Just Sayn'

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Guillermou's avatar
Guillermou
Mar 17

A friend has Parkinson's disease and is being treated by a holistic neurologist. I also help him with some recommendations. Parkinson's disease (PD) is the fastest-growing neurological disorder worldwide, and the burden is predicted to double from six million to more than 12 million between 2015 and 2040.

In PD, mitochondrial dysfunction acts as the main triggering factor. Specifically, pathogenic factors (such as mutations in the PINK1/Parkin gene or environmental toxins) compromise mitochondrial integrity and function, while also impairing the PINK1/Parkin-dependent mitochondrial autophagy mechanism. This alteration prevents the timely elimination of dysfunctional mitochondria, leading to their excessive accumulation. This results in reduced ATP generation, massive ROS production, and increased permeability of the outer mitochondrial membrane.

Mitochondria are organelles with a central role in maintaining and executing key metabolic processes and cellular homeostasis. Neurons are particularly susceptible to mitochondrial dysfunction due to their high bioenergetic demands. Mitochondrial impairment has been implicated in the etiopathogenesis of Parkinson's disease (PD). This includes environmental toxins that affect the electron transport chain (ETC) and, consequently, oxidative phosphorylation; mutations in mitochondrial DNA (mtDNA) and nuclear DNA (nDNA); increased oxidative stress; and disturbances in mitochondrial quality control.

Oxidative stress is a central trigger for the loss of dopaminergic neurons, representing a common endpoint where various pathogenic influences converge. Genetic mutations and environmental factors can alter mitochondrial function, promote neuroinflammation, impair lysosomal and autophagic clearance, and disrupt protein and lipid turnover, leading to the accumulation of dysfunctional cellular components. Collectively, these alterations amplify ROS generation and oxidative damage, positioning ROS as a key factor in the integration of multiple pathological processes in Parkinson's disease (PD). PD is accompanied by mitochondrial dysfunction characterized by alterations in the electron transport chain, reduced ATP, and increased mitochondrial ROS production.

Neuroinflammation plays a key role in the progression of Parkinson's disease (PD), a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to motor impairment. The main pathogenic mechanisms of PD are metabolic dysfunctions, mitochondrial alterations, and an inflammatory response determined by microglial activation.

The results of a pilot study contribute to a growing body of evidence that PD also constitutes a systemic metabolic syndrome with impaired cellular energy and function in peripheral tissues. The significant impairment of both mitochondrial ATP production and resting metabolite levels in the transverse axonal (TA) muscles of PD patients suggests that skeletal muscle mitochondrial function could be an important tool for mechanistic understanding and clinical application in PD patients.

Following the demonstration of dopamine deficiency in PD, dopamine-enhancing strategies have become an essential part of PD management. Similarly, the recent identification of NAD+ and ATP metabolic deficiencies in the brain of PD patients, and now in skeletal muscle in vivo, provides a compelling argument for mitochondrial augmentation as a therapeutic strategy.

Furthermore, NR decreased serum and cerebrospinal fluid levels of inflammatory cytokines. Our findings suggest NR as a potential neuroprotective therapy for PD, warranting further investigation in larger-scale clinical trials.

Improving NAD metabolism could potentially act on several processes involved in PD pathogenesis, such as mitochondrial dysfunction, epigenomic dysregulation, neuroinflammation, and increased DNA damage.

The accelerated pathology in PD models is likely mediated by impaired mitochondrial quality control, and increasing cellular NAD+ levels alleviates mitochondrial proteotoxic stress and mitigates PD phenotypes.

Supplementation with or production of nicotinamide adenine dinucleotide (NAD) has become a promising disease-modifying strategy, targeting multiple key pathways in various neurodegenerative diseases, such as mitochondrial dysfunction, energy deficits, proteostasis, and neuroinflammation.

Dr. Conlon has concluded, and Dr. Mercola fully agrees, that the best single precursor to NAD+ is niacinamide, not niacin, NR, or NMN.

Fasting, calorie restriction, a healthy diet, exercise, sleep, social interaction and contact with nature, and dedication to a chosen profession all contribute to happiness. These factors enhance certain molecules, such as NAD, which are vital for health. NAD levels in our bodies determine the rate of the aging process. In younger cells and tissues, NAD levels are higher, associated with better physical activity, cognitive function, and potential for cellular repair and regeneration.

https://articles.mercola.com/sites/articles/archive/2023/12/03/nad-plus-optimal-health.aspx (2023).--

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112140/ (2014)

https://pubmed.ncbi.nlm.nih.gov/19286518/ (2009)

https://www.mdpi.com/2072-6643/15/4/943 (2023).--

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(22)00045-6 (2022).—

https://www.nature.com/articles/s43587-022-00217-9 (2022).--

https://advanced.onlinelibrary.wiley.com/doi/full/10.1002/advs.202408503 (2025).--

https://www.cell.com/trends/endocrinology-metabolism/fulltext/S1043-2760(25)00070-0 (2025).—

https://www.mdpi.com/2076-3921/15/2/187 (2025).--

https://link.springer.com/chapter/10.1007/978-981-97-9877-3_35 (2025).--

https://link.springer.com/article/10.1134/S1990750824601140 (2025).--

https://link.springer.com/chapter/10.1007/978-981-97-9877-3_39 (2025).--

https://www.sciencedirect.com/science/chapter/handbook/abs/pii/B9780443219924000269 (2026).--

https://www.mdpi.com/1422-0067/27/3/1301 (2026).--

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