Natural Options to Reverse Parkinsons Symptoms

Category: Parkinsons Disease Information (Page 4 of 15)

Access 20 years of research focused on identifying natural approaches, therapies and treatments that offer the opportunity to celebrate relief from the symptoms associated with a diagnosis of Parkinsons disease.

Many Causes of Parkinsons

Is a deficiency of dopamine the only reason for Parkinsons? Actually, there are many causes of Parkinsons which include toxins, trauma and infections.  

Some people take medications or supplements to boost dopamine levels. They welcome a temporary relief of symptoms. A conclusion drawn particularly by individuals who celebrate quick, though temporary relief, is that the only cause of symptoms centers on dopamine deficiencies.

Actually, infections are only one of the many causes of Parkinsons. Not convinced? Consider research that links Tuberculosis to Parkinsons, an infection becoming more prevalent in many countries.

I know. You are probably thinking: How could there be any connection between Tuberculosis and Parkinsons?

The study abstracts below document that there is a connection between Tuberculosis and Parkinsons. And get this. Tuberculosis is only one among other infections that have been documented to cause neurological problems. Others include Lyme disease, Mononucleosis, Epstein Barr and many others as well.

The study abstracts below document that there is a connection between Tuberculosis and Parkinsons. And get this. Tuberculosis is only one among other infections documented by studies to cause neurological problems. Others include Lyme disease, Mononucleosis, Epstein Barr and others as well.

For some people, dopamine deficiencies play a minor role when it comes to identifying the cause of symptoms. Recovery for some people requires treating infections that may be contributing to their symptoms. Taking L-dopa supplements or medications do not address infections in the body, though they may offer temporary relief.

Tuberculosis is one of Many Causes of Parkinsons

Can J Neurol Sci. 2025 Sep 29:1-10. Movement Disorders in Central Nervous System Tuberculosis: A Systematic Review

Abstract

Background: Tuberculosis (TB) affecting the central nervous system (CNS) can lead to a broad range of movement disorders, which are frequently overlooked in clinical settings. This review explores the various presentations, underlying mechanisms and patient outcomes related to these disorders.

Methods: We systematically reviewed published case reports, series and cohort studies that described patients with CNS TB who developed movement disorders. Extracted data included patient characteristics, type of CNS TB, imaging and CSF findings, types of movement disorders, treatments used and outcomes.

Results: A total of 61 patients with CNS TB and associated movement disorders were analyzed. The most common manifestations were ataxia, dystonia, chorea or hemiballismus and parkinsonism. Less frequent symptoms included opsoclonus-myoclonus, segmental myoclonus, tremors, cervical dystonia and stereotypy. TB meningitis was the predominant form, often accompanied by infarcts, hydrocephalus or tuberculomas. Proposed causes included vascular injury, inflammatory lesions, immune mechanisms and drug-related effects. All patients received anti-tuberculosis treatment, and nearly half required corticosteroids or surgical procedures. About 25 patients (41%) fully recovered, 17 (27.9%) had significant improvement, 13 (21.3%) showed partial improvement, 11 (18.0%) had ongoing problems and 1 (1.6%) died. Cohort studies also reveal that movement disorders – particularly tremors, dystonia, parkinsonism and ataxia – are frequent but underrecognized in CNS TB. These typically emerge early, often within three weeks, and are linked to lesions in the basal ganglia or thalamus.

Conclusions: Movement disorders in CNS TB are more common than generally recognized. Prompt diagnosis through imaging and timely therapy can greatly improve neurological outcomes.

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Tuberculosis (Edinb). 2025 Jul:153:102653. Hippocampal syndrome secondary to tuberculosis: From neuroinflammation to neurodegeneration

Abstract

Background: Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a primary global health concern, with significant long-term sequelae. Central nervous system TB (CNS-TB) is a clinical spectrum with entities such as tuberculous meningitis and tuberculomas. Emerging evidence suggests that Mtb may directly or indirectly affect the hippocampus, a critical memory, learning, and cognition structure.

Objectives: This review aims to summarize the current biological understanding of Mtb’s impact on the hippocampus, elucidate its potential role in neurodegeneration, and introduce the concept of “Hippocampal syndrome secondary to tuberculosis (HSST)” as a novel chronic entity within the CNS-TB spectrum.

Methods: A comprehensive literature review was conducted to analyze how Mtb gains access to the brain, its neurotropism, and the resulting neuroinflammatory and neurodegenerative effects on the hippocampus. Data from clinical, histopathological, and experimental studies were evaluated to assess potential links between TB and cognitive impairment.

Results: Mtb can access the CNS through hematogenous dissemination, the “Trojan Horse” mechanism, or via the olfactory pathway, bypassing the blood-brain barrier (BBB). Once in the brain, Mtb induces chronic neuroinflammation and disrupts hippocampal structure. Studies suggest that TB increases the risk of Alzheimer’s and Parkinson’s diseases, with evidence of Mtb-driven amyloid-beta accumulation and neuronal loss. Furthermore, specific Mtb strains exhibit neurotropism and produce virulence factors that facilitate CNS invasion.

Conclusions: Understanding the interaction between TB and neurocognitive disorders is critical for improving post-TB care. Recognizing HSST as a chronic condition within the CNS-TB spectrum may support early diagnosis and targeted interventions to mitigate long-term neurological consequences.

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Microorganisms. 2024 Sep 13;12(9):1890. Mycobacterium paratuberculosis: A HERV Turn-On for Autoimmunity, Neurodegeneration, and Cancer?

Mycobacterium paratuberculosis: A HERV Turn-On for Autoimmunity, Neurodegeneration, and Cancer?

Abstract

Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections that, over millions of years, became integrated into the human genome. While normally inactive, environmental stimuli such as infections have contributed to the transcriptional reactivation of HERV-promoting pathological conditions, including the development of autoimmunity, neurodegenerative disease and cancer.

What infections trigger HERV activation? Mycobacterium avium subspecies paratuberculosis (MAP) is a pluripotent driver of human disease. Aside from granulomatous diseases, Crohn’s disease, sarcoidosis and Blau syndrome, MAP is associated with autoimmune disease: type one diabetes (T1D), multiple sclerosis (MS), rheumatoid arthritis (RA) and autoimmune thyroiditis. MAP is also associated with Alzheimer’s disease (AD) and Parkinson’s disease (PD). Autoimmune diabetes, MS and RA are the diseases with the strongest MAP/HERV association.

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Med Hypotheses. 2002 Oct;59(4):373-7. Parkinson’s: another look

Abstract

Recent studies in the Parkinson’s literature have cited a tuberculosis-like germ called Nocardia as being responsible for Parkinson’s disease. Kohbata seemingly cemented a relationship between Nocardia and Parkinson’s by finding serologic evidence in 20 of 20 Parkinson’s patients, acknowledging that blood tests for Nocardia and the mycobacteria such as tuberculosis often cross-react, as they belong to the same order of bacteria, the Actinomycetales. Besides this difficulty in differentiation, a well-used medical school textbook of microbiology, Atlas, points out that even among experts, different observers may classify the same strain of bacteria as Nocardia or Mycobacterium tuberculosis.

Parkinson’s: another look is a theoretical article which presents compelling, well-documented evidence for an infectious cause for Parkinson’s disease on historical, epidemiological, pharmacologic, microbiological, and biochemical levels.

Why Are People with Parkinsons Skinny?

Most people diagnosed with Parkinson’s disease struggle to gain weight. Why are people with Parkinsons Skinny?

Reason Why People with Parkinsons Skinny

Researchers have recently identified a primary cause of Parkinson’s symptoms to be a faulty digestive system. Constipation is a prevalent problem for many people. Efforts to improve it often fail. People are understandably frustrated from being physically and emotionally constipated all the time.

Why are digestion problems so common among persons with Parkinsons? Their sympathetic nervous system – the one that is our “get up and make things happen” – is on overdrive. While this energy makes people successful in their jobs and careers, it can also lead to neurological problems when its “on-off” switch remains stuck on the “on” switch.

What happens when anxiety and stress are forever present? What happens when we are rarely able to quiet down the intensity of an overactive nervous system that causes tremors, mobility challenges and other neurological problems?

Answer: The digestion system shuts down. We are never hungry. Eating becomes a huge irritant. We become skinny, so much so that we need to gain some weight.

Why? The wisdom of the body allocates energy to the organs needed for survival. When we are stressed and anxious, our body preserves the ability to …

  • Breath oxygen through our lungs.
  • Receive nourishment to our cells through our cardiac system.

We do not need to eat food when our very survival may be an issue. Digestion will always be suspended when the body allocates resources to our lungs and heart during stressful times.

This problem is solved when a better balance is achieved between our active life and our “chill out and relax and have fun” life. When we shut down anxiety, our body reallocates resources to our digestive system. We finally are hungry.

To support those of you who want gain weight and get anxieties under control, I teach a three month online class that covers ways proven by research to Shut Down Anxiety in a flash. Visit the link below to register. Use the coupon code succeed to claim a 50% discount.

Shut Down Anxiety Online Class

I am always surprised at the many people with Parkinsons who devote their attention and resources to improving their digestive system which seldom succeed. The reason for this failure? Attention and resources need first be devoted to shutting down the continuous problem of anxiety and anxiety attacks.

When anxieties are shut down, digestion resumes. Gaining weight becomes possible. At long last we want to eat good food rather than force ourselves to eat something when we are not hungry.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery ®
https://www.parkinsonsrecovery.com
robert@parkinsonsrecovery.com

Eating Too Much Sugar?

I have a clever way for you to determine if you are eating too much sugar.

Studies conclude the toxin that causes the most neurological damage is sugar of all forms. The word sugar is rarely listed as an ingredient in packaged foods, but I can assure you sugar is an ingredient in most of them. Rather, you will likely see listed other names of ingredients that sweeten the product such as:

  • Fructose
  • High-fructose corn syrup
  • Corn syrup
  • Glucose
  • Maple syrup
  • Maltose
  • Rice syrup
  • Dextrose
  • Malt syrup
  • Lactose
  • Brown rice syrup
  • Galactose
  • Barley malt
  • Sucrose
  • Carob syrup
  • Golden syrup
  • Sorghum syrup

Is your head spinning? Mine is. And this is only a partial list of how sugars are listed as an ingredient in packaged food products. Often the ingredient appears at the top of the list.

Your body may well be able to tolerate some of these sweeteners but not others. In the end the most toxic substance that damages neural networks is sugar in whatever form it is eaten.

OK. Everyone knows that it is best to avoid sugars whenever possible. But when your grandmother Perl or your Aunt Betty makes her favorite Tipsy cake during the holidays, are you going to turn it down? Certainly not! That is food that nourishes our emotions. 

When we are honest with ourselves, we all have to admit that we do eat sugar now and then despite knowing it is bad for us. How then can you know if you are eating too much sugar which has a direct impact on your neurological symptoms?

Are You Eating Too Much Sugar?

My answer is simple. It does not involve an expensive diagnostic test or a visit to a medical clinic. Your finger nails reveal the truth about your intake of sugars.

White dots on your finger nails reveal the degree and timing of when we have eaten foods contaminated with sugars. If you have no white dots, you are not eating too much sugar.

If you do have white dots on any (or all) of your fingers nails, the location of the spot on the nail reveals the approximate date when the sugars were eaten. Nails take 6 to 9 months to grow. If your entire nail grows in 6 months and if a white spot appears at the middle of the nail, sugar was eaten 3 months ago. If the spot appears a third up your nail from the root, the contamination occurred two months ago.

What was happening in your life two or three months ago? Was this when you ate Grandma Perl’s Tipsy Cake? Ah – there it is.

When I ask members of my audience whether sugar might be an issue for them the typical answer is “I try my best to avoid eating sugar.” Well, so do I. Are your attempts succeeding? Our bodies can process a limited quantity of sugar over time. But when we eat too much sugar, the body has to eliminate it in several ways – one of which is to send the sugar to our nails.

Summary: You can quickly determine the success or failure of your efforts to avoid eating package products that contain harmful sugars. How? Look whether your finger nails have white spots on them. If they do, re-examine your intention to avoid eating sugars. Your body is struggling to eliminate the toxins from ingesting too much sugar.

And yes. You can even figure out when approximately you ingested too much sugar for your body to process. If the white spots are up and down many of your finger nails, please set a firm intention to stop eating foods sweetened with sugar toxins in whatever name they are listed on any packaged food product you eat.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery ®
https://www.parkinsonsrecovery.com
robert@parkinsonsrecovery.com

Vitamin B12 Deficiencies with Parkinsons


Vitamin B12 with Methylcobalamin is recommended as a treatment for Parkinson’s symptoms. Why? It reduces neurotoxicity and helps reverse symptoms. Research studies report high-dose B12 methylcobalamin inhibits enzymes related to PD, thereby protecting neurons and improving motor/non-motor symptoms.

The bottom line: vitamin B12 supplement plays a leading role in helping to reverse symptoms associated with a diagnosis of Parkinsons.

One of B12’s key roles is helping to maintain myelin, the insulating sheaths covering the nerve endings in the brain, spinal cord, and optic nerve. A lack of sufficient B12 is responsible for faulty sheaths that result in nerve dysfunction.  Deficiencies cause issues with neurological conditions including gait, instability and cognitive decline.

There is a two edged sword at play here. People with Parkinsons avoid foods enriched with B12 including meat products because they can interfere with absorption of their medications.

More importantly, levodopa depletes vitamin B12. The positive results when persons on medications take a B12 supplement are supported by research studies posted below.

There are several forms of B12. The natural form known as methylcobalamin is recommended as a therapy for neurological conditions. It has superior absorption. If you are currently taking a B12 supplement make sure it is the methycobalamin form. If not, purchase a B12 supplement that has it

Studies on Vitamin B12 Deficiencies with Parkinsons

J Gerontol A Biol Sci Med Sci. 2026 Mar 14:glag048. Dietary One?Carbon Nutrients and Genetic Risk in Parkinson’s Disease: A Prospective Cohort Study

Abstract

Background: Several studies have investigated the effects of dietary one-carbon metabolism (OCM) nutrients, such as methionine, folate, vitamin B6, and vitamin B12, on Parkinson’s disease (PD). However, current evidence remains insufficient to definitively establish a link between OCM intake, PD incidence, and genetic risk.

Methods: Among 202171 individuals aged 37-73 in the UK Biobank, we assessed dietary OCM nutrient intake via repeated 24?hour recalls, determined PD incidence via validated ICD?10 codes, and quantified genetic risk with polygenic risk scores. Employing Cox proportional hazards models supplemented by sensitivity analyses, we evaluated the associations and potential interactions among OCM nutrient intake, genetic risk, and PD incidence.

Results: Over a median 12.27-year follow-up of 202171 participants, 1037 incident PD cases occurred. In multivariable-adjusted Cox models, compared with participants in the lowest quartile, those in the highest quartile of methionine, vitamin B6, folate, and vitamin B12 had a lower risk of PD [HR (95% CI)=0.83 (0.69-1.00), 0.75 (0.62-0.90), 0.71 (0.59-0.85), and 0.79 (0.65-0.94)]. Genetically-stratified analyses showed folate inversely associated with PD risk in the low-risk group [HR (95% CI)= 0.65 (0.48-0.88)] (P for interaction = 0.48); vitamin B12 linked to lower risk in the high-risk group [HR (95% CI)= 0.78 (0.63-0.99)] (P for interaction = 0.83); and vitamin B6 inversely associated across both strata [high-risk HR (95% CI)= 0.77 (0.62-0.97); low-risk HR (95% CI) = 0.59 (0.44-0.80)](P for interaction = 0.08).

Conclusions: Higher OCM nutrient intake is inversely associated with PD risk. 

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Front Psychiatry. 2025 Aug 19:16:1569826. Exploring neuropsychiatric manifestations of vitamin B complex deficiencies

Abstract

B complex vitamins, a group of eight water-soluble vitamins, play interconnected roles in maintaining nervous system health. Thiamine (B1), riboflavin (B2), and niacin (B3) are essential as co-enzymes in numerous metabolic reactions related to energy production. Thiamine is involved in the Krebs cycle, riboflavin in the electron transport chain, and niacin plays a key role in both glycolysis and the Krebs cycle. These metabolic processes are vital for sustaining the integrity of the nervous system, as the energy produced is critical for the functioning of nerve cells.

Deficiencies in these vitamins can lead to significant neurological and psychiatric conditions, including Wernicke Korsakoff syndrome, Parkinson’s disease, and various mental illnesses.

Additionally, pyridoxine (B6), folate (B9), and cobalamin (B12) are indispensable coenzymes for the methylation of homocysteine to methionine, a process critical to nervous system function. Elevated homocysteine levels, resulting from deficiencies of these vitamins, are associated with higher risks of depression and dementia.

Imbalances in these vitamins can disrupt key biochemical pathways, leading to neuropsychiatric disorders. The literature reviewed underscores the importance of daily intake of B complex vitamins to maintain normal serum levels and optimal neuronal function. This review aims to elucidate the neuropsychiatric manifestations associated with deficiencies in these vitamins.

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J Neural Transm (Vienna). 2024 Dec;131(12):1495-1509. Parkinson’s disease and vitamins: a focus on vitamin B12

Abstract

Parkinson’s disease (PD) has been linked to a vast array of vitamins among which vitamin B12 (Vit B12) is the most relevant and often investigated specially in the context of intrajejunal levodopa infusion therapy. Vit B12 deficiency, itself, has been reported to cause acute parkinsonism. Nevertheless, concrete mechanisms through which B12 deficiency interacts with PD in terms of pathophysiology, clinical manifestation and progression remains unclear.

Recent studies have suggested that Vit B12 deficiency along with the induced hyperhomocysteinemia are correlated with specific PD phenotypes characterized with early postural instability and falls and more rapid motor progression, cognitive impairment, visual hallucinations and autonomic dysfunction. Specific clinical features such as polyneuropathy have also been linked to Vit B12 deficiency specifically in context of intrajejunal levodopa therapy.

In this review, we explore the link between Vit B12 and PD in terms of physiopathology regarding dysfunctional neural pathways, neuropathological processes as well as reviewing the major clinical traits of Vit B12 deficiency in PD and Levodopa-mediated neuropathy.

Finally, we provide an overview of the therapeutic effect of Vit B12 supplementation in PD and posit a practical guideline for Vit B12 testing and supplementation.

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Neurol Res. 2014 Dec;36(12):1121-8. Involuntary movements due to vitamin B12 deficiency

Abstract

Deficiency of vitamin B12 produces protean effects on the nervous system, most commonly neuropathy, myelopathy, cognitive and behavioural symptoms, and optic atrophy. Involuntary movements comprise a relatively rare manifestation of this readily treatable disorder. Both adults and infants deficient in vitamin B12 may present with chorea, tremor, myoclonus, Parkinsonism, dystonia, or a combination of these, which may precede diagnosis or become apparent only a few days after parenteral replacement therapy has begun. The pathogenesis of these movement disorders shows interesting parallels to certain neurodegenerative conditions.

The clinical syndrome responds well to vitamin B12 supplementation in most cases, and an early diagnosis is essential to reverse the haematological and neurological dysfunction characteristic of this disorder.

We elucidate the association of vitamin B12 deficiency with movement disorders in adults and in infants, discuss the pathogenesis of this association, review previously reported cases, and present a young adult male with severe generalized chorea that showed a salutary response to vitamin B12 supplementation.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery ®
https://www.parkinsonsrecovery.com

Vitamin D Deficiencies

Studies consistently find vitamin D3 deficiencies in persons diagnosed with Parkinsons. On the one hand, you might say to yourself – so what? There are so many presumed deficiencies reported for subjects in the studies. Should you take this one that seriously?

My answer is yes. While there are over 120 natural treatments and therapies that help reverse symptoms, the sunshine vitamin (D3) lies at the foundation of what keeps us alive.

Put aside the complexity of the dozens of recommendations reported to help people celebrate relief from their symptoms. What is really necessary?

  • Sunshine
  • Water
  • Air

We become ill when any of these are missing or deficient. These are the essentials that keep us alive day in and day out.

None of us would have issues with vitamin D3 if the sun shined every day. In the pacific northwest, we do not see the sun for months on end some winters. Most people who live in sunshine deprived areas have a life threatening Vitamin D3 (sunshine) deficiency.

Cardiologists will be the first to tell you heart disease is more common in the winter months. Blood pressure is highest in the winter and for persons who live far from the equator.

Studies have also reported the lowest levels of vitamine D3 are associated with the highest rates of breast cancer.

In any season of the year, the lower the vitamin D3, the higher the blood glucose. This poses problems for the many people with Parkinsons symptoms that have insulin resistance.

In short, optimizing your exposure to the sun and taking supplements to address D3 deficiencies is one of the most important steps you can take to support recovery and sustain overall health.

The best option is always to spend as much time outdoors in the possible. There are benefits even when the sun is not shining brightly. When the sun is not shining, supplementation is recommended.

Studies on Vitamin D3 and Parkinsons

Adv Exp Med Biol. 2026:1493:51-67. Vitamin D and Brain Health

Abstract

Vitamin D is widely known for its influence on the homeostasis of calcium and phosphate levels in the body and its involvement in maintaining musculoskeletal health. In its active form, 1,25-dihydroxy cholecalciferol has immunomodulatory effects on both the innate and adaptive immune systems.

The active form of vitamin D plays a neuroprotective role in the central nervous system, highlighting its importance in maintaining brain health. Studies have noted the role of vitamin D in the formation of antioxidants, reduction of pro-inflammatory cytokines, lowering of oxidative stress, improvement of mitochondrial respiratory health, and slowing of the progression of neuronal damage. This vitamin may also influence development by facilitating the differentiation of cells, the expression of neurotrophic factors, the regulation of cytokines, the synthesis of neurotransmitters, intracellular calcium signaling, and the expression of genes involved in neuronal differentiation.

An association has been noted between vitamin D deficiency and the risk of developing several neuronal diseases, including Parkinson’s disease, headaches, multiple sclerosis, and Alzheimer’s disease. The neuroprotective role of vitamin D suggests the potential benefit of vitamin supplementation in slowing the progression of such conditions and promoting brain health.

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Curr Nutr Rep. 2025 Jun 4;14(1):77. Vitamin D and Neurodegenerative Diseases Such as Multiple Sclerosis (MS), Parkinson’s Disease (PD), Alzheimer’s Disease (AD), and Amyotrophic Lateral Sclerosis (ALS): A Review of Current Literature

Abstract

Purpose of review: This review explores the role of Vitamin D3 and its derivatives as inhibitors of pathological metabolic modifications in neurodegenerative diseases. The manuscript investigates how Vitamin D3 impacts neuronal calcium regulation, antioxidative pathways, immunomodulation, and neuroprotection during detoxification, beyond its known functions in intestinal, bone, and kidney calcium and phosphorus absorption, as well as bone mineralization.

Recent findings: Recent studies have highlighted the synthesis of the active metabolite 1,25(OH)2D3 (vitamin D) in glial cells via the hydroxylation process of CY-P24A1, an enzyme in the cytochrome P450 system in the brain. The effects of vitamin D occur through the vitamin D receptor (VDR), a nuclear steroid receptor, which has been identified in various brain regions, including the cerebellum, thalamus, hypothalamus, basal ganglia, hippocampus, olfactory system, temporal, and orbital regions.

Neurodegeneration is primarily associated with oxidative stress, protein aggregation, neuro-inflammation, mitochondrial dysfunction, apoptosis, and autophagy changes, all of which Vitamin D and VDR are believed to influence. Vitamin D and VDR are recognized as both environmental and genetic factors in the etiopathogenesis of neurodegenerative diseases such as Multiple Sclerosis (MS), Parkinson’s Disease (PD), Alzheimer’s Disease (AD), and Amyotrophic Lateral Sclerosis (ALS).

A deficiency in Vitamin D is postulated to have detrimental effects on the brain and other diseases throughout various stages of life. This review consolidates findings from clinical and experimental studies, as well as past publications, focusing on the implications of Vitamin D deficiency in these neurodegenerative conditions. Current articles published in PubMed were extensively considered for this review.

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ReviewMolecules. 2025 Sep 21;30(18):3823. Vitamin D Associated with Exercise Can Be Used as a Promising Tool in Neurodegenerative Disease Protection

Abstract

Neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, and Huntington’s disease, represent unmet medical and social needs. Still, no definitive cure exists for these illnesses, hence a therapeutic approach with molecules able to prevent/downtone/modify the disease seems highly attractive.

Remarkably, a higher risk of neurodegenerative disease is associated with low vitamin D levels. Vitamin D is a multifaceted molecule able to target critical neuroinflammatory processes underlying neurodegeneration, acting through genomic or rapid signaling. This narrative review aims to focus on vitamin D’s potential to be an optimal neuroprotective molecule, based on its ability to target and counteract aberrant biomolecular processes involved in neuroinflammation/neurodegeneration.

Noticeably, exercise can potentiate vitamin D’s protective effect through some anti-inflammatory actions exerted on shared biomolecular targets. Thus, although vitamin D is not strictly a drug, it could be potentially allocated within the therapeutic approach to neurodegenerative diseases in combination with adapted exercise, best as an early intervention.

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Front Nutr. 2025 Jun 9:12:1500875. Effect of vitamin D supplementation on motor symptoms in Parkinson’s disease: a meta-analysis of randomized controlled trials

Abstract

Introduction: Lower serum vitamin D levels may associate with higher motor symptom severity in Parkinson’s disease (PD). This study aimed to test the efficacy of supplemental vitamin D on ameliorating motor symptoms in PD, which is the most comprehensive study to assess the relationship between vitamin D supplementation and PD motor symptoms to date.

Methods: An electronic literature search supplemented by hand searching up to Sep 2024 identified 8 randomized controlled trials involving 646 cases of PD. Weighted mean difference (WMD) and 95% confidence interval (CI) of PD were assessed through pooling the collected data from eligible studies using Stata software.

Results: The results indicated that supplemental vitamin D did not reduce the Unified Parkinson’s Disease Rating Scale part III score (WMD=-0.56, 95% CI=[-2.34, 1.23]), 10/8 m walk test time (WMD=0.59, 95% CI=[-0.46, 1.64]) and timed up and go (TUG) test time (WMD=-0.57, 95% CI=[-1.45, 0.31]). A statistically significant benefit of supplemental vitamin D was observed on 6-Minute walking test distance (WMD=24.85, 95% CI=[6.54, 43.16]).

Discussion: This meta-analysis suggested that supplemental vitamin D may extend 6-Minute walking test distance, improve partial motor symptoms. Vitamin D supplementation may play an active inhibitory role in the mechanisms of the development of PD.

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J Health Popul Nutr. 2025 Jul 3;44(1):235. Outdoor light spending time, genetic predisposition and incident Parkinson’s disease: the mediating effect of lifestyle and vitamin D

Abstract

Background: Previous studies suggest that outdoor sunlight exposure was associated with a lower risk of Parkinson’s disease (PD). However, the interaction of genetic predisposition and the potential role of lifestyle risk factors in mediating this association remains unclear from prospective evidence.

Methods: A cohort study based on the UK Biobank enrolled participants between 2006 and 2010, with the latest follow-up in November 2022. In the prospective population-based study 375,599 UK adults aged 37–73 years were enrolled. The outdoor light time was assessed using a questionnaire survey to investigate how many hours were spent outdoors on typical summer and winter days. New-onset PD was identified through linkage with inpatient hospitalization and death registers. Multivariate Cox proportional hazard regression models were used. The polygenic risk score (PRS) for PD comprised 44 single-nucleotide variants. The mediation analysis of lifestyle risk factors and vitamin D on this association was performed.

Results: A total of 375,599 participants (mean age, 56.8 years; 46.3% males) were included, and 2,824 individuals were first-ever diagnosed with PD. Compared with the individuals with shorter outdoor light time, those with longer time in summer (HR 0.77; 95% CI, 0.68–0.88), in winter (HR 0.85; 95% CI, 0.75–0.96), and on average (HR 0.83; 95% CI, 0.73–0.93), were prone to have lower PD risk. There was a joint association between outdoor light time and genetic predisposition in PD incidence, and higher genetic risk of PD could be modifiably decreased through longer outdoor light exposure. In mediation analyses, physical activities mainly explained 15.83% on average, while the mediating effects of sleep patterns (2.71%) and vitamin D (4.91%) were relatively mild of the association between outdoor light time and PD, respectively.

Conclusion: In this cohort study, a longer duration of outdoor sunlight exposure was associated with a lower risk of PD, and was more pronounced in individuals with high genetic risk. This association was partly mediated by physical activity, sleep patterns, and vitamin D. These findings highlight the potential of promoting regular outdoor activities as a practical strategy to mitigate PD risk, especially among genetically susceptible individuals.

Robert Rodgers Phd
Founder 2004
Parkinsons Recovery ®
https://www.parkinsonsrecovery.com

Has Your Recovery Flopped?

Everyone with neurological symptoms embraces one approach or another to celebrate either temporary or long lasting relief from their symptoms.

  • Some people focus on medicines as a therapy
  • Some focus on supplements
  • Others focus on diet
  • Still others focus on exercise

All of these approaches can yield welcome benefits. Regardless of what has been your focus,

  • Has your recovery flopped?
  • Are you disappointed with the meager results that resulted from whichever approach you embraced?
  • Is your recovery at a stand still?

If answers to these questions are yes, you are not alone. You have good reason to be depressed. All of these options are known to be beneficial, so why have they not generated symptom relief?

There are hundreds of possible reasons why any program of recovery may have flopped. One strategy is to investigate why your current approach to recovery is not succeeding. The answer to this question will involve expensive diagnostic tests and assessments that may well reveal important insights. Still …

If whatever you are doing to get well is not working, think of yourself as digging a deep hole you cannot dig yourself out of.

If you are focused on medicines as the answer, then the idea is to have your doctor prescribe other medications. If supplements are not helping, the idea is to find more supplements to take. Although other options are adopted, you continue to pursue the same strategy.

I have another approach for you to consider. What is my suggestion? Step back and embrace an entirely different set of options known to facilitate recovery.

For example, sound therapies have proven successful for many persons as have light therapies (or photobiomodulation) and energy healing of one form or another. Acupuncture helps some people. Chiropractic adjustments help others.

I have now documented over 120 natural therapies including those listed above that offer the opportunity for symptom relief. Consider embracing natural options that research demonstrates can be beneficial.

In summary, if your recovery is stuck in the mud, jump out of the hole you have been digging. Embrace other approaches proven by research to reverse one symptom or another. A little experimental makes the difference between success and failure.

I have documented partial or full recovery of many individuals who confronted neurological challenges. They jumped out of the hole they were digging and embraced a fresh approach that flipped a failing recovery into one that was successful.

Are you curious about the many natural options that can help offer symptom relief? Natural options proven by research that reverse one symptom or another are covered in my Parkinsons Recovery online courses.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery ®
https://www.parkinsonsrecovery.com

Unconscious Dynamics of Trauma

Many people believe trauma plays little role in contributing to the symptoms of Parkinsons. The unconscious dynamics of trauma would suggest otherwise.

Why do people conclude trauma is not a problem for them to address? Answer: Because they have no memory of troublesome past traumas in their life.

When I press the issue in my conversations with individuals currently experiencing symptoms of Parkinsons – I will often ask a few follow-up questions.

Have you ever been in an automobile accident?

Have you ever been hospitalized?

Have you visited family and friends who were hospitalized?

  • Have you ever lost a family member to an untimely death at a young age?
  • Were you confronting unrelenting stress, particularly before your systems reared their ugly head?
  • Does a close member of your family have a mental illness?
  • Have you or a member of your family served in the military in a war zone?
  • Have you ever been divorced?

I could devote the next 10 pages to adding questions like the above. Some people will acknowledge that yes – one or a few of these apply to them, but still do not believe trauma could contribute to their symptoms.

There is another dynamic at play here which embodies the unconscious dynamics of trauma. When experiences become too overwhelming for a child to tolerate before their prefrontal lobes in their brains have developed, the brain will not record them as experiences. There is no stored memory of “this is what happened to me.”

Rather, the child (and keep in mind I am referring to all of us adults when we were children) will record these scary experiences as fragments in the form of images, emotions, kinesthetic sensations, smells, sounds, tastes or impulses to take action or shout out certain words. These are all implicit memories stored in the right side of our brain as unconscious fragments.

We will often be triggered by the most harmless of situations. Perhaps a smell. Perhaps a song. Perhaps a taste. Perhaps a food that makes us vomit. Perhaps certain sounds.

In short we are triggered by events that have no impact on others whatsoever. My point?

If you have concluded trauma plays no role as the foundational cause of your symptoms, please evaluate that conclusion. My research conclusively reveals trauma of one form or another is a leading cause of neurological symptoms.

The earlier past traumas are acknowledged, released and cleared, the sooner the opportunity for symptoms to resolve.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery ®
https://www.parkinsonsrecovery.com

Benefits of SAM-e for Parkinsons

People who experience Parkinson’s symptoms are low in S-Adenosyl-L-Methionine – otherwise known as SAM-e. There is a logical reason for this widespread deficiency. Levodopa depletes SAM-e in the body relatively quickly.

Benefits of SAM-e for Parkinsons

SAM-e stimulates the dopamine system as well as other neurotransmitters like serotonin and norepinephrine. It acts a methyl donor, a crucial step in the synthesis and regulation of dopamine in the brain.

SAM-e is crucial for maintaining energy metabolism, as well as maintaining the integrity of nerve membranes. It contributes to more than 100 biochemical reactions in every cell of the body. SAM-e protects against free radical damage, repairs damaged cells and produces essential neurotransmitters, proteins and antioxidants. It is a highly effective treatment for depression, a frequent problem for persons with neurological challenges.

SAM-e is responsible for a multitude of essential functions in the body which include boosting levels of glutathione. It is a protective agent for livers that have been overloaded with too many toxins. In short, it removes the trash and slug out of the body.

What specific functions does SAM-e deliver? It:

  • Boosts high energy molecules
  • Protects the body against the harmful effects of stress
  • Recharges the neurological system
  • Sharpens mental clarity
  • Enhances concentration
  • Holds attention to tasks
  • Heightens pleasure
  • Serves as a natural anti-depressant
  • Improves mood
  • Heals nerve cell membranes

SAM-e is used to address many conditions including depression, anxiety, heart disease, fibromyalgia, pain, osteoarthritis, bursitis, tendonitis, chronic lower back pain, dementia, Alzheimer’s disease, the aging process, chronic fatigue syndrome (CFS), dementia, liver disease as well as Parkinson’s disease.

SAM-e Boosts Effectiveness of Medications

A welcome benefit of SAM-e is that it increases the effectiveness of medications. This means the dosage of medications will not necessarily need to be increased to celebrate symptom relief. If you now take the maximum dose of medications your doctor is willing to prescribe, talk with them about the option of taking SAM-e to increase the absorption and effectiveness of the medications.  

Richard Brown MD is a useful resources for additional informaton about SAM-e and other useful treatments for many diseases including Parkinsons. His  research has revealed persons with Parkinson’s symptoms tend to be very low in SAM-e and benefit greatly from supplementation. www.haveahealthymind.com 

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery ®
https://www.parkinsonsrecovery.com

Cistus Incanus Tea as Therapy for Parkinson’s

About Cistus Incanus Tea as Treatment for Parkinson’s

Dietrich Klinghardt MD discusses a simple treatment for many illnesses including Parkinsons in this 11 minute video. Click the link below to watch (scroll down to find his video)

Release of Retro Viruses are a foundational cause of Parkinson’s

Here are Dr. Klinghardt’s instructions for brewing the tea:

  1. Boil slowly with the lid on.
  2. Steam for 5 minutes
  3. Add Stevia
  4. Drink 6-8 cups every day
  5. Re-brew the tea several times

Below is the source of the tea Dr. Klinghard recommends

 

Research Evidence on Cistus Incanus Tea

Int J Mol Sci. 2025 Jan 23;26(3):947. Antiviral Activity of Water-Alcoholic Extract of Cistus incanus L

Abstract

Recently, previously known viruses have changed their pathogenicity and encompassed new types of host populations. An example of such an infection is that caused by SARS-CoV, belonging to the “well-known” coronavirus family. Another group of viruses that are of great importance to the human population are the herpes viruses.

Due to increasing viral resistance to existing antiviral drugs, plant extracts are attracting increasing interest due to their complex composition and their simultaneous attack of different viral targets. Based on the above, we tested the antiviral potential of water-alcoholic extract obtained from a commercial sample of the plant Cistus incanus L. against the enveloped viruses SvHA1, SvHA2 (ACV resistant) and HCoV 229E.

The results showed both complete inhibition of the intracellular stages of the viral replication and a strong effect on extracellular virions in the three viral models. In a study of the effect on the replication of SvHA 2, the calculated selectivity index was over 10. From the experiments on the virucidal effects on the two herpes viruses, it was found that the viral titer of the samples decreased by about 4 lg compared to the control sample. The extract is of interest for introduction into practice.

Photobiomodulation Studies

There has been an explosion of photobiomodulation studies over the past several years. I have previously reported results of studies that conclude photobiomodulation (light therapy) offers relief from neurological conditions such as Parkinsons and Alzheimers. These, however, are only a few of the conditions photobiomodulation studies conclude offer symptom relief.

Given the explosion of photobiomodulation studies recently – over 1500 studies alone published since 2025 – what conditions do the studies find photobiomodulation offer relief from symptoms?

Here is the list. Get ready to be surprised at the diversity of conditions photobiomodulation studies find this therapy to be effective.

  • Mitochondrial function
  • Cognition
  • Parkinsons
  • Alzheimers
  • Traumatic Brain Injury
  • Transmission of stem cells
  • Macular degeneration
  • Diabetic retinopathy
  • Sperm motility
  • Wound healing
  • Inflammation
  • TMJ
  • Pain
  • Cancer
  • Alopecia
  • Brain function
  • Port wine birthmarks in infants
  • Bone regeneration
  • Carpal Tunnel Syndrome
  • Cardiovascular disese
  • Retinal Disease
  • Sleep
  • Spinal injuries
  • Neuropathy

And this is not even an exhaustive list!

As you can see above, there is at long last compelling evidence that light therapy is a medicine of the future. This prediction is no longer an idle speculation on my part!

Vielight.com is the gold standard company that has been inventing photobiomodulation devices since 2016. They deliver light therapy with patented helmet and nasal applicators. There have now been 25+ published studies using their devices that address many of the conditions listed above.

Vielight offers a 10% discount on purchases – coupon code is healing4me. If users do not celebrate a welcome relief from symptoms, the company offers an 80% refund for units returned within 6 months of use.

Over the past two decades I have documented dozens of natural treatments that offer the opportunity to experience relief from neurological symptoms. My top recommendation in 2026 is the Vielight photobiomodulation therapy which has been documented in studies to produce consistent welcome relief from neurological conditions.

The company has humans (not AI) who answer the phone and answer your questions – 1-877-355-8012. They are a Canadian company but units are shipped from the USA to USA destinations so no tariffs are involved. https://www.vielight.com

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery®
https://www.parkinsonsrecovery.com
360-789-1658

Top Recommendation of a Treatment for Parkinsons

Studies have now systematically documented over 120 natural therapies that offer relief from symptoms of Parkinson’s disease to one extent or another. After over two decades of conducting research focused on Parkinsons, what is my top recommendation of a treatment option for Parkinsons?

My answer: photobiomodulation (light therapy). Why?

The gold standard company that first invented photobiomodulation devices beginning in 2016 is Vielight.com. Twenty-five studies have now been published using a Vielight photobiomodulation device. Every single study reports significant findings for a surprising variety of conditions including Parkinsons and Alzheimers.

I first learned about the Vielight photobiomodulation devices from interviewing Vielight’s CEO Dr. Lew Lim in 2018. At that time there was only one published study that reported significant findings for a sample of 5 subjects with early Alzheimers. Today there are 25 published studies using one of the Vielight devices.

Eight years later, hundreds of members of the Parkinsons Recovery audience have used the Neuro Gamma Vielight device. Feedback I have received has been consistently favorable which is why I rank their device as my top recommendation as a treatment for Parkinsons.

There has been an explosion of studies that evaluated photobioomodulation for one condition or another. Fifteen hundred studies that focus on photobiomodulation alone have been published since January, 2025.

Vielight offers a generous warranty on their photobiomodulation devices. If a user does not celebrate relief from symptoms they had anticipated within six months of use, they need only return the device for an 80% refund!

Only 10% of individuals in my audience have returned their device for a refund. The risk of getting one of the Vielight devices is clearly minimal given their generous 80% warranty offered by no other company.

Vielight (https://www.vielight.com) also offers members of the Parkinsons Recovery audience a 10% discount on any of their devices with the coupon code healing4me. Keep in mind that everyone in the family can use the device, not just the person who confronts neurological challenges.

A study published in 2026 offers groundbreaking evidence that the Vielight devices make the brain more resilient. Each of their devices include a helmet that emits the light and a nasal applicator that sends the light through the blood stream. A brief summary of this new study follows.

The Brain Becomes More Resilient with Photobiomodulation Home Treatments

A 2026 published study evaluated the effectiveness of a Vielight photobiomodulation device using a treatment group and a control group, the gold standard for any study. The study population consisted of active, healthy NCAA Division I collegiate football players over the course of their season. The treatment group administered the Vielight photobiomodulation at home three times a week. The control group wore an identical device that delivered no therapeutic light.

Both groups of players were subjected to head traumas from falls and other injuries typical of any college football season.

The active group showed no significant increases in inflammation or axonal remodeling markers in their brains while the control group exhibited significant increases.

This is truly a ground breaking result. Instead of always treating head traumas when they happen (such as head traumas to college football players or persons with Parkinsons), photobiomodulation makes the brain more resilient, better able to withstand repeated traumas to the head.

Some people who experience Parkinson’s symptoms fall frequently, causing repeated injury to their body and head. Making the brain more resilient makes it possible to avert problematic symptoms that result from repeated falls.

Studies using the Vielight devices using Parkinson’s subjects and Alzhiemer’s subjects have documented significant outcomes from regular use. This is still another reason why I make the Vielight photobiomodulation devices my top recommendation as a therapy to address symptoms of both conditions.

The Neuro Gamma device is recommended for persons with Parkinsons. The Duo device can be used if sleep and/or memory are also issues in addition to other Parkinsons symptoms.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery®
https://www.parkinsonsrecovery.com
robert@parkinsonsrecovery.com

Studies Recommend Betaine for Parkinsons

Studies recommend Betaine for Parkinsons. Trimethylglycine (TMG) is also called glycine betaine. The name trimethylglycine signifies that it has three methyl groups attached to each molecule of glycine.

 Wheat bran and beets are a good dietary source of TMG, with smaller amounts available in other cereal grains. TMG can also be made in the body from choline, an essential nutrient found in eggs, soybeans and other foods.

Why Studies Recommend Betaine for Parkinsons

Trimethylglycine or TMG is a recent and potential  addition to a Parkinson’s treatment program.  It helps as an anti-oxidant, anti-inflammatory, detoxification and energy enhancement.

TMG is also called betaine because it was first isolated from sugar beets.  It is not the same however as betaine hydrochloride.

It is now part of all development programs.  A dosage to consider is 1000 mg daily for women and 3000 mg daily for men.  Children need less, depending on their size. Always consult with your doctor about dosages.

SOURCES OF TMG

Dietary sources of TMG.  The main foods high in TMG are broccoli, beets and many other vegetables.  Cooking does not destroy the TMG in vegetables.

The problem is that most people do not eat nearly enough of these foods to get a sufficient amount of TMG from their diet.  Even if you eat plenty of these vegetables, it is usually not enough.

WHY SUPPLEMENT WITH TMG?

TMG is excellent for the liver and for detoxification.  Stress, infections, inflammation and other disease conditions may use up the TMG the body makes, so more is needed.  Toxic metals and toxic chemicals require more TMG in our bodies for their detoxification and removal.

Toxic Metals Delete Availability of TMG

Mercury interferes with the natural TMG production in the body and thus increases the body’s requirement for TMG.  If you have silver/mercury dental amalgams, you also likely need more of it.  Mercury can contribute to hundreds of health conditions.

Copper toxicity interferes with the production of TMG in the body and increases the need to supplement  it.  One cause of the copper toxicity is widespread zinc deficiencies in the soil and in food.  This tends to cause more accumulation of copper in the body.  Women tend to be more copper toxic than men, although it affects both men and women.

Cadmium also increases the need for TMG, either by interfering with its production or enhancing the demand for it in order to detoxify and remove cadmium from the body through the liver. Cadmium toxicity is very common. In part, this is due to widespread zinc deficiency in the soil, the food and in refined food diets.  The body takes up cadmium if there is insufficient zinc available in the diet.

Below find two studies that recommend Betaine (TMG) as a treatment for Parkinsons and other conditions as well.

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Curr Neuropharmacol. 2025 Aug 8. Betaine: A Promising Natural Product for Neurological and Psychiatric Diseases

Abstract

Neurological and psychiatric diseases pose a considerable global burden. Exploring additional potential prevention strategies and therapies is ongoing. As a prevalent natural product and nutraceutical from food, betaine’s pharmaceutical applications suggest benefits for both health and disease in multiple organs.

Recently, its efficacy on neurological and psychiatric health has been proposed and has drawn considerable attention. In addition to its well-known osmotic protection, due to methyl donation, it regulates metabolism, alleviates oxidative stress, and reduces inflammation. To manifest neurological and psychiatric health benefits, betaine acts by affecting gamma-aminobutyric acid associated with its transporters, related neurotransmitters, downstream and neurological pathways, and other specific mechanisms in the nervous system.

Betaine demonstrates therapeutic potential against various neurological and psychiatric diseases, such as epilepsy, neurocognitive disorders (including Alzheimer’s disease), Parkinson’s disease, stroke, multiple sclerosis, traumatic brain injury, depression, anxiety, schizophrenia, autism spectrum disorder, sleep disorders, fetal alcohol syndrome, syringomyelia, neonatal brain injury, neuropathic pain, and motor dysfunction.

Basic Clin Pharmacol Toxicol. 2023 Nov;133(5):485-495. Betaine-The dark knight of the brain

Abstract

The role of betaine in the liver and kidney has been well documented, even from the cellular and molecular point of view. Despite literature reporting positive effects of betaine supplementation in Alzheimer’s, Parkinson’s and schizophrenia, the role and function of betaine in the brain are little studied and reviewed. Beneficial effects of betaine in neurodegeneration, excitatory and inhibitory imbalance and against oxidative stress in the central nervous system (CNS) have been collected and analyzed to understand the main role of betaine in the brain.

What Makes Us Crazy

Two forms of energy dominate the universe as well as our bodies. The state of expansion and the state of contraction. Disease results when these two states become unbalanced which is what makes us crazy.

Our ancestors were unable to open up bodies. They instead became keen observers of our behavior. Two very different energies have been documented century after century. The Chinese refer to these two opposing energies as Yang (the state of expansion) and Yin (the state of contraction).

When neurological systems rear their ugly head, the two energies are unbalanced. Yang energy becomes the driving force of our life. What is wrong with Yang energy? Nothing! That is what makes us successful in whatever we choose to in our life. We focus, set goals and activate the energy required to manifest our dreams.

It is indeed difficult to surrender the get up and go energy that makes us successful in life. But when this expansive state dominates our life day in and day out, our neurons become stressed out and exhausted. It is this imbalance that is what makes us crazy as troublesome symptoms of Parkinsons surface.

While medicines and supplements thankfully suppress problematic symptoms, the solution to soothing overexcited neurons is to learn over time how to balance the two energies so that there is not too much Yang nor too little Yin.

The four seasons best describe the energetic state that is necessary to engage a successful journey down the road to recovery.

  • Summer: Mostly yang (expansion)
  • Fall: More in balance
  • Winter: More Yin (contraction)
  • Spring: Balance of two energies

Yang is known as hot energy. Yin is known as having cool energy. The liver (which gets overloaded with toxins with symptoms of Parkinsons and the brain are both considered the hot organs of the body.

Cooling down what makes us crazy requires an ongoing balance of the two diametrically opposed energies. Members of the Parkinsons Recovery audience tell me frequently that their symptoms seem to vanish for a day or week, then explode. It becomes a vicious juggling act.

What is happening here? The welcome relief surfaces when the two energies are at long last balanced: Not too much expansion nor too little contraction.

To summarize, we can always turn down the volume of what makes us crazy and frantic with confronting tremors that flare up and impaired mobility. It is not a question of medications or supplements. It is all about living a day to day existence that balances the “get up and go” energies with the “let go and relax” energies.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery
Road to Recovery from Parkinsons Disease
robert@parkinsonsrecovery.com

Lavender Calms Anxiety and Supports Sleep

Guess what. A treatment as simple as lavender calms anxiety and supports sleep. The plant also protects you from radiation exposure. This harmful exposure can be emitted by WIFI, cell phone towers, radiation treatments for cancer, smart phones or even new cars.

Energy healers will often recommend that their clients locate lavender plants in their home or office. Why? Lavender offers protection from EMF exposures. People report that they have more energy and feel better when placing a lavender plant next to their computer.

The plant can also be particularly helpful to persons undergoing radiation therapy.

If a plant dies, it has served its purpose. Do not hesitate to get a replacement.

The studies below report that lavender shuts down anxiety, promotes beneficial sleep and helps with depression.

Why not give a lavender plant an opportunity to serve a useful purpose? The cost is minimal. Potential benefits significant. Sometimes the simplest solutions offer the greatest benefits.

Three studies below confirm the benefit effects of lavender.

Asian Nurs Res (Korean Soc Nurs Sci). 2021 Dec;15(5):279-290. Effects of Lavender on Anxiety, Depression, and Physiological Parameters: Systematic Review and Meta-Analysis

Abstract

Purpose: The recent evidence suggested substantial anxiolytic efficacy of lavender. The aim of this study was to examine the efficacy of lavender for anxiety, depression, and physiological parameters and to elucidate the differential effects of lavender on anxiety and depression by study characteristics.

Methods: A systematic review and meta-analysis was performed following the PRISMA guidelines. We searched PubMed, Embase, Cochrane Library, Web of Science, and Cumulative Index of Nursing and Allied Health Literature databases for randomized controlled trials investigating the efficacy of lavender on anxiety, depression, or physiological parameters in humans. We assessed the risk of bias within studies with the revised Cochrane risk of bias tool for randomized trials. We used random effect model to estimate the average effect and computed bias-corrected standardized mean difference as effect size metric, Hedges’ ? for all outcomes.

Results: Lavender was superior to placebo or no treatment in reducing anxiety (Hedges’ ? = -0.72, 95% confidence interval [CI] -0.90 to -0.55, p value <.001), depression (Hedges’ ? = -0.43, 95% CI, -0.59 to -0.27, p value <.001), and systolic blood pressure (Hedges’ ? = -0.23, 95% CI, -0.41to -0.05, p value = .01). The moderator analysis by meta-regression indicated that route of administration accounted 6.5% (p value = .187) for the heterogeneity in anxiolytic effects, sessions of treatment accounted 13.2% (p value = .055), and participants’ health state accounted 8.9% (p value = .131) for the variance in anxiolytic effects.

Conclusion: Lavender aromatherapy showed substantial effect in reducing anxiety and depression, and sessions of administration increased the anxiolytic effects.

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Complement Ther Med. 2022 Sep:68:102832. The effect of lavender on stress in individuals: A systematic review and meta-analysis

Abstract

Background: Lavender is considered as one of the medicinal plants to manage stress. Although many preliminary studies evaluated the effect of lavender on individuals’ stress level, to the best of our knowledge, we did not find a study that summarizes the results. Therefore, the present study aimed to estimate the Pooled effect of lavender on the stress level of individuals using systematic review and meta-analysis.

Method: A systematic literature review based on PRISMA 2020 was performed on the SID, MagIran, Embase, PubMed, Scopus, Web of Science (WoS) databases, and Google Scholar motor engine using related MeSH/Emtree and ?Free Text words,? including “Lavender*”, “Lavandula*”, “Stress*”, “Stress Disorders, Traumatic”, and “Stress, Psychological” with no time limitation until August 2021: We also searched two Iranain free local resourses including MagIran https://www.magiran.com and Scientific Information Database (SID) https://www.sid.ir. The quality assessment of studies was performed using JBI checklist. Heterogeneity among studies was quantified using I2 index and Random Effects model was used to combine the data and perform the meta-analysis.

Results: In the initial search, 1520 articles were found. After excluding the irrelevant studies, finally, 21 articles with a sample size of 791 in the intervention group and 804 in the control group were included in the meta-analysis. As a result of combining the studies, stress score after using lavender in the intervention group showed a significant decrease of 0.63 ± 0.13 (95% CI) more than that in the control group (P < 0.001). The results of subgroup analysis demonstrated that the highest standardized mean difference (SMD) before and after the intervention in the intervention group compared to the control group was related to L. angustifolia species with 0.73 ± 0.22, student groups with 2.27 ± 1.34, and diagnostic tool of Perceived Stress Scale (PSS) with 0.82 ± 0.42, indicating that the difference between the groups was statistically significant (P < 0.001).

Conclusion: The pooled estimation of this systematic reiew and meta-analysis revealed that lavender significantly reduces individuals’ stress. Therefore, it seems that the use of lavender can be considered as a part of a stress management programs.

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Exp Gerontol. 2025 Nov:211:112919. A systematic review and meta-analysis of clinical trials on lavender for sleep disorders in older adult

Abstract

Background: The present study aimed to gather existing findings related to the effect of lavender on improving sleep disorders in older adults.

Methods: In this systematic review, PubMed, Web of Science, Embase, and Scopus databases were searched using keywords ((lavender OR Lavandula) AND (sleep OR insomnia OR “sleep disturbance” OR “sleep quality” OR “sleep disorder”) AND (elderly OR elder OR aging OR aging OR “older adult” OR geriatric OR geriatrics)) from their inception up to August 20, 2025. Only clinical trials evaluating the effect of lavender on aged patients (more than 60 years old) with sleep disorders were included. Then, data about drug formulation, dosage, duration of treatment, measurements, findings, and adverse events were recorded. A random-effects meta-analysis was used to calculate the pooled standardized mean differences (SMD) and their corresponding 95 % confidence intervals (CI).

Results: In this study, 84 articles were evaluated, and ten articles were selected for full review. In nine studies (90 %), lavender significantly improved sleep disorders. The most used scale among the articles was the Pittsburgh Sleep Quality Index (PSQI), which was used in seven studies (70 %). All the studies reported using lavender in the medicinal form of inhalation. The results of the meta-analysis indicated a significant improvement in the total score of sleep quality (SMD: -1.20, 95 % CI: -1.73, -0.68, I2: 87.5 %), with a more pronounced effect observed in studies that utilized the PSQI questionnaire.

Conclusion: Based on preliminary evidence from this review, lavender may effectively treat sleep disorders, especially in the elderly. 

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery®
https://www.parkinsonsrecovery.com

Platelet Rich Plasma (PRP) Therapy

What is Platelet Rich Plasma (PRP) Therapy? When asked the question: What do Platelets in the blood do? Most people say they have one function: to clot the blood. This answer is correct, but it is a tiny fraction of the functions platelets perform for us and our body.

Platelet-rich plasma (PRP) therapy is a regenerative, minimally invasive procedure using a patient’s own blood platelets to accelerate healing in injured tendons, ligaments, muscles, joints, and skin.

It was originally used for musculoskeletal conditions (e.g., tennis elbow, arthritis), hair loss, and cosmetic facial rejuvenation but applications have spread to many other applications, including neurodegenerative diseases like Parkinsons where pain can affect symptoms. 

The process involves drawing blood, spinning it in a centrifuge, and injecting it into a part of the body that exhibits excessive inflammation.  The procedure promotes tissue repair and reduces pain. 

The procedure typically involves withdrawing blood from the patient which is then spun to create a concentrated body of platelets which are reinserted into the body. 

  • What it does: The high concentration of platelets (up to 10 times more than the concentration of platelets in a normal blood) releases growth factors. This  stimulates healing, reduces inflammation and supports tissue regeneration.

This concentration of platelets can be injected into places in the body that have a high inflammation and as a consequence pain.

  • The Procedure: A blood sample is taken from the patient, placed in a centrifuge for 15–30 minutes to concentrate the platelets, and then injected into the target area. Imaging guidance (like ultrasound) is often used for accuracy.

Research on Platelet Rich Plasma (PRP) Therapy

Neurochem Res. 2025 Mar 4;50(2):112. Systemic Rejuvenating Interventions: Perspectives on Neuroinflammation and Blood-Brain Barrier Integrity

Abstract

The aging process results in structural, functional, and immunological changes in the brain, which contribute to cognitive decline and increase vulnerability to neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and stroke-related complications. Aging leads to cognitive changes and also affect executive functions. Additionally, it causes neurogenic and neurochemical alterations, such as a decline in dopamine and acetylcholine levels, which also impact cognitive performance.

The chronic inflammation caused by aging contributes to the impairment of the blood-brain barrier (BBB), contributing to the infiltration of immune cells and exacerbating neuronal damage. Rejuvenating therapies such as heterochronic parabiosis, cerebrospinal fluid (CSF) administration, plasma, platelet-rich plasma (PRP), and stem cell therapy have shown potential to reverse these changes, offering new perspectives in the treatment of age-related neurological diseases. 

Research on Aspartame and Parkinsons

Nutr Neurosci. 2024 May;27(5):506-519. Aspartame use and Parkinson’s disease: review of associated effects on neurotransmitters, oxidative stress, and cognition

Abstract

Objective: The purpose of this review was to assess the current evidence regarding the associated physiological and cognitive effects of aspartame (APM) consumption and Parkinson’s Disease (PD).

Methods: A total of 32 studies demonstrating effects of APM on monoamine deficiencies, oxidative stress, and cognitive changes were reviewed.

Results: Multiple studies demonstrated decreased brain dopamine, decreased brain norepinephrine, increased oxidative stress, increased lipid peroxidation, and decreased memory function in rodents after APM use. In addition, PD animal models have been found to be more sensitive to the effects of APM.

Discussion: Overall, studies of APM use over time yielded more consistent results.

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Neurology. 2025 Oct 7;105(7):e214023. Association Between Consumption of Low- and No-Calorie Artificial Sweeteners and Cognitive Decline: An 8-Year Prospective Study

Abstract

Background and objectives: Consumption of low- and no-calorie sweeteners (LNCSs) has been associated with adverse health outcomes. However, little is known about the association between consumption of LNCSs and cognition. The aim of this study was to investigate the association between consumption of LNCSs and cognitive decline.

Methods: We conducted a longitudinal observational study using data from civil servants aged 35+ years at baseline who were enrolled in the Brazilian Longitudinal Study of Adult Health and evaluated across 3 study waves (2008-10, 2012-14, and 2017-19). Participants with incomplete dietary data, extreme caloric intake (<1st percentile or >99th percentile), and incomplete data for cognitive tests and covariates at baseline were excluded. A Food Frequency Questionnaire was used to calculate combined and individual consumption of 7 LNCSs (aspartame, saccharin, acesulfame k, erythritol, xylitol, sorbitol, and tagatose). We estimated z-scores across 6 cognitive tests. The association of LNCSs with cognitive decline was evaluated using linear mixed-effects models.

Results: Among 12,772 participants (mean age 51.9 ± 9.0 years, 54.8% women, 43.2% Black/mixed race), the mean consumption of LNCSs was 92.1 ± 90.1 mg/d. Among participants aged younger than 60 years, consumption of combined LNCSs in the highest tertiles was associated with a faster decline in verbal fluency (second tertile: ? = -0.016, 95% CI -0.040 to -0.008; third tertile: ? = -0.040, 95% CI -0.064 to -0.016) and global cognition (second tertile: ? = -0.008, 95% CI -0.024 to 0.008; third tertile: ? = -0.024, 95% CI -0.040 to -0.008). There was no association between tertiles of LNCSs and cognitive decline in participants aged 60+ years.

Consumption of aspartame, saccharin, acesulfame k, erythritol, sorbitol, and xylitol was associated with a faster decline in global cognition, particularly in memory and verbal fluency domains. Consumption of combined LNCSs in the highest tertiles was associated with a faster decline in verbal fluency and global cognition in participants without diabetes and faster decline in memory and global cognition in participants with diabetes.

Discussion: Consumption of LNCSs was associated with an accelerated rate of cognitive decline during 8 years of follow-up. Our findings suggest the possibility of long-term harm from LNCS consumption, particularly artificial LNCSs and sugar alcohols, on cognitive function. 

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery®
https://www.parkinsonsrecovery.com

The Reason for Mobility Difficulties

When I ask people if walking is improved when they are in nature, the answer 100% of the time is yes. Why should hanging out in nature be such a tremendous support to rock solid walking?

The straightforward answer is – nature helps ground our energetic system.

As I describe in the video – problematic walking is directly connected to energy which is top heavy. Effortless mobility requires that our energy be distributed evenly from our head to our feet. When more energy is circulating around our head and the top of our body we become top heavy and are much more likely to fall, stumble and freeze.

The one criteria for energy healers to help their clients manifest improved mobility is for them to become grounded. If their energy is running haphazardly from left to right or spinning at the top of the body, they will simply exaggerate the problems a client confronts.

Another way of understanding what it means to be grounded is to “be in our body.”  When we reside only in our mind and brain with thoughts of worry and regret we are not grounded and will confront mobility challenges.

How to Become Grounded

  • Take off shoes and walk in the grass
  • Wear the color red
  • Spend your day out in nature as much as possible even if it means standing outside for a few minutes
  • Take off shoes when walking around your home.
  • Get grounding mats for your bed or a chair where you sit often
  • Use your intention to shift the energy from your head to your legs and feet.
  • Become mindful of each and every step you take.

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery
https://www.parkinsonsrecovery.com 
Road to Recovery from Parkinsons Disease

 

How to Identify Your Dominant Eye in 10 Seconds or Less

Here are your instructions on how to identify your dominant eye:

  • Put one hand in front of you.
  • Focus on an object like a picture (or a person) beyond you a short distance away.
  • Close one eye with the other hand.
  • Then close the other eye.
  • Notice what happens
  • When one of the two eyes is closed the object will be directly in front of you.
  • When the other eye is closed, the object will shift.

The dominant eye is revealed when your hand is directly in front of you. My dominant eye is the left eye which comes as no surprise to me. I have always been a right brain (big picture) person.

My eye classes prescription for long distance sight is stronger for my right eye and weaker for my dominant eye. Makes sense, eh?

What is the big deal here with whether one eye is dominate or not? Put a patch over your dominant eye, then challenge yourself with tossing a ball to another person. Having trouble? Then catch the ball. Having trouble? It is not so easy when your dominant eye is patched closed

Wobbly walking involving freezing and shuffling can be due in part to a stark difference between your dominant eye and your other eye. Equalizing out both eyes can boast rock solid walking.

Neuro-Optometrists can be of great assistance in this regard.

For more information about neuro optometry visit: https://noravisionrehab.org/

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery®
https://www.parkinsonsrecovery.com

Swallowing Safely

Difficulty with swallowing safely is a typical symptom of Parkinsons. How do you know for sure that you have a swallowing problem and if you do, what do you do about it?

Dr. Joel Herskowitz, M.D. and Dr. Roya Sayadi, Ph.D., authors Swallow Safely answer these questions and explain the critical role of swallowing safely for persons with Parkinson’s symptoms.

Swallow Safely presents in non-technical language how swallowing works normally, how things can go wrong and what symptoms to watch out for. The book is written primarily for persons with neurological challenges problems such as stroke, Parkinson disease, multiple sclerosis, cancer, and Alzheimer disease, all of which are commonly associated with swallowing problems. Appendices include a Letter For Your Doctor and Suggestions For Safe Swallowing.

You can order Swallow Safely by clicking on Swallow Safely

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery®
Road to Recovery from Parkinsons Disease
https://www.parkinsonsdisease.me
robert@parkinsonsrecovery.com

Broccoli Seed Tea

Below find directions for preparing Broccoli Seed Tea which contains the bioactive compound sulforaphane. This process involves a crucial two-step reaction using both broccoli seeds and ground white mustard seeds as a myrosinase enzyme source. 

Broccoli Seed Tea Recipe

Ingredients:

  • Dry, high-quality broccoli seeds: 1 tablespoon (or about 15g to 35g, depending on the desired strength)
  • Ground white mustard seeds (sinapis alba): 1/8 to 1 teaspoon
  • Water: Approximately 1 cup (or 100-200ml) 

Instructions:

  1. Heat the water: Bring water to approximately 60°C (140°F). This deactivates an enzyme (ESP) that reduces sulforaphane yield in broccoli. Do not boil, as high heat destroys the necessary myrosinase enzyme.
  2. Combine seeds and water: Add the desired amount of dry broccoli seeds to the hot water.
  3. Allow extraction: Let the mixture sit for about 10 minutes. This step helps extract the precursor compound, glucoraphanin, from the seeds.
  4. Add myrosinase source: Stir in the ground white mustard powder. This provides the active myrosinase enzyme needed to convert the glucoraphanin into sulforaphane.
  5. Activate sulforaphane: Let the mixture sit for an additional 10 minutes to allow the conversion reaction to occur.
  6. Consume: The mixture can be consumed as is. Or, blend the preparation into a smoothie with other ingredients like fruit, nuts, or protein powder to improve the taste and texture. 

Early evidence suggests that this tea was most helpful for addressing symptoms including fatigue, sleep quality, and lack of motivation. Urinary incontinence and nocturnal urinary frequency showed significant improvement as well.

The studies posted below suggest it should also be useful to treat the symptoms of neurological conditions such as Parkinsons and Alzheimers.

The primary role of sulforaphane is to enhance energy production in neurons by reducing damage to mitochondria. Oxidative stress is likely to be the predominant mechanism in the development of the process that gives rise to these non-motor symptoms.

Research on Sulforaphane as a Treatment for Neurological Conditions

Nutrients. 2025 Apr 15;17(8):1353. Sulforaphane and Brain Health: From Pathways of Action to Effects on Specific Disorders

Abstract

The brain accounts for about 2% of the body’s weight, but it consumes about 20% of the body’s energy at rest, primarily derived from ATP produced in mitochondria. The brain thus has a high mitochondrial density in its neurons because of its extensive energy demands for maintaining ion gradients, neurotransmission, and synaptic activity. The brain is also extremely susceptible to damage and dysregulation caused by inflammation (neuroinflammation) and oxidative stress.

Many systemic challenges to the brain can be mitigated by the phytochemical sulforaphane (SF), which is particularly important in supporting mitochondrial function. SF or its biogenic precursor glucoraphanin, from broccoli seeds or sprouts, can confer neuroprotective and cognitive benefits via diverse physiological and biochemical mechanisms. SF is able to cross the blood-brain barrier as well as to protect it, and it mitigates the consequences of destructive neuroinflammation.

It also protects against the neurotoxic effects of environmental pollutants, combats the tissue and cell damage wrought by advanced glycation end products (detoxication), and supports healthy glucose metabolism. These effects are applicable to individuals of all ages, from the developing brains in periconception and infancy, to cognitively, developmentally, and traumatically challenged brains, to those in later life as well as those who are suffering with multiple chronic conditions including Parkinson’s and Alzheimer’s diseases.

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Biochem Pharmacol. 2025 Mar:233:116797. Sulforaphane: An emerging star in neuroprotection and neurological disease prevention

Abstract

Neurological diseases, including both acute injuries and chronic neurodegenerative disorders, represent major contributors to morbidity and mortality worldwide. Chronic neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), which require long-term management, present significant challenges in the search for neuroprotective agents with reduced adverse effects and enhanced therapeutic efficacy.

Sulforaphane (SFN), a bioactive compound found in cruciferous vegetables like broccoli and cauliflower, has garnered considerable attention for its potent neuroprotective properties and overall health benefits. Marketed primarily as a dietary supplement, SFN has shown a variety of biological activities and therapeutic potential in neurological diseases.

Recent surging studies including ours have highlighted its ability to impede the progression of AD, PD, and cerebral ischemia by fostering neurogenesis and inhibiting apoptosis, oxidative stress, and neuroinflammation. This review aims to summarize the latest research on SFN, exploring its advanced therapeutic potential and underlying mechanisms in various neurological diseases, offering a comprehensive overview for researchers focused on neurological pathogenesis and drug development in neuroprotection.

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Int J Mol Sci. 2020 Nov 16;21(22):8637. Efficacy of Sulforaphane in Neurodegenerative Disease

Abstract

Sulforaphane (SFN) is a phytocompound belonging to the isothiocyanate family. Although it was also found in seeds and mature plants, SFN is mainly present in sprouts of many cruciferous vegetables, including cabbage, broccoli, cauliflower, and Brussels sprouts. SFN is produced by the conversion of glucoraphanin through the enzyme myrosinase, which leads to the formation of this isothiocyanate.

SFN is especially characterized by antioxidant, anti-inflammatory, and anti-apoptotic properties, and for this reason, it aroused the interest of researchers.

The aim of this review is to summarize the experimental studies present on Pubmed that report the efficacy of SFN in the treatment of neurodegenerative disease, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Therefore, thanks to its beneficial effects, SFN could be useful as a supplement to counteracting neurodegenerative diseases.

Robert Rodgers PhD
Founder Parkinsons Recovery ®
https://www.parkinsonsrecovery.com

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