Dr. Richard Cheng, Cheng Integrative Health Center

Introduction

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to motor and non-motor symptoms. While conventional treatments focus on dopamine replacement therapy, they do not address the underlying causes of neurodegeneration. Integrative Orthomolecular Medicine (I-OM) provides a comprehensive approach to managing PD by optimizing nutrition, reducing inflammation and oxidative stress, and utilizing innovative therapies such as photobiomodulation (PBMT) and methylene blue.

1. Dietary Approach: Low-Carb, Ketogenic, and Anti-Inflammatory Diet

Low-Carb and Ketogenic Diet

A low-carbohydrate, ketogenic diet is highly beneficial for Parkinson’s patients due to its neuroprotective effects. The ketogenic diet provides an alternative energy source (ketones) to the brain, reducing dependence on glucose metabolism, which is often impaired in PD. Benefits include:

• Mitochondrial Support: Enhances mitochondrial function and reduces oxidative stress.
• Neuroprotection: Ketones, especially β-hydroxybutyrate, have anti-inflammatory and antioxidant properties.
• Stabilizing Dopamine Levels: Ketogenic metabolism may help modulate neurotransmitter balance and slow neuronal loss.

Avoiding Ultra-Processed Foods and Omega-6 Seed Oils

Ultra-processed foods are linked to systemic inflammation and oxidative stress, exacerbating neurodegeneration. Reducing the intake of industrial seed oils (soybean, corn, canola, sunflower) is crucial, as excessive Omega-6 fatty acids promote neuroinflammation.

Optimizing Omega-3 Intake

Omega-3 fatty acids (EPA/DHA) have anti-inflammatory and neuroprotective effects, supporting synaptic plasticity and reducing neuronal apoptosis. Sources include fatty fish, fish oil supplements, and grass-fed meats.

2. Orthomolecular Nutrient Optimization

Correcting nutrient deficiencies and optimizing high-dose supplementation are fundamental in I-OM for Parkinson’s Disease.

B-Vitamins: Thiamine (B1), Riboflavin (B2), Niacin (B3)

• Thiamine (B1, high-dose therapy): Studies suggest that high-dose thiamine (up to 3,000 mg/day) significantly improves motor symptoms and cognitive function in PD.
• Riboflavin (B2): Enhances mitochondrial function and reduces oxidative stress.
• Niacin (B3, Nicotinamide Riboside/Nicotinic Acid): Supports NAD+ synthesis, essential for mitochondrial health and energy production.

Vitamin C & D

• Vitamin C: A powerful antioxidant that reduces oxidative stress and protects dopaminergic neurons.
• Vitamin D: Essential for immune regulation, neuroprotection, and reducing neuroinflammation.

Magnesium (Mg)

Magnesium supports dopaminergic neurotransmission and prevents excitotoxicity. Deficiency is common in PD and contributes to increased oxidative stress and neurodegeneration.

Antioxidants (Glutathione, CoQ10, Alpha-Lipoic Acid, NAC)

• Glutathione: A crucial antioxidant that detoxifies oxidative stress in dopaminergic neurons.
• Coenzyme Q10 (CoQ10): Supports mitochondrial energy production and reduces neurodegeneration.
• Alpha-Lipoic Acid (ALA): Helps regenerate other antioxidants and supports mitochondrial function.
• N-Acetylcysteine (NAC): Increases glutathione levels, reducing oxidative damage in PD patients.

3. Near-Infrared Light Therapy (NIR) / Photobiomodulation (PBMT)

Photobiomodulation (PBMT), specifically Near-Infrared (NIR) light therapy, has emerged as a promising therapy for PD. It works by:

• Stimulating Mitochondria: Enhancing ATP production and reducing oxidative stress.
• Reducing Inflammation: Decreasing microglial activation and promoting neuronal survival.
• Improving Dopaminergic Function: Studies suggest that PBMT improves motor function and cognitive performance in PD patients.
• Neuroplasticity: Promotes brain repair and synaptic plasticity.

Common NIR/PBMT devices include 810nm and 1064nm wavelength light therapy, which penetrate deep into brain tissues.

4. Methylene Blue (MB) Therapy

Methylene Blue (MB) is a mitochondrial enhancer with neuroprotective, antioxidant, and cognitive-enhancing properties in PD. Key benefits:

• Enhances Mitochondrial Function: Acts as an alternative electron carrier, bypassing mitochondrial dysfunction in PD.
• Antioxidant Effects: Reduces oxidative stress and improves neuronal survival.
• Increases ATP Production: Supports brain energy metabolism.
• Prevents Protein Aggregation: Helps reduce misfolded alpha-synuclein accumulation, a hallmark of PD.

Low-dose MB (0.5-4 mg/kg) has been shown to improve cognitive function and neuroprotection in neurodegenerative diseases.

5. Detoxification and Environmental Considerations

Environmental toxins, including pesticides, heavy metals (lead, mercury), and industrial pollutants, have been linked to increased PD risk. Strategies to support detoxification include:

• Glutathione supplementation to enhance detox pathways.
• Chelation therapy (e.g., EDTA, ALA) for heavy metal removal.
• Infrared sauna therapy to promote detoxification through sweating.

Conclusion

Integrative Orthomolecular Medicine (I-OM) offers a holistic approach to preventing and managing Parkinson’s Disease by addressing root causes rather than just symptoms. A low-carb, ketogenic diet, combined with optimal doses of essential nutrients (B1, B2, B3, C, D, magnesium, omega-3, and antioxidants), Near-Infrared Light Therapy (PBMT), and Methylene Blue, provides neuroprotection and enhances mitochondrial function. Additionally, environmental detoxification plays a critical role in slowing disease progression. This multi-targeted approach holds great promise for improving the quality of life and long-term health of individuals with Parkinson’s Disease.

To reach Dr. Cheng for a consultation, please email richzc@gmail.com. Or call: 1.803.344.3420.

Multiple studies have demonstrated that intracellular glutathione (GSH) deficiency is a common feature across various pathological conditions and tissue types. This review summarizes the evidence of decreased GSH levels in immune deficiencies, neurodegenerative diseases, mitochondrial disorders, and other chronic conditions. Despite variations in study designs, measurement techniques, and sample types, the overall findings indicate that reduced GSH levels are associated with enhanced oxidative stress, impaired immune function, mitochondrial dysfunction, and neuronal vulnerability. These observations underscore the crucial role of glutathione in maintaining cellular health and suggest that GSH deficiency may be a prominent feature in several disease states.

Introduction

Glutathione is a key intracellular antioxidant that plays a vital role in redox homeostasis, immune regulation, and energy metabolism. In recent years, numerous studies have reported abnormalities in intracellular GSH levels in conditions such as common variable immunodeficiency (CVI), HIV infection, Parkinson’s disease, and mitochondrial dysfunction. This review aims to systematically collate current literature, analyze the prevalence of GSH deficiency in different pathological contexts, and discuss the potential molecular mechanisms underlying these observations.

Literature Search and Selection

The studies included in this review were identified through extensive literature searches across multiple academic databases. The selection criteria were as follows:

• The study must measure intracellular GSH levels in human subjects.
• Validated measurement techniques (e.g., high-performance liquid chromatography, enzymatic assays, or flow cytometry) were employed.
• The study included a healthy control or disease control group for baseline comparison.
• A minimum sample size of 10 subjects was required.
• The measurements focused on chronic or baseline GSH status rather than acute changes.
• Direct quantification of GSH levels in cellular components (not solely in plasma or extracellular fluid) was conducted.

Based on these criteria, studies involving CVI, HIV, Parkinson’s disease, mitochondrial disorders, and other related conditions were selected for review.

Results

Prevalence of GSH Deficiency in Various Conditions

1. Immune-Related Disorders
   • Common Variable Immunodeficiency (CVI): Aukrust et al. (1995) reported that patients with CVI exhibit significantly lower total and reduced GSH levels in CD4⁺ lymphocytes compared to healthy controls. Some studies also noted differential findings, with monocytes showing increased GSH levels, suggesting cell-type specific regulation.
   • HIV Infection: Several studies (e.g., Staal et al., 1992; Herzenberg et al., 1997) have documented markedly reduced GSH levels in both CD4⁺ and CD8⁺ T cells of HIV-infected individuals. Low GSH levels in these cells are associated with impaired immune function and poorer clinical outcomes.
2. Neurodegenerative Diseases
   • Parkinson’s Disease: Perry et al. (1982) found that the substantia nigra of patients with Parkinson’s disease has an almost complete absence of reduced GSH, whereas other brain regions maintain detectable levels. This localized deficiency may increase the susceptibility of the substantia nigra to oxidative injury. In addition, Martin and Teismann (2009) noted that reduced GSH levels constitute an early biochemical change in Parkinson’s disease.
3. Mitochondrial Disorders
   • Electron Transport Chain (ETC) Defects: Hargreaves et al. (2005) used HPLC analysis of skeletal muscle biopsies to show that patients with ETC defects have significantly lower GSH concentrations compared to controls (7.7 ± 0.9 nmol/mg protein versus 12.3 ± 0.6 nmol/mg protein). This reduction may reflect increased oxidative stress and impaired energy metabolism.
4. Other Conditions
   • Additional Diseases: Reid and Jahoor (2001) reviewed altered glutathione metabolism in a range of conditions, including protein–energy malnutrition, seizures, Alzheimer’s disease, sickle cell anemia, and various chronic diseases associated with aging.

Tissue- and Cell-Specific Patterns

• Immune Cells:
  CD4⁺ T cells consistently show reduced GSH levels in both CVI and HIV infection, with CD8⁺ T cells exhibiting similar trends. The observed differences between lymphocytes and monocytes in some studies suggest that glutathione regulation may vary by cell type.
• Skeletal Muscle:
  In patients with mitochondrial dysfunction, decreased GSH concentrations in skeletal muscle are indicative of impaired mitochondrial function and heightened oxidative stress.
• Brain Tissue:
  The near absence of reduced GSH in the substantia nigra of Parkinson’s disease patients highlights the vulnerability of specific brain regions to oxidative damage.

Mechanistic Insights

Relationship with Oxidative Stress

Glutathione plays a central role in cellular antioxidant defense. The reviewed studies suggest a bidirectional relationship between GSH deficiency and oxidative stress:

• In CVI, low GSH levels may be linked to increased oxidative stress and activation of the tumor necrosis factor system.
• In mitochondrial disorders, diminished GSH may result from both elevated oxidative stress and decreased ATP availability.
• In Parkinson’s disease, the deficiency of GSH in the substantia nigra may render neurons more vulnerable to oxidative injury.

Impact on Cellular Function

The consequences of GSH deficiency extend to several aspects of cellular physiology:

• Immune Function: Reduced GSH levels are associated with impaired T cell function and compromised immune responses.
• Mitochondrial Function: GSH deficiency may lead to dysfunction of the electron transport chain, adversely affecting energy production.
• Neuroprotection: The lack of GSH in vulnerable neuronal populations, as seen in Parkinson’s disease, may contribute to neurodegenerative processes.
• Cell Survival: In conditions of chronic infection or inflammation, low GSH levels have been linked to decreased cell viability and poorer survival outcomes.

Discussion

The reviewed literature demonstrates that intracellular glutathione deficiency is observed across a wide range of pathological conditions, including immune deficiencies, neurodegenerative disorders, and mitochondrial diseases. Although the degree of deficiency varies depending on the disease context and the specific cell or tissue examined, the consistent finding of reduced GSH levels underscores its importance in maintaining cellular health. Further research is needed to quantify these differences more precisely and to explore targeted interventions that might restore optimal GSH levels.

Conclusion

Current evidence indicates that intracellular glutathione deficiency is a prevalent feature in several disease states. The association of low GSH levels with increased oxidative stress, impaired immune function, mitochondrial dysfunction, and neurodegeneration highlights the critical role of glutathione in cellular homeostasis. Future studies should aim to clarify the quantitative aspects of GSH deficiency in different conditions and develop clinical strategies to mitigate its impact.

References

1. Staal FJ, Roederer M, Israelski DM, Bubp J, Mole LA, McShane D, Deresinski SC, Ross W, Sussman H, Raju PA, et al. Intracellular glutathione levels in T cell subsets decrease in HIV-infected individuals. AIDS Res Hum Retroviruses. 1992 Feb;8(2):305-11. doi: 10.1089/aid.1992.8.305. PMID: 1540417.
2. Martin HL, Teismann P. Glutathione–a review on its role and significance in Parkinson’s disease. FASEB J. 2009 Oct;23(10):3263-72. doi: 10.1096/fj.08-125443. Epub 2009 Jun 19. PMID: 19542204.
3. Hargreaves IP, Sheena Y, Land JM, Heales SJ. Glutathione deficiency in patients with mitochondrial disease: implications for pathogenesis and treatment. J Inherit Metab Dis. 2005;28(1):81-8. doi: 10.1007/s10545-005-4160-1. PMID: 15702408.
4. Herzenberg LA, De Rosa SC, Dubs JG, Roederer M, Anderson MT, Ela SW, Deresinski SC, Herzenberg LA. Glutathione deficiency is associated with impaired survival in HIV disease. Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1967-72. doi: 10.1073/pnas.94.5.1967. PMID: 9050888; PMCID: PMC20026.
5. Reid M, Jahoor F. Glutathione in disease. Curr Opin Clin Nutr Metab Care. 2001 Jan;4(1):65-71. doi: 10.1097/00075197-200101000-00012. PMID: 11122562.
6. Aukrust P, Svardal AM, Müller F, Lunden B, Berge RK, Frøland SS. Decreased levels of total and reduced glutathione in CD4+ lymphocytes in common variable immunodeficiency are associated with activation of the tumor necrosis factor system: possible immunopathogenic role of oxidative stress. Blood. 1995 Aug 15;86(4):1383-91. PMID: 7632946.
7. Perry TL, Godin DV, Hansen S. Parkinson’s disease: a disorder due to nigral glutathione deficiency? Neurosci Lett. 1982 Dec 13;33(3):305-10. doi: 10.1016/0304-3940(82)90390-1. PMID: 7162692.

Naturally occurring plant toxins can contribute to skin rash diseases, including neurodermatitis, eczema, psoriasis, and other inflammatory skin conditions. Many of these compounds act as immune triggers, inflammatory agents, or gut disruptors, which can exacerbate skin issues through systemic inflammation, immune dysregulation, or histamine-related pathways.

How Plant Toxins Can Trigger Skin Conditions Like Neurodermatitis

1. Histamine & Mast Cell Activation

• Certain plant compounds can increase histamine release or block histamine breakdown, leading to skin itching, hives, and chronic rashes.
• Key Plant-Based Histamine Triggers:
  • Lectins (found in legumes, grains, nightshades)
  • Saponins (quinoa, soy, legumes)
  • Tannins (tea, coffee, nuts)
  • Fermented plant foods (sauerkraut, kombucha)
  • High-histamine plant foods (spinach, eggplant, avocado, tomato)

➡ Solution: Follow a low-histamine diet, avoid fermented foods, and supplement with DAO enzyme if necessary.

2. Gut Inflammation & Increased Intestinal Permeability (“Leaky Gut”)

• Many plant toxins can damage the gut lining, leading to increased intestinal permeability. This can allow toxins, undigested food particles, and bacterial byproducts (LPS) to enter the bloodstream, triggering immune activation and skin inflammation.
• Key Gut-Disrupting Plant Compounds:
  • Lectins – Found in wheat, legumes, nightshades; can damage gut lining.
  • Phytates & Oxalates – Can bind minerals, impair gut health.
  • Gluten & Gliadin – Found in wheat; associated with autoimmune skin disorders.
  • Saponins – Can act as detergents, damaging intestinal cells.

➡ Solution: Follow a gut-healing diet (low-lectin, low-gluten, high-collagen foods). Consider bone broth, L-glutamine, and probiotics.

3. Autoimmune & Immune Dysregulation

• Some plant-derived compounds mimic human proteins, leading to molecular mimicry and autoimmune activation. Many autoimmune skin diseases, including psoriasis, lupus-related skin conditions, and eczema, can be worsened by these triggers.
• Key Autoimmune-Triggering Plants:
  • Nightshades (Solanine, Chaconine) – Found in potatoes, tomatoes, peppers, eggplants; can trigger eczema, psoriasis, and lupus-related rashes.
  • Soy & Phytoestrogens – May worsen hormonal skin conditions.
  • Gluten-Containing Grains – Linked to dermatitis herpetiformis (Celiac-related rash).

➡ Solution: Consider an autoimmune-friendly, low-nightshade diet.

4. Oxalates & Skin Irritation

• Oxalates (oxalic acid) found in spinach, almonds, beets, chocolate, and sweet potatoes can form crystals in tissues, leading to skin irritation, rashes, and delayed wound healing.
• Conditions Linked to Oxalates:
  • Chronic eczema
  • Psoriasis
  • Fibromyalgia-related skin pain

➡ Solution: Reduce high-oxalate foods, supplement with calcium citrate, and increase B6 intake to help oxalate metabolism.

5. Mycotoxins & Mold-Contaminated Plant Foods

• Mycotoxins from mold-contaminated grains, nuts, coffee, and dried fruits can increase oxidative stress and inflammation, contributing to chronic skin conditions.
• Common Mycotoxin Sources:
  • Peanuts, cashews, walnuts
  • Stored grains (corn, wheat, oats)
  • Coffee beans (low-quality brands)

➡ Solution: Choose mold-free nuts, organic coffee, and fresh grains if consuming.

6. Salicylates & Phenolic Compounds

• Salicylates are found in many fruits, vegetables, and plant oils. Some people with salicylate sensitivity experience hives, eczema, and itchy rashes.
• High-Salicylate Foods:
  • Berries, tomatoes, grapes, oranges
  • Mint, cinnamon, curry spices
  • Tea, coffee, nuts

➡ Solution: If sensitive, follow a low-salicylate diet.

Conclusion: Can Plant Toxins Promote Neurodermatitis & Skin Rashes?

Yes, naturally occurring plant toxins can contribute to skin diseases, including neurodermatitis, eczema, psoriasis, and allergic rashes. The key mechanisms include:

• Histamine release & mast cell activation
• Gut inflammation & leaky gut
• Autoimmune activation
• Oxalate accumulation & skin irritation
• Mycotoxin exposure from plant-based foods
• Salicylate & phenolic compound sensitivity

Recommended Approach for Skin Issues

✔ Low-lectin, low-nightshade diet (Avoid tomatoes, potatoes, eggplants, legumes)
✔ Reduce high-histamine foods (Fermented foods, spinach, avocado)
✔ Optimize gut health (Bone broth, L-glutamine, probiotics)
✔ Check for oxalate issues (Avoid spinach, almonds, beets)
✔ Limit mycotoxin exposure (Choose organic nuts, fresh grains)
✔ Consider a low-salicylate diet if skin symptoms persist

References:

Plant toxins, including phytoalexins, lectins, and oxalic acid, can contribute to skin conditions like neurodermatitis through various mechanisms.

## Phytoalexins

Phytoalexins are antimicrobial compounds produced by plants in response to stress or pathogen attack. They serve as a defense mechanism against infections, but can also induce skin reactions in sensitive individuals. These compounds may cause irritation and inflammation when they come into contact with the skin, particularly when exposed to sunlight, leading to conditions such as phytophotodermatitis, which resembles sunburn or eczema[1][2].

## Lectins

Lectins are proteins found in many plants that can bind to carbohydrates and may trigger immune responses. While specific studies linking lectins directly to neurodermatitis are limited, their ability to provoke inflammatory responses suggests a potential role in exacerbating skin conditions. Lectins can cause cell damage and inflammation, which may contribute to the symptoms associated with neurodermatitis.

## Oxalic Acid

Oxalic acid is a naturally occurring compound in various plants that can lead to skin irritation and allergic reactions. In some cases, high levels of oxalic acid have been linked to atopic dermatitis in children, indicating that metabolic disturbances involving this compound can aggravate skin conditions[3]. The irritant effect of oxalic acid may be due to its ability to form insoluble calcium oxalate crystals in the body, which can lead to inflammation and discomfort.

## Conclusion

In summary, plant toxins such as phytoalexins, lectins, and oxalic acid can promote neurodermatitis through mechanisms involving skin irritation and immune response activation. Individuals with sensitivities or pre-existing skin conditions may be particularly vulnerable to these effects.

References:

1. https://newsnetwork.mayoclinic.org/discussion/sun-related-skin-condition-triggered-by-chemicals-in-certain-plants-fruits/
2. https://en.wikipedia.org/wiki/Phytoalexin
3. https://childshealth.zaslavsky.com.ua/index.php/journal/article/view/1137
4. https://krishi.icar.gov.in/jspui/bitstream/123456789/14140/1/ABNL%20SEED%20LONGEVITY.pdf
5. https://www.actasdermo.org/en-allergic-contact-dermatitis-plants-understanding-articulo-S1578219012001989
6. https://pmc.ncbi.nlm.nih.gov/articles/PMC6271817/
7. https://pmc.ncbi.nlm.nih.gov/articles/PMC7733371/
8. https://naturalingredient.org/wp/wp-content/uploads/leungs-encyclopedia-of-common-natural-ingredients-3rd-edition.pdf
9. https://pmc.ncbi.nlm.nih.gov/articles/PMC3276901/
10. https://www.plantsjournal.com/archives/2022/vol10issue2/PartB/10-2-24-532.pdf
11. https://www.amazon.com/s?k=carnivore+code+paul+saladino&crid=25SIVOMDH0ENQ&sprefix=carnivore+code%2Caps%2C463&ref=nb_sb_ss_ts-doa-p_2_14

Both Thomas E. Levy’s book “Hidden Epidemic: Silent Oral Infections Cause Most Heart Attacks and Breast Cancers” and Robert Kulacz, DDS and Thomas E. Levy’s “The Toxic Tooth: How a Root Canal Could Be Making You Sick” explore the connection between root canal-treated teeth (and other oral infections) and systemic diseases, particularly atherosclerotic cardiovascular disease (ASCVD) and breast cancer. These works highlight that bacteria trapped in root canal-treated teeth may be a source of chronic low-grade infections, leading to systemic inflammation that may contribute to diseases like ASCVD and breast cancer.

Key Studies and Data Supporting the Connection:

1. Root Canal-Treated Teeth and Systemic Infections:

• The Bacterial Link Between Root Canals and Systemic Disease:
  • Dr. Levy and Dr. Kulacz discuss how root canal-treated teeth can become breeding grounds for bacteria that are difficult to eliminate. These bacteria can migrate through the bloodstream and enter other tissues, potentially causing inflammation that contributes to systemic diseases like ASCVD and breast cancer.
  • Study Example: A study by Dr. Weston Price in the early 20th century suggested that bacteria from root canal-treated teeth could travel through the bloodstream and contribute to various systemic diseases. Although some aspects of his work have been critiqued, his findings sparked further investigation into the connection between oral infections and systemic diseases.

2. Root Canals and ASCVD:

• Root Canal Infections and Cardiovascular Disease:
  • A study published in the Journal of Periodontology (2006) found that oral pathogens, including those commonly found in root canal infections, can trigger inflammation that spreads to other parts of the body, including the cardiovascular system. This inflammation has been implicated in atherosclerosis, which can lead to heart attacks and other forms of cardiovascular disease.
  • Study Example: A 2009 study in Arteriosclerosis, Thrombosis, and Vascular Biology examined the connection between oral infections (including root canal infections) and cardiovascular disease. The study found that root canal bacteria such as Fusobacterium nucleatum and Porphyromonas gingivalis were present in atherosclerotic plaques, contributing to plaque instability and inflammation. This is believed to accelerate atherosclerosis. (Source: Göran H. Hedblad et al., Arteriosclerosis, Thrombosis, and Vascular Biology, 2009)
• Periodontal Disease and Atherosclerosis:
  • A study in Circulation (2008) showed that periodontal disease, which is often linked with untreated root canal infections, increases the levels of C-reactive protein (CRP). CRP is a well-known marker for systemic inflammation and is associated with an increased risk of atherosclerosis and cardiovascular disease. This link supports the idea that chronic infections in the mouth, including from root canal-treated teeth, contribute to cardiovascular pathology.
  • Study Example: Taba, M., et al. “Periodontal disease and cardiovascular risk: Systemic inflammation and atherosclerosis.” Circulation, 2008.

3. Root Canals and Breast Cancer:

• Systemic Inflammation and Cancer:
  • Dr. Levy’s work also touches on how the chronic inflammation associated with root canal infections can create an environment conducive to cancer cell growth. Root canal infections can lead to the release of pro-inflammatory cytokines, which can promote tumor growth and metastasis. These mechanisms are well-understood in cancer biology, and chronic inflammation from oral infections could be one of the many contributing factors to breast cancer.
  • Study Example: A 2014 study in the American Journal of Pathology suggested that oral pathogens like Porphyromonas gingivalis, commonly found in root canal-treated teeth, can trigger inflammation pathways that may contribute to the development of cancers, including breast cancer. This inflammation can lead to changes in the immune system that make it easier for tumor cells to evade detection and spread. (Source: Zhou, X. et al. “Oral bacteria and cancer risk.” American Journal of Pathology, 2014)
• Cytokine Release and Cancer Progression:
  • Chronic oral infections, including those from root canal-treated teeth, release pro-inflammatory cytokines such as IL-6 and TNF-α, both of which have been linked to increased cancer progression. These cytokines play a key role in the tumor microenvironment, supporting the idea that root canal infections could contribute to breast cancer development and metastasis.
  • Study Example: A 2012 study published in Breast Cancer Research explored the role of IL-6 in breast cancer and found that chronic inflammation, potentially originating from oral infections, could play a significant role in promoting tumor growth. (Source: Yun, Z., et al. “Cytokine IL-6 as a key mediator in the progression of breast cancer.” Breast Cancer Research, 2012)

4. The Toxicity of Root Canal Materials:

• Toxins Released from Root Canal Materials:
  • Both Dr. Levy and Dr. Kulacz argue that root canal materials, such as gutta-percha and formaldehyde-based compounds, could be harmful over time, contributing to chronic toxicity that worsens systemic inflammation. These toxins may not only trigger immune responses but also exacerbate conditions like ASCVD and breast cancer.
  • Study Example: A study published in Environmental Toxicology and Pharmacology (2011) showed that materials used in root canal treatments, such as formocresol, can release formaldehyde and other toxic compounds that could potentially contribute to systemic diseases, including cancer. (Source: Santos, A. et al. “The toxic effects of dental materials on systemic health.” Environmental Toxicology and Pharmacology, 2011)

5. General Mechanism of Root Canal Pathology:

• Chronic Infection and Systemic Inflammation:
  • Dr. Levy and Dr. Kulacz emphasize that root canal infections are often “silent” and do not present with overt symptoms, but they can release harmful toxins and bacteria into the bloodstream. These microorganisms can trigger systemic inflammation, which can spread to other parts of the body and contribute to both ASCVD and breast cancer.
  • General Mechanism: Chronic oral infections (including root canal-treated teeth) lead to bacteremia, which is the presence of bacteria in the bloodstream. This can induce systemic inflammatory responses, contributing to atherosclerosis, endothelial dysfunction, and cancer by promoting tissue damage, immune suppression, and tumor growth.

Conclusion:

The connection between root canal-treated teeth and diseases like ASCVD and breast cancer is supported by evidence linking oral infections to systemic inflammation. The bacteria and toxins associated with root canal infections can contribute to a pro-inflammatory environment that is a well-known contributor to both atherosclerosis and cancer. Dr. Levy and Dr. Kulacz’s works provide a strong foundation for the hypothesis that root canal-treated teeth may play a significant role in the development of these systemic diseases.

References:

1. Thomas E. Levy, M.D., J.D., Hidden Epidemic: Silent Oral Infections Cause Most Heart Attacks and Breast Cancers. https://www.amazon.com/s?k=Hidden+Epidemic%3A+Silent+Oral+Infections+Cause+Most+Heart+Attacks+and+Breast+Cancers&ref=nb_sb_noss
2. Robert Kulacz, DDS, Thomas E. Levy, M.D., J.D., The Toxic Tooth: How a Root Canal Could Be Making You Sick. https://www.amazon.com/Toxic-Tooth-canal-could-making/dp/0983772827/ref=sr_1_1?crid=1R2JRCFJBXE2H&dib=eyJ2IjoiMSJ9.z7-6BOhVh_IceiGWy-g9ig.HkpME-HgxgokYQJtOYFBwlNWgdP9pkSLYdZXvjTpzE4&dib_tag=se&keywords=The+Toxic+Tooth%3A+How+a+Root+Canal+Could+Be+Making+You+Sick%2C&qid=1739662240&sprefix=the+toxic+tooth+how+a+root+canal+could+be+making+you+sick%2C%2Caps%2C457&sr=8-1

Recently, I consulted on an elderly woman (in her 90’s) with T2DM and Parkinson’s disease. She has been on ketogenic diet for 8 months and high dose orthomolecular nutrition supplementation based on my previous consultation. Her ketogenic diet is pretty strict since she has a feeding tube and her daily dietary intake is well calculated. She has been maintained relatively well.

Recently she had urinary tract infection, along with seizures.  She was admitted to ICU.  Lab tests showed metabolic acidosis. But she quickly recovered. Some questions arose whether ketogenic diet was the cause.

The short answer to the above question is No. The ketogenic diet offers more immediate concerns for ketosis and DKA, but with proper management, it can be safer than a conventional diet for long-term metabolic acidosis in T2DM. 

When comparing the risks of metabolic acidosis between a ketogenic diet for a T2DM patient accustomed to the ketogenic diet and on multiple nutritional supplements versus a conventional diet, several factors come into play. Let’s break it down:

1. Ketogenic Diet for a T2DM Patient Already Accustomed to It

• Risk of Metabolic Acidosis:
  • For a patient already accustomed to the ketogenic diet, the body has likely adapted to ketosis, meaning it has developed the ability to manage ketone production and avoid diabetic ketoacidosis (DKA).
  • Chronic ketosis (from long-term adherence to a ketogenic diet) means the body is less likely to enter a dangerous state of DKA unless there are other contributing factors such as insulin resistance, infection, or severe dehydration.
  • The presence of nutritional supplements (such as electrolytes, magnesium, potassium, calcium, and B-vitamins) can help mitigate the risks associated with ketosis, including electrolyte imbalances and dehydration, both of which can exacerbate acidosis.
  • Insulin management: In T2DM, some insulin production remains, so the risk of DKA is generally lower than in type 1 diabetes, but it still exists if insulin therapy is improperly adjusted (e.g., not reducing insulin doses when switching to ketosis).
  • Hydration and electrolytes: If the patient is consuming adequate electrolytes (sodium, potassium, magnesium) through supplements or food, it reduces the risk of dehydration, which can elevate ketone levels and increase acidosis risk.
  • Overall, the risk of acidosis is low if the individual is well-adapted to the ketogenic diet, actively managing insulin, and supplementing electrolytes as needed.

2. Conventional Diet for T2DM

• Risk of Metabolic Acidosis:
  • The conventional diet for T2DM typically includes higher carbohydrate intake, which can lead to insulin resistance and chronic hyperglycemia if not properly managed. This increases the likelihood of hyperglycemic crises such as hyperosmolar hyperglycemic state (HHS), but not DKA.
  • In cases of poorly controlled diabetes, where blood glucose remains chronically high, renal function can deteriorate over time, leading to chronic metabolic acidosis or diabetic nephropathy. This is more related to the progression of T2DM rather than the diet itself.
  • If the conventional diet is not optimized with nutritional supplements, especially electrolytes (e.g., magnesium, potassium), vitamins, and minerals, it could lead to nutritional deficiencies or imbalances that contribute to acidosis, especially if kidney function is compromised.
  • Chronic insulin resistance in patients with T2DM may lead to metabolic derangements, but the risk of diabetic ketoacidosis is extremely low in the context of a conventional, carbohydrate-rich diet, unless there is an acute event like infection or stress that exacerbates glucose dysregulation.

3. Comparing the Two Approaches:

Summary:

• Ketogenic Diet (Accustomed & Supplemented): For a T2DM patient who is well-accustomed to the ketogenic diet and supplements appropriately, the risk of metabolic acidosis is generally low. The body is more efficient at managing ketones, and with proper hydration and electrolyte balance, the risk of DKA or chronic metabolic acidosis is minimal. However, there is still a potential risk of DKA if insulin or hydration is not carefully managed.
• Conventional Diet: The risk of metabolic acidosis in the conventional diet is primarily linked to long-term uncontrolled diabetes, leading to chronic hyperglycemia and renal complications (e.g., diabetic nephropathy), which could eventually result in acidosis. The risk of DKA is very low, but hyperglycemic crises (HHS) or chronic metabolic acidosis can develop with poor blood sugar management.

Thus, the ketogenic diet offers more immediate concerns for ketosis and DKA, but with proper management, it can be safer than a conventional diet for long-term metabolic acidosis in T2DM.

The book One Minute Cure suggests using hydrogen peroxide (H2O2) orally as part of its proposed therapy. However, it’s crucial to proceed with extreme caution, as ingesting hydrogen peroxide can be dangerous if not done properly.

According to the book, the hydrogen peroxide used for this therapy should be food-grade (usually 35% concentration) and highly diluted with water before consumption. The typical recommendation involves the following steps:

1. Start with a low dose: The initial dose starts with a very diluted solution—typically 3 to 5 drops of food-grade hydrogen peroxide in about 8 ounces (240 mL) of water. The idea is to introduce the compound slowly and allow the body to adapt.
2. Gradually increase the dosage: As the body becomes accustomed to the hydrogen peroxide, the dosage is slowly increased. The book suggests increasing the dose by 1 drop every few days, aiming for a maximum of 25 drops in the same 8 ounces of water.
3. Frequency: The hydrogen peroxide solution is usually taken once or twice per day, preferably on an empty stomach.
4. Dilution is key: It’s essential to ensure the hydrogen peroxide is always heavily diluted. At full strength (35%), hydrogen peroxide is corrosive and can cause severe harm to the tissues of the mouth, esophagus, stomach, and intestines. Only the food-grade version, diluted to around 3%, should be used.

Important Warnings:

• Medical supervision: While Cavanaugh claims that this method is safe and effective for treating a wide range of conditions, it is important to seek medical advice before attempting any hydrogen peroxide therapy. Many healthcare professionals warn against ingesting hydrogen peroxide, even in diluted forms.
• Potential side effects: Some people may experience nausea, stomach irritation, or more severe reactions if they consume hydrogen peroxide. Long-term use could potentially harm the gastrointestinal tract and other internal organs.
• Risks: Hydrogen peroxide is a reactive compound, and improperly diluting or using too much can lead to oxygen embolism (bubbles in the bloodstream), severe damage to tissues, and other life-threatening issues.

Given these risks, while some individuals report benefits from using hydrogen peroxide as outlined in One Minute Cure, the therapy is controversial, and its safety and efficacy remain unproven by mainstream medical research.

Ref:

The One-Minute Cure: The Secret to Healing Virtually All Diseases – 2nd Edition – Kindle edition by Cavanaugh, Madison. Health, Fitness & Dieting Kindle eBooks @ Amazon.com.

Mitral valve prolapse (MVP) is a condition where the mitral valve in the heart doesn’t close properly, causing it to bulge or “prolapse” into the left atrium during systole. While MVP is often benign, it can lead to complications such as mitral regurgitation, where blood leaks backward into the left atrium. Some individuals with MVP may also experience symptoms like palpitations, chest pain, fatigue, and shortness of breath.

Orthomolecular medicine focuses on the use of nutrients and lifestyle changes to support optimal health and manage conditions. When it comes to managing mitral valve prolapse, orthomolecular approaches may target several aspects of heart health, including reducing inflammation, improving cardiovascular function, and supporting connective tissue integrity. Here are some orthomolecular medicine strategies that may help:

1. Magnesium

• Magnesium deficiency is common in people with cardiovascular problems, and it plays a critical role in muscle function, including the heart’s muscle and the smooth muscle of blood vessels.
• Magnesium helps in relaxing the heart muscle, which can be beneficial in reducing palpitations and promoting normal rhythm. It may also support the structural integrity of connective tissue, which is vital in the mitral valve’s functioning.
• Dosage: Magnesium citrate or glycinate at 200–400 mg daily is commonly recommended.

2. Vitamin C

• Vitamin C is essential for the synthesis of collagen, a key component of connective tissue. Since MVP often involves abnormal connective tissue (such as Marfan’s syndrome or other connective tissue disorders), adequate vitamin C may support the structural health of the mitral valve.
• Dosage: 500–2000 mg per day, depending on individual needs and tolerance.

3. Vitamin E

• Vitamin E has antioxidant properties that can help reduce oxidative stress in the cardiovascular system, improving endothelial function and overall heart health.
• Vitamin E may also help reduce arrhythmias (irregular heartbeats) commonly associated with MVP.
• Dosage: A typical dose is 100–400 IU per day, although higher doses should be taken cautiously.

4. Coenzyme Q10 (CoQ10)

• CoQ10 is a powerful antioxidant that supports mitochondrial energy production in heart muscle cells. It helps in maintaining overall heart health and may improve symptoms such as fatigue and shortness of breath in individuals with MVP.
• CoQ10 also enhances the function of the left ventricle and left atrium, which can be beneficial in mitigating the effects of mitral regurgitation.
• Dosage: 100–300 mg per day.

5. Omega-3 Fatty Acids

• Omega-3 fatty acids (found in fish oil, flaxseeds, or algae) can help reduce inflammation in the cardiovascular system, which may be beneficial in managing symptoms of MVP.
• These fatty acids are also known to improve blood flow and reduce the risk of arrhythmias.
• Dosage: 1000–2000 mg per day of EPA and DHA.

6. L-Carnitine

• L-Carnitine supports mitochondrial function and fatty acid metabolism, providing energy to heart cells. It may help improve heart function in those with MVP and reduce symptoms like chest discomfort.
• Dosage: 500–1000 mg daily.

7. B Vitamins (Especially B6, B12, and Folate)

• B vitamins, particularly B6, B12, and folate, play an essential role in homocysteine metabolism. Elevated levels of homocysteine are a risk factor for cardiovascular disease and may exacerbate heart valve problems.
• Adequate levels of these vitamins may help reduce homocysteine levels and support heart health.
• Dosage: A B-complex vitamin supplement with 50–100 mg of B6, 400 mcg of folate, and 100–1000 mcg of B12 daily.

8. Collagen Support (Gelatin, Collagen Peptides)

• Since mitral valve prolapse often involves weakened connective tissue, collagen supplementation may help support the integrity of the valve. Collagen also supports overall cardiovascular health and elasticity of blood vessels.
• Dosage: 10–20 grams of collagen peptides or gelatin powder daily.

9. Antioxidants (Alpha-Lipoic Acid, Selenium, Zinc)

• Alpha-lipoic acid (ALA) is a potent antioxidant that can reduce oxidative stress and support overall cardiovascular health. Selenium and zinc also play important roles in the body’s antioxidant defense mechanisms.
• These antioxidants help protect heart tissues from damage and reduce the risk of inflammation and plaque formation in blood vessels.
• Dosage: 100–300 mg of ALA, 100 mcg of selenium, and 15–30 mg of zinc daily.

10. Lifestyle and Dietary Changes

• Diet: A heart-healthy diet is crucial for managing MVP. The low-carb, anti-inflammatory diet can help reduce inflammation and support overall cardiovascular health. Foods high in antioxidants, such as fruits, vegetables, and whole grains, as well as healthy fats from sources like olive oil and avocados, can benefit heart function.
• Exercise: Regular, moderate-intensity exercise can improve heart health, regulate blood pressure, and help prevent complications related to MVP.
• Stress Management: Stress can exacerbate palpitations and arrhythmias in people with MVP. Practices such as yoga, meditation, or deep breathing exercises can help manage stress and improve overall heart function.

Conclusion

Orthomolecular medicine offers several promising avenues for managing mitral valve prolapse, primarily through the use of nutritional interventions and lifestyle modifications. These strategies can help improve heart health, alleviate symptoms like palpitations, and support the integrity of connective tissue, which is essential in the proper functioning of the mitral valve.

While magnesium, vitamin C, CoQ10, and other nutrients can be effective in improving MVP-related symptoms and overall heart function, it is crucial for individuals to work with a qualified healthcare provider to tailor these recommendations to their specific needs.

A holistic approach that combines orthomolecular medicine with conventional treatment options—such as monitoring heart function, managing regurgitation, and possibly using beta-blockers or other medications—can help ensure the best outcomes for those with MVP.

Highlights: Fat induced mild diarrhea is a common complication of (high fat) ketogenic diet. One of the expected consequences of such a high fat diet is ‘Fat Flush“ which not only helps to improve constipation, but also to excrete fat soluble toxins including plastic particles.  

Microplastic contamination is increasingly recognized as a significant health concern due to its widespread presence in the environment and its potential to accumulate in the human body. These tiny particles, ingested primarily through contaminated food and water, can lead to metabolic disturbances and inflammation (1).

A promising approach to mitigating the harmful effects of microplastics is enhancing their excretion through dietary fat modifications. Specifically, increasing fecal fat excretion with non-absorbable dietary fats has been shown to enhance the removal of lipophilic pollutants, including microplastics, by disrupting their enterohepatic circulation (2, 3). This “fat-flush” mechanism facilitates the absorption of microplastics and their subsequent excretion, reducing their retention in the body (4).

Studies have detected microplastics in human stool samples, further highlighting their widespread presence in the food chain and their potential health implications (5). Additionally, research indicates that dietary fat can interact with environmental pollutants, potentially altering lipid metabolism gene expression (6).

Non-absorbable fats and fat absorption inhibitors are emerging as potential dietary interventions to lower the body burden of lipophilic contaminants, including microplastics. These interventions offer a promising, practical strategy to combat environmental pollutant exposure and its associated health risks (7).

Summary

Microplastic contamination poses significant health risks due to its ability to accumulate in the body, leading to metabolic disturbances and inflammation. Recent research suggests that dietary modifications, particularly the use of non-absorbable dietary fats, may enhance the excretion of microplastics and other lipophilic contaminants by disrupting their enterohepatic circulation. This “fat-flush” mechanism offers a potential strategy to mitigate the harmful effects of microplastic exposure. Further research into the role of dietary fat in reducing the body burden of environmental pollutants could pave the way for innovative and effective interventions.

Ref:

1. Okamura T, Hamaguchi M, Hasegawa Y, Hashimoto Y, Majima S, Senmaru T, Ushigome E, Nakanishi N, Asano M, Yamazaki M, Sasano R, Nakanishi Y, Seno H, Takano H, Fukui M. Oral Exposure to Polystyrene Microplastics of Mice on a Normal or High-Fat Diet and Intestinal and Metabolic Outcomes. Environ Health Perspect. 2023 Feb;131(2):27006. doi: 10.1289/EHP11072. Epub 2023 Feb 22. PMID: 36821708; PMCID: PMC9945580.
2. Meijer L, Hafkamp AM, Bosman WE, Havinga R, Bergman A, Sauer PJ, Verkade HJ. Nonabsorbable dietary fat enhances disposal of 2,2′,4,4′-tetrabromodiphenyl ether in rats through interruption of enterohepatic circulation. J Agric Food Chem. 2006 Aug 23;54(17):6440-4. doi: 10.1021/jf0608827. PMID: 16910742.
3. Jandacek RJ, Tso P. Factors affecting the storage and excretion of toxic lipophilic xenobiotics. Lipids. 2001 Dec;36(12):1289-305. doi: 10.1007/s11745-001-0844-z. PMID: 11834080.
4. Schlummer M, Moser GA, McLachlan MS. Digestive tract absorption of PCDD/Fs, PCBs, and HCB in humans: mass balances and mechanistic considerations. Toxicol Appl Pharmacol. 1998 Sep;152(1):128-37. doi: 10.1006/taap.1998.8487. PMID: 9772208.
5. Schwabl P, Köppel S, Königshofer P, Bucsics T, Trauner M, Reiberger T, Liebmann B. Detection of Various Microplastics in Human Stool: A Prospective Case Series. Ann Intern Med. 2019 Oct 1;171(7):453-457. doi: 10.7326/M19-0618. Epub 2019 Sep 3. PMID: 31476765.
6. Arzuaga X, Ren N, Stromberg A, Black EP, Arsenescu V, Cassis LA, Majkova Z, Toborek M, Hennig B. Induction of gene pattern changes associated with dysfunctional lipid metabolism induced by dietary fat and exposure to a persistent organic pollutant. Toxicol Lett. 2009 Sep 10;189(2):96-101. doi: 10.1016/j.toxlet.2009.05.008. Epub 2009 May 23. PMID: 19467301; PMCID: PMC2729430.
7. Jandacek RJ, Genuis SJ. An assessment of the intestinal lumen as a site for intervention in reducing body burdens of organochlorine compounds. ScientificWorldJournal. 2013;2013:205621. doi: 10.1155/2013/205621. Epub 2013 Feb 7. PMID: 23476122; PMCID: PMC3582106.

Disclaimer: The following information is provided for educational and informational purposes only. It is not intended as medical advice, diagnosis, or treatment. Always consult with a qualified and experienced healthcare professional before starting, stopping, or altering any medical regimen or treatment plan. This content should be used under the direct supervision of a licensed healthcare provider to ensure safety and appropriateness for your individual health needs.

The following supplements and practices should be incorporated into your daily routine. Not only can they help prevent viral infections, but if you do contract an infection, this protocol may reduce its severity. Additionally, adhering to this protocol can significantly enhance your overall health and well-being.

1. Vitamin C:
   • Dosage: 3,000 mg – 10,000 mg/day, divided into 2-3 doses.
   • Alternatively, use Liposomal Vitamin C (Liposomal-Vit C): 1-2 grams/day.
2. Vitamin D3:
   • Dosage: 5,000 IU/day.
   • Regularly check blood vitamin D3 levels and adjust your Vit D dosing to maintain blood levels within 50-100 ng/ml.
3. Vitamin E:
   • Dosage: 400-2,000 IU/day.
4. Zinc:
   • Dosage: 15-30 mg/day.
5. Quercetin:
   • Dosage: 500 mg per dose, 3-4 times daily.
6. Melatonin:
   • Dosage: 5-20 mg nightly.
7. Magnesium Ion:
   • Dosage: 500-1,000 mg/day.
8. Hydrogen Peroxide Nebulization Inhalation:
   • Use a 1-3% hydrogen peroxide solution (do not exceed 3%).
   • Inhale for 5-15 minutes after returning from outside or following suspected exposure.
9. Other Recommendations:
   • Maintain healthy lifestyle, including adequate sunlight exposure, regular exercise, and a healthy diet that is low on carb, plenty of healthy fats, low ultra-processed foods, low seed oil.
   • Other vitamins, micronutrients, antioxidants, methylene blue, NIR/PBMT and mitochondrial nutrients all play critical roles in optimizing immunity, maintaining health, and treating diseases—a concept Dr. Cheng refers to as TotoCell Nutrition™.
     

Disclaimer: The following information is provided for educational and informational purposes only. It is not intended as medical advice, diagnosis, or treatment. Always consult with a qualified and experienced healthcare professional before starting, stopping, or altering any medical regimen or treatment plan. This content should be used under the direct supervision of a licensed healthcare provider to ensure safety and appropriateness for your individual health needs.

Acute Infectious Diseases: Recommended Nutritional and Therapeutic Protocols

1. Vitamin C:
   • Begin with a high dose to achieve mild watery diarrhea (dosage varies by individual and disease; generally recommended starting dose: 10,000-20,000 mg/day).
   • After reaching bowel tolerance, take 1,000-3,000 mg per hour during waking hours daily. Adjust dosage to just below the threshold that causes diarrhea.
   • Alternatively, use liposomal vitamin C: 1-3 grams per dose, 1-3 times daily.
2. Vitamin D3:
   • Take 50,000 IU/day for 5-7 days initially.
   • Transition to a maintenance dose of 5,000 IU/day.
   • After 1-2 months, measure blood vitamin D3 levels and maintain them between 50-100 ng/ml.
3. Vitamin E:
   • Dosage: 400-2,000 IU/day.
4. Liposomal Glutathione (Liposomal-GSH):
   • Dosage: 1-2 grams/day.
5. Zinc:
   • Dosage: 50-100 mg/day for 7 days.
6. Melatonin:
   • Dosage: 5-20 mg nightly.
7. Magnesium Ion:
   • Dosage: 500-1,500 mg/day.
8. Quercetin:
   • Dosage: 500 mg per dose, 3-4 times daily.
9. Hydrogen Peroxide Nebulization Inhalation:
   • Use 1-3% hydrogen peroxide solution (do not exceed 3%).
   • Inhale for 5-15 minutes, 3-4 times daily.
10. Methylene Blue:
    • Administered orally or intravenously as per medical guidance.
11. Other Recommendations:
    • Maintain a healthy lifestyle, including adequate sunlight exposure, regular exercise, sufficient hydration and a healthy diet that is low on carb, plenty of healthy fats, low ultra-processed foods, low seed oil.
    • Other vitamins, micronutrients, antioxidants,  methylene blue, NIR/PBMT and mitochondrial nutrients all play critical roles in optimizing immunity, maintaining health, and treating diseases—a concept Dr. Cheng refers to as TotoCell Nutrition™.