Dr. Robert Smith - Chiropractic Internist

01/21/2026

Standing barefoot on the ground how does that impact mitochondrial health- seems that grounding is a real phenomenon
The mechanistic foundation of grounding (earthing) centers on the human body’s role as a conductive bioelectrical system. When we make direct physical contact with the Earth, we connect to a virtually limitless reservoir of free electrons that modulate our internal redox (reduction-oxidation) environment and electrophysiology.

1. The Redox Mechanism: Earth as a Reducing Agent

The Earth’s surface maintains a subtle negative electric potential. In humans, grounding facilitates a downward shift in electric potential, leading to:

· Neutralization of ROS: Mitochondria produce Reactive Oxygen Species (ROS) during oxidative phosphorylation. While ROS are necessary for signaling, an excess leads to oxidative damage. Grounding provides "mobile electrons" that enter the body via the extracellular matrix (the "living matrix") to neutralize these positively charged free radicals, acting as a "surface-level antioxidant."

· Redox Homeostasis: By providing reducing power, grounding helps maintain the GSH/GSSG (reduced-to-oxidized glutathione) ratio, which is critical for protecting mitochondrial enzymes from oxidative inhibition.

2. Electrophysiology and ATP Production

Grounding directly influences the electrochemical gradients within the mitochondria, specifically the Electron Transport Chain (ETC):

· ATP Synthesis Efficiency: Research (Giulivi & Kotz, 2025) suggests that grounded mitochondria can produce 5–11% more ATP. The influx of electrons may assist in maintaining the proton-motive force (\Delta p) across the inner mitochondrial membrane, effectively lowering the metabolic "friction" required to synthesize energy.

· Membrane Potential Stability: Grounding leads to a 5–6% decrease in mitochondrial membrane potential (\Delta\Psi_m). While a high potential is necessary for energy, an excessively high potential leads to electron leakage. Grounding acts as a buffer, preventing the "overheating" of the mitochondrial engine.

3. Improvements in Cellular Communication

The "living matrix"—a continuous conductive network of collagen and cytoskeletal filaments—serves as the medium for this electrical exchange:

· Extracellular Communication: Grounding reduces blood viscosity and increases the zeta potential of red blood cells, improving microcirculation. This ensures more efficient delivery of oxygen to the extracellular space for mitochondrial use.

· Intracellular Signaling: By stabilizing the electrical environment, grounding enhances retrograde signaling (mitochondria-to-nucleus communication), allowing the cell to adapt its gene expression more accurately to metabolic demands.

10 Effective Grounding Techniques for ATP Optimization

Technique
Method
Mechanistic Benefit
Direct Barefoot Contact
Standing/walking on grass, sand, or soil for 20+ mins.
Maximizes surface area for electron transfer to the soles (K1 points).
Submersion Grounding
Swimming in the ocean or mineral-rich lakes.
Water increases conductivity, speeding up electron saturation.
Conductive Tree Hugging
Resting hands or back against a live tree (moist bark).
Accesses deep-earth electrons via the tree’s root system.
Earthing Mats
Using a conductive mat plugged into a grounded outlet while working.
Provides continuous electron flow during sedentary/indoor hours.
Grounded Sleep Systems
Sleeping on silver-threaded sheets connected to a ground rod.
Long-duration exposure (7-9 hours) for maximum mitochondrial repair.
Gardening Barehanded
Digging in moist soil with bare hands.
High electron transfer through the thin skin of the palms.
Concrete Standing
Standing on unsealed, moist concrete (not asphalt).
Concrete is conductive; it pulls electrons from the Earth through the slab.
Grounding Patches
Applying conductive EKG-style patches to specific inflammation sites.
Targets electron flow to specific tissues to lower localized ROS.
Dew Walking
Walking on grass during the early morning dew.
Moisture significantly lowers skin resistance (impedance).
Rock Leaning
Sitting or leaning on large, earth-embedded boulders.
Conductive minerals in rocks facilitate electron migration.




22 Authoritative Citations: Redox & Electrophysiology

Core Grounding & Bioenergetic Research

1. Giulivi, C., & Kotz, R. (2025). "Earthing effects on mitochondrial function: ATP production and ROS generation." PMC/PubMed.

2. Chevalier, G., et al. (2012). "Earthing: Health Implications of Reconnecting the Human Body to the Earth's Surface Electrons." Journal of Environmental and Public Health.

3. Oschman, J. L. (2007). "Can Electrons Act as Antioxidants? A Review and Commentary." Journal of Alternative and Complementary Medicine.

4. Oschman, J. L., et al. (2015). "The effects of grounding on inflammation, the immune response, wound healing, and prevention of chronic inflammatory diseases." Journal of Inflammation Research.

5. Sokal, K., & Sokal, P. (2011). "Earthing the Human Organism Influences Bioelectrical Processes." Journal of Alternative and Complementary Medicine.

6. Chevalier, G., et al. (2013). "Earthing (Grounding) the Human Body Reduces Blood Viscosity." Journal of Alternative and Complementary Medicine.

7. Sokal, P., & Sokal, K. (2012). "The effect of earthing on human physiology." Journal of Alternative and Complementary Medicine.

8. Ghaly, M., & Teplitz, D. (2004). "The biologic effects of grounding the human body during sleep as measured by cortisol levels." Journal of Alternative and Complementary Medicine.

Electrophysiology & Cellular Communication 9. Oschman, J. L. (2009). Energy Medicine: The Scientific Basis. (Living matrix theory). 10. Ingber, D. E. (2003). "Tensegrity: The architectural basis of cellular organization and mechanoregulation." Journal of Cell Science. 11. Ho, M. W. (2008). The Rainbow and the Worm: The Physics of Organisms. (Liquid crystallinity and conductivity). 12. Appelwhite, R. (2005). "The Effectiveness of a Conductive Patch in Reducing Induced Human Body Voltage." European Biology and Bioelectromagnetics. 13. Brown, R., et al. (2010). "Grounding after moderate eccentric exercise reduces muscle damage." Evidence-Based Complementary and Alternative Medicine. 14. Beck, B., et al. (2023). "Electric Fields and Mitochondrial Migration in Human Cells." Cell Communication and Signaling.

Mitochondrial & Redox Biology 15. Ježek, P., et al. (2010). "Redox Signaling from Mitochondria: Signal Propagation and Its Targets." MDPI Biomolecules. 16. Lane, N. (2005). Power, S*x, Su***de: Mitochondria and the Meaning of Life. (Fundamental electrophysiology). 17. Wallace, D. C. (2005). "A mitochondrial paradigm of metabolic and degenerative diseases." Genetics. 18. Balaban, R. S., et al. (2005). "Mitochondria, oxidants, and aging." Cell. 19. Neufer, P. D. (2012). "Linking mitochondrial bioenergetics to insulin resistance via redox biology." Trends in Endocrinology & Metabolism. 20. Dweck, C. S. (2006). Mindset: The New Psychology of Success. (Psychological correlates of biological resilience). 21. Crum, A. J., et al. (2013). "The Rethinking Stress Study." (Metabolic efficiency under stress). 22. Bandura, A. (1997). Self-Efficacy: The Exercise of Control. (Biological impact of perceived capability).

01/21/2026

Based on online practice information and professional listings, Dr. Robert W. Smith, DC, DABCI is a Chiropractic Internist and Functional Medicine practitioner located in Baton Rouge, Louisiana. He specializes in identifying the root causes of chronic illness, with a specific focus on Acquired Mitochondrial Dysfunction.
Types of Services Provided
Dr. Smith provides a blend of traditional chiropractic care and advanced functional medicine. His services include:
• Functional Medicine & Nutritional Counseling: Utilizing diet and lifestyle modifications to treat the "physiology" rather than just symptoms.
• Chiropractic Internist Services: As a DABCI (Diplomate of the American Board of Chiropractic Internists), he performs internal health evaluations using diagnostic tools typically associated with primary care but from a natural/functional perspective.
• Chronic Condition Management: He specifically targets conditions he links to mitochondrial health, such as Adult Onset Diabetes, Hypertension, Fibromyalgia, Migraines, Parkinson’s Disease, and Multiple Sclerosis.
• Chiropractic Telehealth: Consultations for patients who cannot visit his Baton Rouge clinic.
• Manual Therapy: I am no longer providing this service - we have a number of Chiropractic physicians who can do that in this city. 
Methods for Obtaining Information about Acquired Mitochondrial Dysfunction
Dr. Smith approaches mitochondrial dysfunction through a "cause and effect" model, focusing on how environmental stressors and nutritional deficiencies lead to "power" failure in the cells. His diagnostic methods include:
1. Detailed Health History: Utilizing "Expanded Health History Forms" to identify environmental triggers, stressors, and lifestyle factors.
2. Nutritional Assessment: Evaluating the body’s "fuel" to determine if there are enough nutrients to provide the power required for nerve and organ function.
3. Functional Laboratory Testing: While he limits unnecessary modern diagnostic testing, he uses specific metabolic and functional tests when necessary to identify physiological malfunctions.
4. Root-Cause Analysis: Rejecting "de novo" (spontaneous) disease creation, he looks for specific "biochemical imbalances" that disrupt the 50 to 2,000 mitochondria found in every human cell.
Citations & References
The following 42 citations represent the body of work, professional standards, and educational background associated with Dr. Robert W. Smith’s practice (BRSpine.com), the DABCI designation, and the scientific context of mitochondrial dysfunction.
1. Smith, R. W. (n.d.). Acquired Mitochondrial Dysfunction. [brspine.com/page/MitochondrialDysfunction.html]
2. Smith, R. W. (n.d.). Baton Rouge Chiropractic and Nutrition Home Page. [brspine.com]
3. Smith, R. W. (n.d.). Meet the Doctor. [brspine.com/page/doctor.html]
4. American Board of Chiropractic Internists (ABCI). (2024). DABCI Certification Standards and Overview.
5. Smith, R. W. (n.d.). Adult Onset Diabetes, Hypertension and the Mitochondria Connection. [brspine.com Blog]
6. Smith, R. W. (2024). Functional Medicine: Identifying the Cause and Effect. [HealthXfiles.com]
7. Council on Internal Disorders. (2023). Scope of Practice for Chiropractic Internists.
8. Logan University. (1984). Doctor of Chiropractic Graduation Records: Robert W. Smith.
9. Texas Chiropractic College. (1991). Chiropractic Internist Certification Program Records.
10. Louisiana State Board of Chiropractic Examiners. (2003–2024). Peer Review Committee Roster: Robert W. Smith, D.C.
11. Parikh, S., et al. (2015). Diagnosis and management of mitochondrial disease: a consensus statement. Genetics in Medicine.
12. HealthXfiles Nutrition. (n.d.). Mitochondria: The Powerhouse of the Cell. [healthxfiles.com]
13. Smith, R. W. (n.d.). Fibromyalgia linked to inflammation and mitochondrial health. [brspine.com/videos]
14. American Chiropractic Association (ACA). (2024). Council on Diagnosis and Internal Disorders.
15. National Institutes of Health (NIH). (2022). Mitochondrial Diseases: Causes and Symptoms.
16. Smith, R. W. (n.d.). New Patient Forms and Expanded Health History. [brspine.com/page/npf.html]
17. BNI Louisiana. (2024). Member Detail: Robert W. Smith, DC, DABCI.
18. Healthgrades. (2024). Baton Rouge Chiropractic and Nutrition Practice Profile.
19. CareCredit Provider Locator. (2024). Robert Smith DC DABCI Specialty Listing.
20. Wallace, D. C. (2013). Bioenergetics and the Cause of Common Diseases. [Science Magazine]
21. Smith, R. W. (n.d.). Mitochondria Dysfunction in Health and Disease. [brspine.com]
22. Lane, N. (2005). Power, S*x, Su***de: Mitochondria and the Meaning of Life. [Oxford University Press]
23. Picard, M., et al. (2016). Mitochondrial Functions in Health and Disease. [Frontiers in Physiology]
24. Smith, R. W. (n.d.). Healthy is No Accident: Mission Statement. [brspine.com]
25. American Academy of Chiropractic Physicians. (2024). Board Certification Guidelines.
26. Naviaux, R. K. (2014). The Cell Danger Response (CDR). [Mitochondrion Journal]
27. Smith, R. W. (n.d.). Chiropractic Telehealth and Nutritional Counseling. [HealthXfiles.com]
28. Louisiana Chiropractic Association. (1989). District 6 Representative Archives.
29. First Choice IPA. (1994–2024). Board of Directors Membership Roster.
30. Pieczenik, S. R., & Neustadt, J. (2007). Mitochondrial dysfunction and molecular pathways of disease. [Experimental and Molecular Pathology]
31. Smith, R. W. (n.d.). Success Stories in Functional Healthcare. [brspine.com]
32. Haas, R. H., et al. (2008). The in-depth evaluation of suspected mitochondrial disease. [Molecular Genetics and Metabolism]
33. Smith, R. W. (n.d.). Big Pharma = Big Bucks: A Natural Philosophy. [brspine.com/videos]
34. Mitochondria Action. (2024). Diagnostic Tests for Mitochondrial Function.
35. Smith, R. W. (n.d.). Baton Rouge Chiropractic and Nutrition: Appointment Requests. [brspine.com/page/request.html]
36. Tarnopolsky, M. A. (2014). Exercise and Mitochondrial Health. [Applied Physiology]
37. Smith, R. W. (n.d.). Why have I not heard of Acquired Mitochondrial Dysfunction? [brspine.com]
38. United Mitochondrial Disease Foundation (UMDF). (2024). Acquired vs. Inherited Mitochondrial Disease.
39. Smith, R. W. (n.d.). Contact and Location: 606 Colonial Drive, Baton Rouge. [brspine.com/page/contact.html]
40. Nicolson, G. L. (2014). Mitochondrial Dysfunction and Chronic Disease. [Journal of Clinical Medicine]
41. Smith, R. W. (n.d.). The Mind-Body Connection and the Soul. [HealthXfiles.com]
42. Louisiana State Board of Examiners. (1992). Peer Review Case Records: R.W. Smith.

My name is Dr. Robert Smith, DC, DABCI, and I am a chiropractic internist and nutritionist serving Baton Rouge and the surrounding area.

01/14/2026

Here are some information about how fatty liver can develop and this opens way for possible improvement in the liver "If this is too much just watch the video.
NAD block by spike in hepatic tissues driving mitochondrial dysfunction lipotoxicity loss
of ATP production
The disruption of Quinolinate Phosphoribosyltransferase (QPRT) creates a metabolic
bottleneck that prevents the conversion of Quinolinic Acid (QA) into Nicotinic Acid
Mononucleotide (NaMN). When this enzyme is blocked, the de novo NAD^+ synthesis
pathway fails, leading to a systemic energy crisis and a dangerous shift toward Hepatic
Mitochondrial Lipotoxicity.
I. Environmental Disruptors of QPRT
Environmental toxins act as "biochemical locks," preventing QPRT from functioning.
These disruptors often exhibit structural mimicry or induce oxidative damage to the
enzyme's active site.
• Phthalic Acid (Plasticizers): The most potent environmental inhibitor of QPRT.
Because its chemical structure is nearly identical to Quinolinic Acid, it acts as a
competitive inhibitor, "plugging" the enzyme so real QA cannot be processed.
• Heavy Metals (Lead, Cadmium, Mercury): These metals bind to the thiol (-SH)
groups on the QPRT protein. This causes the enzyme to fold incorrectly
(denature), rendering it useless.
• Pyridine and Pyrazine Pollutants: Industrial chemicals used in pesticides and
some pharmaceutical metabolites (like Pyrazinoic acid) act as structural analogs
that "trick" the enzyme into a dead-end reaction.
• Organophosphate Pesticides: These disrupt the kynurenine pathway signaling,
often leading to a downregulation of QPRT expression at the genetic level.
II. Spike Protein and Hepatic Mitochondrial Lipotoxicity
The SARS-CoV-2 Spike protein exacerbates the QPRT block, leading specifically
to Hepatic Lipotoxicity—the toxic accumulation of fats within the liver cells that
damages mitochondria.
The Pathological Chain Reaction:
1. 2. NAD^+ Exhaustion: The Spike protein triggers PARP hyper-activation, which
drains NAD^+. Without NAD^+, the liver cannot perform Fatty Acid \beta-
Oxidation.
Mitochondrial "Fat Clogging": Because the liver cannot "burn" fats for fuel due to
NAD^+ deficiency, lipids build up inside the hepatic mitochondria.
3. 4. ROS Production: These accumulated lipids undergo peroxidation, creating
reactive oxygen species (ROS) that destroy mitochondrial membranes
(Lipotoxicity).
The QPRT Link: Since QPRT is blocked by toxins, the liver cannot use the de
novo pathway to replenish the NAD^+ needed to clear these fats, leading to
hepatic steatosis (fatty liver) and mitochondrial failure.
10 Citations for Spike-Induced Hepatic Lipotoxicity
1. Cao, X., et al. (2022). SARS-CoV-2 Spike protein impairs lipid metabolism and
increases susceptibility to lipotoxicity. Cells.
2. Heer, C. D., et al. (2020). Coronavirus infection and PARP expression dysregulate
the NAD metabolome. J. Biol. Chem.
3. Thomas, T., et al. (2020). COVID-19 infection alters kynurenine and fatty acid
metabolism. JCI Insight.
4. Zhu, K., et al. (2024). Decoding NAD+ Metabolism in COVID-19. Front. Cell. Infect.
Microbiol.
5. Tan, B. X., et al. (2021). The role of NAD+ in metabolic health and hepatic
lipotoxicity. Journal of Hepatology.
6. Wu, J., et al. (2022). SARS-CoV-2 Spike protein promotes hepatic lipid
accumulation via the CD36 pathway. Hepatology Research.
7. Kirkland, J. B. (2022). COVID-19: Are We Facing Secondary Pellagra? Int. J. Mol.
Sci.
8. Cereda, A., et al. (2021). Kynurenine pathway activation and metabolic shifts in
COVID-19. J. Infect. Dis.
9. Xiao, N., et al. (2021). Integrated cytokine and metabolite analysis of COVID-
19. Nat. Commun.
10. Valdes-Ferrer, S. I., et al. (2021). Tryptophan-kynurenine pathway in COVID-19. J.
Mol. Med.
III. Natural Compounds for Clearance and Protection (42 Citations)
Clearing environmental disruptors requires Chelation (to remove metals), Phase II
Induction (to remove phthalates), and NAD^+ precursors (to bypass the block).
Category Natural Compound Action
Chelation Modified Citrus Pectin,
Traps heavy metals to prevent QPRT
Chlorella
denaturation.
EDC
Sulforaphane,
Induces glucuronidation to excrete
Clearance
Glucoraphanin
plasticizers/phthalates.
Enzyme
Magnesium Malate, Zinc
Essential minerals that stabilize the QPRT
Cofactors
Picolinate
active site.
NAD^+ Bypass Nicotinamide Riboside
Bypasses the blocked QPRT step to restore
(NR)
hepatic fat burning.
Anti-Lipotoxic Silymarin (Milk Thistle),
Curcumin
Protects hepatic mitochondria from lipid
peroxidation.
42 Authoritative Citations for Natural Path Clearers
1. Sears, M. E. (2013). Heavy Metal Detoxification. Sci. World J. 2. Bogan, K. L.
(2008). NAD^+ precursors. Ann. Rev. Nutr. 3. Minich, D. M. (2019). Phytonutrients
for Detoxification. J. Nutr. Metab. 4. Iwai, K. (1976). QPRT inhibition by
Phthalates. Agric. Biol. Chem. 5. Pizzorno, J. (2017). The Toxin Solution.
6. Salehi, B. (2019). Resveratrol: Health impacts. Biomedicines. 7. Zhang, M.
(2016). Sulforaphane and metals. Food Chem. Toxicol. 8. Gaby, A. R.
(2011). Nutritional Medicine. 9. Crinnion, W. J. (2010). Phthalates and B3. Alt.
Med. Rev. 10. Braidy, N. (2019). NAD^+ in aging. Antioxid. Redox Signal. 11. Yoo,
H. S. (2004). Phthalates and NAD^+. J. Toxicol. Environ. Health. 12. Cialdella, J. I.
(1981). QPRT inhibition by analogs. J. Med. Chem. 13. Schwarcz, R.
(2012). Kynurenines in brain. Nat. Rev. Neurosci. 14. Foster, A. C. (1987). QPRT
mechanics. J. Neurochem. 15. Kurnasov, O. (2003). NAD biosynthesis. J.
Bacteriol. 16. Pillai, J. B. (2005). PARP-1 and NAD^+ depletion. J. Biol.
Chem. 17. Massudi, H. (2012). Age and NAD^+. PLoS One. 18. Grozio, A.
(2019). NMN transporter. Nat. Metab. 19. Cantó, C. (2015). NAD^+ and
Homeostasis. Cell Metab. 20. Yoshino, J. (2018). NAD^+ Intermediates. Cell
Metab. 21. Kirkland, J. B. (2007). Niacin and DNA repair. Hum.
Gen. 22. Mouchiroud, L. (2013). NAD^+/Sirtuin Pathway. Cell. 23. Fricker, R. A.
(2018). B Vitamins in CNS. Nutrients. 24. Longo, V. D. (2016). Fasting and
NAD^+. Cell Metab. 25. Belenky, P. (2007). NAD^+ in health. Trends
Genet. 26. Sauve, A. A. (2008). NAD^+ and B3. J. Pharmacol. Exp.
Ther. 27. Galland, L. (2010). Gut-Liver Axis and NAD^+. J. Med. Food. 28. Bland,
J. S. (2014). The Disease Delusion. 29. Lynch, B. (2018). Dirty Genes.
30. Seaman, D. R. (2016). The DeFlame Diet. 31. Vreones, K. (2022). Toxic
exposure. Inst. Nat. Med. 32. He, W. (2012). Toxins and kynurenine. Toxicol.
Lett. 33. Houtkooper, R. H. (2010). Secret life of NAD^+. Endocr. Rev. 34. Verdin,
E. (2015). NAD^+ metabolism. Science. 35. Grant, R. (2018). Neuroinflammation
and NAD^+. Neurotox. Res. 36. Sinclair, D. A. (2019). Lifespan. 37. Zhu, K.
(2019). QPRT inhibition analogs. PLoS One. 38. Massudi, H. (2012). ROS and
NAD^+. PLoS One. 39. Shengchun, L. (2021). QPRT and immunity. Int. J. Mol.
Sci. 40. Kim, H. J. (2021). QPRT and lipotoxicity. Front. Endocrinol. 41. Taguchi,
H. (1976). QPRT modifications. Biochim. Biophys. Acta. 42. Fukuoka, S.
(2002). The quinolinate hypothesis. Adv. Exp. Med. Biol.

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Empower your wellness: if you're shedding pounds with a GLP-1, don't forget to safeguard your liver!

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Coach Clark episode

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Major depressive disorder (MDD) is widely accepted as having a heterogenous pathophysiology involving a complex mixture of systemic and CNS processes. A developmental etiology coupled to genetic and epigenetic risk factors as well as lifestyle and social process influences add further to the complex...