Baton Rouge Chiropractic and Nutrition

07/07/2026

Here is news on food that is good.

07/05/2026

This is why sick mitochondria matter-

Your kid is the first generation to go backwards. It happened in school. In your office. Now AI. Dr Jared Horvath studied this across 80 countries. Every country that adopted screens saw scores drop. The system chose the tool. Never asked what it cost. It called that progress. Horvath called it surr...

07/04/2026

Hereis a new post from HHS Sec. Kennedy

07/04/2026

This is the original idea for the class of drugs working on hunger the GLP-1s

A lizard that eats a handful of times a year runs on chemistry so precise it barely wastes a single calorie. The protein hiding in Gila monster venom does not just mimic the signal that tells a body it is full — it holds that signal open for hours. In people, the natural version of that signal collapses in minutes, constantly needing to be rebuilt. The Gila monster's version, called exendin-4, stays active long enough to stretch one meal across weeks of desert survival. Scientists spent years studying how that molecule kept blood sugar steady across such impossible stretches of time. What they reverse-engineered from it became the foundation for a new class of drugs now used by millions. The lizard did not change to help anyone. It just solved its own problem, quietly, over a very long time, in the dirt and heat of the Sonoran desert. The best medicine was not invented in a lab. It was found in a slow animal nobody was watching. [1NDF5]

07/02/2026

The anti aging factor that is hurt by high blood sugar at the kidneys While the ancient Greeks envisioned Klotho as a goddess holding a spindle of wool, modern biophysics views her as a circulating glycoprotein safeguarding genomic and mitochondrial integrity. In both cases, if her thread unravels, life draws rapidly to its close.
The name Klotho (or Clotho) represents a beautiful intersection where ancient mythology perfectly predicts modern biochemistry. In both realms, Klotho is the ultimate arbiter of lifespan, biological timing, and the thread of existence.
1. The Mythological Goddess: The Spinner of Life
In Greek mythology, Klotho (Greek: Κλωθώ, meaning "The Spinner") is one of the Moirai, or the Three Fates. Alongside her sisters Lachesis and Atropos, she controls the destiny of every mortal and god alike.
The Role: Klotho is the youngest sister and the Spinner of the Thread of Life. Using her spindle, she creates the biological and circumstantial thread of a person's existence from the moment of conception and birth.
The Sisters:
Klotho: Spins the thread (initiates life).
Lachesis: Measures the thread (allocates destiny and determines its length).
Atropos: Cuts the thread with her "abhorred shears" (chooses the mechanism and exact moment of death).
The Power: Even Zeus and the other Olympian gods are bound by the threads spun by Klotho. Her actions represent the unyielding, deterministic laws of nature.
2. The Klotho Protein: The Molecular Arbiter of Longevity
In 1997, Japanese researchers Makoto Kuro-o and his team discovered a gene in mice that profoundly regulated aging. When mutated, the mice aged rapidly and died prematurely. When overexpressed, the mice lived up to 30% longer than average.
Recognizing the undeniable parallel to the Greek Fate who spins the thread of life, they named the gene and its resulting protein Klotho.

Scientific History & Discovery
1997 (The Discovery): Published in Nature, Kuro-o's team identified that disrupting the Klotho gene led to a syndrome closely resembling human aging: arteriosclerosis, osteoporosis, skin atrophy, and cognitive decline.
Early 2000s (The Mechanism): Scientists discovered that Klotho functions primarily as an anti-aging hormone. It exists in two main forms: a membrane-bound form and a secreted (soluble) form that circulates in the blood and cerebrospinal fluid.
3. How the Protein Replicates the Myth
The biological functions of the Klotho protein mirror the mythological goddess's control over life, vitality, and degeneration through specific physiological mechanisms:
Ion Transport & Mineral Homeostasis
Membrane Klotho acts as an essential co-receptor for Fibroblast Growth Factor 23 (FGF23). Together, they regulate phosphate and Vitamin D metabolism in the kidneys. When Klotho is deficient, hyperphosphatemia (excess blood phosphate) occurs, accelerating tissue calcification and systemic "aging" — essentially causing the thread of life to degrade prematurely.
Mitochondrial & Oxidative Stress Protection
Soluble Klotho acts as a circulating hormone that suppresses the Insulin/IGF-1 signaling pathway, a known evolutionary regulator of lifespan across species. This suppression stimulates superoxide dismutase (SOD), an endogenous antioxidant enzyme. By scavenging reactive oxygen species (ROS), Klotho shields cellular structures, particularly mitochondria, from oxidative decay and energetic collapse.
Cognitive Preservation
In neurobiology, high levels of circulating Klotho are strongly correlated with enhanced synaptic plasticity and cognitive resilience. It upregulates the GluN2B subunit of NMDA receptors in the brain, improving learning, memory, and defending against neurodegenerative pathways like Alzheimer's disease.

07/02/2026

A groundbreaking discovery has shed new light on the root cause of Alzheimer's, pinpointing high blood sugar as a key contributor, rather than glucosamine. A recent June 2026 study published in Nature Metabolism, led by researchers at the University of Florida, has revolutionized our understanding of how sugars impact the brain. The study reveals that both hyperglycemia and glucosamine feed into the same metabolic pathway, creating destructive sugar tags that lead to hyperglycosylation, a process where proteins become overloaded with complex sugar chains, misfold, and malfunction.

06/18/2026

When should I take vitamin D and why?

From a chronobiology and biophysical perspective, the optimal time to take a vitamin D supplement is in the morning or early afternoon, ideally with your first fat-containing meal.
To understand why, we have to look at how oral cholecalciferol (vitamin D3) interacts with our central master clock—the suprachiasmatic nucleus (SCN)—and core peripheral clock genes.
1. The Inverse Relationship with Melatonin
In nature, vitamin D synthesis is a pure biophysical marker of midday solar radiation (specifically UVB light). Because our biochemistry evolved under these solar cues, vitamin D and melatonin share a deeply coordinated, inverse relationship:
Daytime (High Vitamin D, Low Melatonin): High sun exposure drives cutaneous vitamin D production while simultaneously suppressing melatonin release through retinal light pathways.
Nighttime (Low Vitamin D, High Melatonin): As darkness falls, the pineal gland ramps up melatonin synthesis to initiate sleep and cellular repair.
Introducing a significant dose of oral vitamin D late in the evening can send a conflicting biochemical signal to the brain, mimicking "midday" biochemistry. Emerging chronobiological research indicates that vitamin D receptors (VDR) are highly expressed in the brain regions responsible for sleep regulation. Flooding these receptors at night can modulate transcriptional regulators (like REV-ERBs and RORs) and potentially disrupt or suppress the natural nocturnal rise in melatonin, leading to sleep fragmentation or delayed sleep onset.
2. Synchronization of Peripheral Clock Genes
Mitochondria and peripheral tissues run on autonomous 24-hour cellular rhythms governed by clock genes like CLOCK and BMAL1. Vitamin D functions less like a standard nutrient and more like a secular secosteroid hormone. When taken in the morning, it acts as a chemical "zeitgeber" (time-giver), helping to entrain and synchronize these peripheral tissue clocks with the central master clock in the SCN. This promotes daytime metabolic alertness and supports the natural nocturnal drop in core body temperature later on.
3. The Bioavailability Constraint
Beyond the circadian rhythm, vitamin D is strictly fat-soluble. Taking it on an empty stomach drastically blunts its absorption. Therefore, tying it to a morning or early afternoon meal that contains healthy lipids (such as eggs, avocado, or yogurt) maximizes its transport via chylomicrons into the lymphatic system and bloodstream.
Summary Checklist for Timing

This is a short recap of how vitamin D helps so many areas of our o...

06/10/2026

Look at the answer to this question!
What part of the Pfizer Covid vaccine?

The unexpected molecular mimicry associated with the vaccine-expressed SARS-CoV-2 spike protein affects several major organ systems. While the primary identified mechanisms of mimicry involve surface receptor interference or autoantibodies attacking structural and signaling proteins, mitochondrial dysfunction can occur as a secondary downstream consequence of these primary insults.
Heart (Cardiovascular System)
Primary Mechanism: Autoantibody Attack (Structural Mimicry).
How it is affected: The immune system generates antibodies targeting the ⁠ELDKY⁠ sequence on the spike protein, which cross-reacts with alpha-tropomyosin, a structural protein highly concentrated in cardiac muscle. This can cause localized inflammation of the heart muscle or surrounding sac.
Mitochondrial Involvement: Secondary. The primary driver is autoimmune-mediated tissue inflammation (myocarditis/pericarditis). However, because cardiac myocytes depend heavily on mitochondria for energy, the resulting local inflammatory stress and altered calcium handling can subsequently induce secondary mitochondrial stress and energetic "brownouts."
Brain (Central Nervous System)
Primary Mechanism: Ion Channel Dysregulation (Signaling Mimicry).
How it is affected: Anti-spike antibodies can cross-react with the ⁠EPLDVL⁠ motif on the human UNC-80 protein, a core component of the NALCN leak sodium channel complex. This channel controls baseline electrical excitability in neurons, and its disruption can alter neurological signaling.
Mitochondrial Involvement: Indirect/Secondary. The primary mechanism disrupts the electrical firing thresholds of neurons. If severe enough, chronic neurological cellular stress or altered calcium influx through dysfunctional channels can overburden the neuron’s mitochondria, leading to localized metabolic strain.
Kidneys and Vascular System
Primary Mechanism: Receptor Blockade & Idiotypic Networks (Conformational Mimicry).
How it is affected: Anti-idiotypic antibodies (antibodies formed against the anti-spike antibodies) can mirror the shape of the spike protein itself, binding to and dysregulating ACE2 receptors. ACE2 is highly expressed on the vascular endothelium (blood vessel linings) and the tubular epithelial cells of the kidneys. Blocking or downregulating ACE2 disrupts the renin-angiotensin-aldosterone system (RAAS), promoting local vasoconstriction, fluid retention, and microvascular inflammation.
Mitochondrial Involvement: Indirect. The primary breakdown happens at the cell surface receptor level. However, the kidneys are among the most mitochondria-dense organs in the body; when ACE2 dysregulation triggers localized vascular hypoxia (low oxygen) and inflammatory cytokine cascades, the renal tubule mitochondria suffer downstream oxidative damage, impairing cellular bioenergetics.
Blood (HematOLOGIC System)
Primary Mechanism: Autoantibody Destruction (Hormonal Mimicry).
How it is affected: The ⁠TQLPP⁠ motif mimics human thrombopoietin (TPO), the primary hormone driving platelet production. Cross-reactive antibodies can bind native TPO or its signaling pathways, occasionally resulting in temporary platelet drops (thrombocytopenia).
Mitochondrial Involvement: Little to none. This is an extracellular, antibody-mediated clearance or inhibition mechanism that bypasses cellular metabolic machinery.

In mRNA vaccines like the Pfizer-BioNTech (BNT162b2) vaccine, the specific component identified as the source of unexpected molecular mimicry is the SARS-CoV-2 Spike (S) Glycoprotein (Arévalo-Cortés et al., 2024; Kanduc & Shoenfeld, 2020).
Because the vaccine works by introducing mRNA that instructs host cells to express the full-length spike protein to trigger a protective immune response, any structural or sequential overlapping between the spike and native human proteins can inadvertently cause the immune system to create cross-reactive autoantibodies (Mizuno et al., 2024; Safary et al., 2023).
Immunoinformatic and biochemical screens have mapped unexpected peptide commonalities (such as 5-mer to 7-mer amino acid sequences) shared between the viral spike protein and critical human tissues (Kanduc & Shoenfeld, 2020; Mizuno et al., 2024; Nunez-Castilla et al., 2021). When the immune system creates antibodies against these specific spike motifs, those antibodies can misidentify and target human structures, potentially triggering transient autoimmune responses (Arévalo-Cortés et al., 2024; Nunez-Castilla et al., 2021).
Observed Cross-Reactive Connections
The following diagrammatic list maps the specific regions (motifs) within the vaccine-expressed Spike protein to the human target structures, using both their common names and specific scientific names.
Affected Structures and Clinical Implications
1. Thrombopoietin
Peptide Motif: ⁠TQLPP⁠ (Nunez-Castilla et al., 2021).
Common Name: Thrombopoietin (TPO).
Specific Structural Name: Human Thrombopoietin Glycoprotein.
Mechanism: The ⁠TQLPP⁠ motif in the spike protein shares highly similar antibody-binding properties with human TPO (Nunez-Castilla et al., 2021). Cross-reactive antibodies generated by the vaccine may target native TPO, which is the primary hormone regulating platelet production in bone marrow, potentially contributing to rare cases of thrombocytopenia (low platelet counts) (Nunez-Castilla et al., 2021).
2. Protein Kinase G 1
Peptide Motif: ⁠ELDKY⁠ (Nunez-Castilla et al., 2021).
Common Name: PRKG1.
Specific Structural Name: cGMP-dependent protein kinase 1.
Mechanism: The ⁠ELDKY⁠ motif is embedded in both the viral spike and several human regulatory proteins (Nunez-Castilla et al., 2021). PRKG1 is essential for smooth muscle relaxation, calcium regulation, and platelet activation inhibition. Autoantibody cross-reactivity here is studied in connection with rare blood-clotting or vascular tone anomalies (Nunez-Castilla et al., 2021).
3. Tropomyosin
Peptide Motif: ⁠ELDKY⁠ (Nunez-Castilla et al., 2021).
Common Name: Tropomyosin.
Specific Structural Name: Striated Muscle Alpha-Tropomyosin Chain.
Mechanism: This structural protein is highly concentrated in cardiac and skeletal muscle tissue. Molecular mimicry between the spike protein and tropomyosin is one of several hypothesized pathways being investigated regarding rare post-vaccine cardiovascular events like myocarditis or pericarditis in susceptible individuals (Bozkurt et al., 2021; Fanti, 2026; Nunez-Castilla et al., 2021).
4. UNC-80 Homolog
Peptide Motif: ⁠EPLDVL⁠ (Mizuno et al., 2024).
Common Name: UNC-80 Protein.
Specific Structural Name: Unc-80 Homolog (NALCN Channel Complex Subunit).
Mechanism: In vitro testing has shown that antibodies raised against specific constituent sequences of the spike protein possess high cross-reactive affinity to the ⁠EPLDVL⁠ peptide sequence inside the human UNC-80 protein (Mizuno et al., 2024). UNC-80 acts as a core component of the leak sodium channel complex, which controls baseline electrical excitability in the central nervous system.
5. Angiotensin-Converting Enzyme 2
Peptide Motif: Structural/Conformational Binding Region.
Common Name: ACE2 Receptor.
Specific Structural Name: Angiotensin-Converting Enzyme 2 (Cell Surface Receptor).
Mechanism: Beyond short linear sequences, the overall shape of the spike protein interacts intimately with the ACE2 receptor to facilitate cellular instruction (Devaux & Camoin-Jau, 2023; Mizuno et al., 2024). The presentation of this massive structural block can cause anti-idiotypic networks (antibodies created against the primary antibodies) to mimic the shape of the spike itself, leading to a transient block or dysregulation of native ACE2 pathways and altering local vascular balance (Devaux & Camoin-Jau, 2023; Guo et al., 2023).
References
Arévalo-Cortés, A., Rodriguez-Pinto, D., & Aguilar-Ayala, L. (2024). Evidence for molecular mimicry between SARS-CoV-2 and human antigens: Implications for autoimmunity in COVID-19. Autoimmune Diseases, 2024, Article 8359683. https://doi.org/10.1155/2024/8359683
Cited by: 28
Balbona, E. J., Neuenschwander, J., Margulis, J., & Seneff, S. (2024). Potential association of Covid-19 mRNA vaccination and infections with the antiphospholipid antibody syndrome. Medical Research Archives, 12(11). https://doi.org/10.18103/mra.v12i11.6049
Cited by: 0
Bozkurt, B., Kamat, I., & Hotez, P. J. (2021). Myocarditis with COVID-19 mRNA vaccines. Circulation, 144(6), 471-484. https://doi.org/10.1161/circulationaha.121.056135
Cited by: 1054
Devaux, C. A., & Camoin-Jau, L. (2023). Molecular mimicry of the viral spike in the SARS-CoV-2 vaccine possibly triggers transient dysregulation of ACE2, leading to vascular and coagulation dysfunction similar to SARS-CoV-2 infection. Viruses, 15(5), 1045. https://doi.org/10.3390/v15051045
Cited by: 39
Fanti, S. (2026). Combined adaptive immune mechanisms mediate cardiac injury after COVID-19 vaccination. Circulation. https://doi.org/10.1161/CIRCULATIONAHA.125.074644
Cited by: 7
Guo, M., Liu, X., & Chen, X. (2023). Insights into new-onset autoimmune diseases after COVID-19 vaccination. Autoimmunity Reviews, 22(7), 103340. https://doi.org/10.1016/j.autrev.2023.103340
Cited by: 127
Kanduc, D., & Shoenfeld, Y. (2020). Molecular mimicry between SARS-CoV-2 spike glycoprotein and mammalian proteomes: Implications for the vaccine. Immunologic Research, 68(5), 310-313. https://doi.org/10.1007/s12026-020-09152-6
Cited by: 339
Karami Fath, M., Jahangiri, A., Ganji, M., Sefid, F., Payandeh, Z., Hashemi, Z. S., Pourzardosht, N., Hessami, A., Mard-Soltani, M., Zakeri, A., Rahbar, M. R., & Khalili, S. (2021). SARS-CoV-2 proteome harbors peptides which are able to trigger autoimmunity responses: Implications for infection, vaccination, and population coverage. Frontiers in Immunology, 12, Article 705772. https://doi.org/10.3389/fimmu.2021.705772
Cited by: 44
Mizuno, Y., Nakasone, W., Nakamura, M., & Otaki, J. M. (2024). In silico and in vitro evaluation of the molecular mimicry of the SARS-CoV-2 spike protein by common short constituent sequences (cSCSs) in the human proteome: Toward safer epitope design for vaccine development. Vaccines, 12(5), 539. https://doi.org/10.3390/vaccines12050539
Cited by: 9
Nunez-Castilla, J., Stebliankin, V., Baral, P., Balbin, C. A., Sobhan, M., Cickovski, T., Mondal, A. M., Narasimhan, G., Chapagain, P., Mathee, K., & Siltberg-Liberles, J. (2021). Potential autoimmunity resulting from molecular mimicry between SARS-CoV-2 Spike and human proteins. bioRxiv. https://doi.org/10.1101/2021.08.10.455737
Cited by: 115
Safary, A., Akbarzadeh-Khiavi, M., Barar, J., & Omidi, Y. (2023). SARS-CoV-2 vaccine-triggered autoimmunity: Molecular mimicry and/or bystander activation of the immune system. BioImpacts, 13(4), 269-273. https://doi.org/10.34172/bi.2023.27494
Cited by: 16

06/10/2026

This is Big -NOW half of the population now in Martha's Vineyard have Alpha gel
Remember Alpha gel is the Lonestar tick Borne illness that makes you not be able to eating beef or any other meat with that type of protein in it?
 that's disturbing 

“It is really a devastating disease.”“You can’t eat red meat for ...

06/08/2026

More information about receptor Fields, and how they reset the system
Think about what spinal adjustment is doing to the articular receptors located the joint capsule of the 48 joints of your back

Your body has a built-in reset switch for stress — and you've been ...