Head Injury

[Peatness]

I’m really sorry this happened to you @Meecho . It must have been terrifying. Mine was just a simple falling and hitting the back of the head on a concrete floor – multiple times. Passing out each time. Not fun. Luckily I had access to the information on the forum and hit the b vitamins/pregnonolone/progesterone within the first few weeks of injury. Everything was healing nicely – then a year later I started to noticed a lot of problems with scar tissue. My spine was twisted and I got plenty of shedding from vaccinated physical therapists and the rest is history. Since then my healing seems to be going in reverse. I believe a combination of shedding and the MRI scan have negatively contributed to my lack of progress. My health was already compromised by a tetanus vaccine I got the year before. Personally, I am staying away from all imaging. Becasue of 5g I don’t know how safe it is – I don’t have evidence that there is danger, just a suspicion. I’m supper sensitive to radiation now that parts of my body are magnetic.

Thiamine is very important for head injuries –see the studies posted in this thread. High doses are needed. In the early days of my injury I was using high doses up to 300mg a day. I’ve also tried other forms of thiamine besides thiamine hcl. Niacinamide has been extremely helpful – in fact when I stopped taking it recently I noticed an increase in hypoxic symptoms. Have a look at this website, there's alot about thiamine.

You searched for thiamine concussion - Hormones Matter

www.hormonesmatter.com

Severe lactic acidosis reversed by thiamine within 24 hours

www.ncbi.nlm.nih.gov

Your Co2 bag/head cap is a great idea. I wonder if you optimize your thiamine levels if you will still need it?

 

[Meecho]

I'm taking B-complex (Energin), but I don’t optimize my thiamine levels, unfortunately. I’ll do that next. What brand do you use?

Lately, I was setting up strong incandescent lights in my place.

 

[Peatness]

I'm taking B-complex (Energin), but I don’t optimize my thiamine levels, unfortunately. I’ll do that next. What brand do you use?

Lately, I was setting up strong incandescent lights in my place.

I do have energin but for thiamine alone these are the brands I have tried. If you search the forum each one has been discussed.

https://www.objectivenutrients.com/products/thiamax-uk/

Vitamin B1 (Thiamine Pyrophosphate)

<p>Vitamin B1 is also known as Thiamine and is one of the 8 B vitamins.</p>

www.metabolics.com

Vitamin B1 Powder Thiamine HCl USP Grade

<ul> <li><span style="font-size: 18px;">Supports Energy Production</span></li> <li><span style="font-size: 18px;">Shown To Protect Nerves</span></li> <li><span style="font-size: 18px;">Anti-Aging</span></li> <li><span style="font-size: 18px;">Supports Digestion</span></li> <li><span...

lifegivingstore.com

The light is a good idea. Lately I've been day dreaming of being on a beach in strong sunlight. It's a beautiful day here in the UK but the sun is not that powerful. I do use red light - not often enough.

 

[Meecho]

Thanks for the info.

I wrote the CO2 hat story to Ray Peat, and here’s his response:
“Vitamin D and vitamin K are other things that help repair.”

As far as I know, for fixing radiation issues, strong light is the best. Also, If I remember correctly, Peat once told a story about one man who applied strong light on his spine, for months, and cured his severe neurological illness.

 

[BRMarshall]

The Androsterone threads speak of myelin sheath repair...to which DHT and Testosterone are important...

Years ago I had a head injury from a fall skiing and I ended up working with the LENS neurofeedback system, which in one session had incredible results. What is interesting about the LENS is that it is homeopathic in its approach, where less is more. Where concussions are caused by a blow, the Lens speaks to the brain through a very discreet signal, that works along lines of the so called "butterfly effect" in chaos theories...Part of the idea is that the brain works in a homeostasis which is actually very stable and steady and takes a wack on the head, to discombobulate things, where the discombobulation becomes a new steady state....The idea, discovered by experiment, is that the brain can be tricked into seeking a new steady state through new information, but the way that can happen is by what is a very subtle signal, so tiny that it gets past the brains sensors, to thus create, as can be detected by the biofeedback instrument, changes in brainwave activity, that then can provide both an awakening and a calming at the same time... it was like I got my brain back and more with the initial treatment providing very dramatic response.

Unfortunately the practitioner is no longer around....

I have unfortunately gone to the use of marijuana when I bang my head, as it seems to be the only thing for immediate relief sometimes, and rather a bad excuse to get stoned, but there are some neuroprotective aspects and other disadvantages, which is why I am interested in this thread, as sometimes it does not take much to disturb my brain...

i do take progesterone, androsterone, asprin, vitamins, etc...

 

[Peatness]

@Meecho I've found D and K very helpful. Is your light set up red light?

@BRMarshall someone else on the forum wrote about using androsterone for spinal issues. I did order some but have been a bit cautious about using it. I've tried one or two drops at night. I don't have the same neurological changes as you guys (at least I am not aware of it) but I worry for the future. Scar tissue is the biggest problem for me, progesterone and vitamin e have been most helpful for this.

 

[Peatness]

I used to use glutamine but once I came to Peat's work I switched to gelatine. Recently I've been thinking about glutamine again and wondering if it has a role in traumatic head/brains injuries. I found this clinical trial that is ongoing. It ends in Dec 2023

Glutamine and Traumatic Brain Injury - Full Text View - ClinicalTrials.gov

Glutamine and Traumatic Brain Injury - Full Text View.

clinicaltrials.gov

The term "brain injury" covers a wide range of conditions and injuries relating to the brain, skull, and scalp. A traumatic brain injury (TBI) usually results when the head or body suffers from a violent blow or jolt that results in swelling, bruising, bleeding, or tearing of the brain tissue which any damage to it has the potential to change the way your body operates.

Now ,(TBI) is considered one of the major causes of disability and deaths ,As It contributes more than 30% Of deaths worldwide . Those who survive a TBI can face effects that last a few days, or the rest of their lives. Effects of TBI can include impaired motor, cognitive and emotional functioning. These issues not only affect individuals but can have lasting effects on families and communities.TBI can also cause some inflammatory mediators to be released in circulation that affect brain and systemic organs such as cortisol,IL6 and TNF etc. A lot of modialities have been introduced to help in decreasing these side effects.

Glutamine,a non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells.glutamine has a restricted passage to the brain from blood but it is synthesised in the brain as a part of the glutamate-glutamine cycle.5,6 so it present in over 90% of all brain synapses and is a naturally occurring molecule that nerve cells use to send signals to other cells in the central nervous system,maintaining normal brain function and can improve situations related to impaired cognitive,motor and emotional functions.

Hypothesis of this study; Does glutamine therapy have a positive effect on traumatic brain injury patients ?

 

[David PS]

Is your light set up red light?

I use near-infrared light. Based in part on this mouse study.

https://www.nature.com/articles/s41598-022-14812-8.pdf

 

[Peatness]

I use near-infrared light. Based in part on this mouse study.

https://www.nature.com/articles/s41598-022-14812-8.pdf

Thanks

 

[Meecho]

The Androsterone threads speak of myelin sheath repair...to which DHT and Testosterone are important...

I’ve noticed that vitamin D and vitamin K increase androgens a lot.

Years ago I had a head injury from a fall skiing and I ended up working with the LENS neurofeedback system, which in one session had incredible results.

I have also heard about rTMS. Both use magnetic fields. I'll look into that more. Also, it appears that significantly improving plant growth via a magnetic field might be real (magnetoculture). I’m in the early stage of research.

Exposure of seeds to static magnetic field enhances germination and early growth characteristics in chickpea (Cicer arietinum L.) - PubMed

Seeds of chickpea (Cicer arietinum L.) were exposed in batches to static magnetic fields of strength from 0 to 250 mT in steps of 50 mT for 1-4 h in steps of 1 h for all fields. Results showed that magnetic field application enhanced seed performance in terms of laboratory germination, speed of...

pubmed.ncbi.nlm.nih.gov

Chinese researchers claim electroculture works as theorized

A team of researchers affiliated with multiple institutions in China reports that electroculture can increase agricultural yields. In their paper published in the journal Nature Food, the group describes growing peas using traditional methods while applying electric shocks to other pea crops.

phys.org

Greenhouse Carbon Dioxide Supplementation - Oklahoma State University

By Megha Poudel and Bruce Dunn. Learn about carbon dioxide, its concentration in relation to plants, supplementation, the effect of supplemental CO2 on different growing factors, sources of carbon dioxide and control and distribution of CO2.

extension.okstate.edu

CO2 enrichment using CRAM fermentation improves growth, physiological traits and yield of cherry tomato (Solanum lycopersicum L.)

Carbon dioxide (CO2) concentration in greenhouses is sub-optimal for vegetable production. Many techniques have been used to increase CO2 concentratio…

www.sciencedirect.com

@Meecho I've found D and K very helpful. Is your light set up red light?

For continuous use, I go with full-spectrum light – two 250W clear incandescent bulbs on one cable. The only difference between red and clear incandescent bulbs is that the red one is tinted red (it only passes red light). Both bulbs are called infrared bulbs because approximately 90% of the energy produced is infrared.

Parts:
* cable for 220V: 3 x 0.75mm (probably better to just use 2 x 0.75mm)
* bulb sockets for 220V: two E27; mine are 4A (E26 for the USA, and apparently, you can screw a standard light bulb in both of them)
* power plug

Then, I put it all together with bulb sockets connected in parallel on one cable – brown on brown, blue on blue (youtube.com/watch?v=8gu3-J8MOGc).

Other notes:
* brown wire is Live, blue wire is Neutral, green & yellow wire is Earth
* I cut wire insulation with small scissors lengthwise, on two sides, and then remove the pieces completely by cutting it crosswise

Recently I've been thinking about glutamine again and wondering if it has a role in traumatic head/brains injuries. I found this clinical trial that is ongoing. It ends in Dec 2023

Interesting. On my side, I've been thinking about creatine supplementation.

Creatine, cognition, and concussion: What does the evidence really show?

Creatine affects muscle but also the brain. Can it be a useful supplement to improve cognitive function or reduce the effects of concussion?

www.mysportscience.com

https://journals.sagepub.com/doi/full/10.1177/03000605211073305

---

I think that if the injury isn’t very recent, the main focus should be growth and repair.

 

[Meecho]

@Peatness

One drop of Metabolics vitamin B1 (Thiamine Pyrophosphate) contains 389 mcg B1 (Vitamin B1 (Thiamine Pyrophosphate)). One pill (lozenge) of Source Naturals Coenzymated B1 contains 13 mg B1 (Source Naturals Coenzymated™ B-1). “Thiamin diphosphate (TDP), also called thiamin pyrophosphate (TPP) or cocarboxylase, is the active, coenzyme form of vitamin B-1.”

That’s a big difference – if I’m not missing something. Probably this is because they say, “The RDA for thiamine in the United States is 1.2 mg everyday for men and 1.1 mg everyday for women.” As a reference, Energin from idealabsdc.com has 50 mg as a daily dosage, and in some studies, they use, for example, 300mg daily (as you have used). I can see that you Peatness use Thiamin HCL for the rest of your daily dosage.

How much do you dose Metabolics vitamin B1 under your tongue?

 

[Peatness]

@Peatness

One drop of Metabolics vitamin B1 (Thiamine Pyrophosphate) contains 389 mcg B1 (Vitamin B1 (Thiamine Pyrophosphate)). One pill (lozenge) of Source Naturals Coenzymated B1 contains 13 mg B1 (Source Naturals Coenzymated™ B-1). “Thiamin diphosphate (TDP), also called thiamin pyrophosphate (TPP) or cocarboxylase, is the active, coenzyme form of vitamin B-1.”

That’s a big difference – if I’m not missing something. Probably this is because they say, “The RDA for thiamine in the United States is 1.2 mg everyday for men and 1.1 mg everyday for women.” As a reference, Energin from idealabsdc.com has 50 mg as a daily dosage, and in some studies, they use, for example, 300mg daily (as you have used). I can see that you Peatness use Thiamin HCL for the rest of your daily dosage.

How much do you dose Metabolics vitamin B1 under your tongue?

I tend to use 2 - 3drops of the metabolics drops under the tongue when I use it. I still don't know how well this form of thiamine is absorbed. I don't use this product everyday.

 

[Meecho]

Related: Restoring Metabolism [with creatine] Prevents / Reverses "permanent" Nerve Damage, by haidut

Restoring Metabolism Prevents / Reverses "permanent" Nerve Damage

Yet another study demonstrating the crucial role cellular metabolism plays in pathological processes. While most of my posts deal with beneficial effects of improving OXPHOS on various chronic diseases, the study below demonstrates that the same may be true in acute pathologies such as traumatic...

raypeatforum.com

Restoring Cellular Energetics Promotes Axonal Regeneration and Functional Recovery after Spinal Cord Injury

Axonal regeneration in the central nervous system (CNS) is a highly energy-demanding process. Extrinsic insults and intrinsic restrictions lead to an …

www.sciencedirect.com

 

[Peatness]

This is so simply and it helps - a lot!

Tension Release Secret​

View: https://www.youtube.com/watch?v=ok5RtO6usN4

 

[Peatress]

Associations and Outcomes Between Chronic Traumatic Encephalopathy and Vasculitis in Adult Patients - PubMed

Chronic traumatic encephalopathy (CTE) results from brain injuries and traumas due to accelerated impacts on the head. In severe cases, the diseases cause brain damage, given the head trauma. On the other hand, vasculitis occurs through antibodies that mistake protein vessels as foreign, hence...

pubmed.ncbi.nlm.nih.gov

Scurvy masquerading as leukocytoclastic vasculitis: a case report and review of the literature - PubMed

Scurvy, a disease rarely seen in modern times, results from dietary deficiency of vitamin C and is characterized in adults by hemorrhagic diathesis, hair follicle abnormalities, and osteopenia. We present a 59-year-old man with perifollicular petechiae of the extremities, a painful lower...

pubmed.ncbi.nlm.nih.gov

Scurvy mimicking systemic vasculitis - PubMed

An 91 years old woman was hospitalized because of lethargy, shortness of breath and diffuse subcutaneous hemorrhage of legs. Clinical features were consistent with the diagnosis of vasculitis with systemic involvement. However dermatologic characteristics of the legs, in association with...

pubmed.ncbi.nlm.nih.gov

 

[Peatress]

If anyone can get access to the full article please post

E12 Two Cases of Giant Cell Arteritis Following Head Trauma, A New Risk Factor?

Disclosure statement: The authors have declared no conflicts of interest.

academic.oup.com

 

[David PS]

@Peatress, while watching this video I as surprised that vitamin D was more effective than the various vitamin D anaologs that the body makes from sunshine. It seems that vitamin D is a much smaller molecule that can pass thru the blood brain barrier. In addition from the papers that I glanced over, it may be important to to have the combination of progesserson and vitamin D in your system.

View: https://www.youtube.com/watch?v=U93z9MleSkk


Here are some of the Vitamin D paper that I found. Some of then are rat studies. They may be already part of this thread.

Vitamin D Protects Human Endothelial Cells from H2O2 Oxidant Injury Through the Mek/Erk-Sirt1 Axis Activation

Progesterone Increases Circulating Endothelial Progenitor Cells and Induces Neural Regeneration after Traumatic Brain Injury in Aged Rats

Vascular remodeling plays a key role in neural regeneration in the injured brain. Circulating endothelial progenitor cells (EPCs) are a mediator of the vascular remodeling process. Previous studies have found that progesterone treatment of traumatic brain ...

www.ncbi.nlm.nih.gov

Vitamin D receptor activation regulates microglia polarization and oxidative stress in spontaneously hypertensive rats and angiotensin II-exposed microglial cells: Role of renin-angiotensin system

Hypertension is one of the major predisposing factors for neurodegenerative disease characterized with activated renin-angiotensin system (RAS) in bot…

www.sciencedirect.com

Deep Vein Thrombosis Prophylaxis Use in Traumatic Brain Injury Patients in Tropical Climate
Efficacy of Vitamin D3 and Progesterone Interactions Following Traumatic Brain Injury

 

[Peatress]

Thanks @David PS . On page two of this thread I posted a study comparing the administration of progesterone versus progesterone and vitamin D in improvement of outcomes in patients with traumatic brain injury. It was a randomized clinical trial with placebo group.

I’ve been thinking about vitamin D again because my recent blood test shows mine is still not optimum. I’ve been doing topical but will switch to oral dosing. Perhaps I need magnesium. As for progesterone I'm never consistent with it because of how it makes me feel.

 

[Peatress]

Posted on the email thread by @Nick

Clinical trials progesterone for treating traumatic brain injury

Question:
In clinical trials (stage I & II) for treating traumatic brain injury progesterone was effective but in stage III the dose was increased from 1 or 2mg/kg/day intravenously to 12mg/kg/day and it had no effect compared to the placebo. It was proposed in several papers that progesterone may have a U-shaped dose response curve which would perhaps explain these results. I wonder if the high dose might be depleting brain glycogen but I have trouble believing that this alone would eliminate all protective effect.

If you are familiar with these trials do you have any idea why a larger dose or some other procedural factor might have eliminated the progesterone's neuroprotective effects?
Are you aware of any evidence of a U-shaped dose response curve for progesterone?

Randy B. Howard, Iqbal Sayeed, Donald G. Stein. Suboptimal dosing parameters as possible factors in the negative Phase III clinical trials of progesterone for TBI. J Neurotrauma 2016
http://sci-hub.ac/10.1089/neu.2015.4179

Ray Peat:
Although the history of phase III studies might suggest that someone doesn’t intend for them to succeed, what’s clear is that ignorance increased the likelihood of failure in the progesterone study. Soybean oil is brain toxic, and it’s not an adequate solvent for progesterone, so much of the progesterone was probably trapped in the spleen, failing to protect the brain from the toxic effect of the fatty acids. Oral progesterone lowers nitric oxide and prostaglandins, protects against histamine and serotonin, and reduces the formation of free fatty acids. Dissolved in vitamin E, it’s taken up from the intestine in chylomicrons, and safely made available to the brain, and the vitamin E and progesterone both protect the brain by inhibiting nitric oxide and heme oxygenase (source of carbon monoxide and free iron). The protective effects increase with dose; extremely high doses produce anesthesia, which wouldn’t be a problem for traumatic brain injury patients, but starting with about 50 mg at a time a person can adjust the dose according to how they feel.

Food Chem. 2012 Sep 15;134(2):920-5.
Comparative effects of tocotrienol-rich fraction, α-tocopherol and α-tocopheryl
acetate on inflammatory mediators and nuclear factor kappa B expression in mouse
peritoneal macrophages.
Ng LT(1), Ko HJ.
(1)Department of Agricultural Chemistry, National Taiwan University, Taipei,
Taiwan. [email protected]
The effects of tocotrienol-rich fraction (TRF), α-tocopherol (T) and α-tocopheryl
acetate (TA) on lipopolysaccharide (LPS)-induced inflammatory responses in mouse
peritoneal macrophages were examined. Results showed that at 5-30 μg/ml, all test
compounds plus 1 μg/ml LPS exhibited no cytotoxic effects on macrophage cells.
Compared with T and TA, TRF showed the strongest anti-inflammatory activity as
demonstrated by its potency in inhibiting the LPS-induced nitric oxide (NO),
prostaglandin E(2) (PGE(2)), and proinflammatory cytokine (TNF-α, IFN-γ, IL-1β
and IL-6) production. At 10 μg/ml, it significantly blocked the LPS induction of
inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression,
but has no effect on cyclooxygenase-1 (COX-1). Furthermore, TRF also showed a
greater inhibition on the nuclear factor kappa B (NF-κB) expression than T and
TA. These results suggest that TRF could be a better agent than T and TA for use
in the prevention of chronic inflammatory diseases.
Copyright © 2012 Elsevier Ltd. All rights reserved.

2. Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11494-9.
gamma-tocopherol and its major metabolite, in contrast to alpha-tocopherol,
inhibit cyclooxygenase activity in macrophages and epithelial cells.
Jiang Q(1), Elson-Schwab I, Courtemanche C, Ames BN.
(1)Division of Biochemistry and Molecular Biology, University of California,
Berkeley, CA 94720, USA.
Cyclooxygenase-2 (COX-2)-catalyzed synthesis of prostaglandin E(2) (PGE(2)) plays
a key role in inflammation and its associated diseases, such as cancer and
vascular heart disease. Here we report that gamma-tocopherol (gammaT) reduced
PGE(2) synthesis in both lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages
and IL-1beta-treated A549 human epithelial cells with an apparent IC(50) of 7.5
and 4 microM, respectively. The major metabolite of dietary gammaT,
2,7,8-trimethyl-2-(beta-carboxyethyl)-6-hydroxychroman (gamma-CEHC), also
exhibited an inhibitory effect, with an IC(50) of approximately 30 microM in
these cells. In contrast, alpha-tocopherol at 50 microM slightly reduced (25%)
PGE(2) formation in macrophages, but had no effect in epithelial cells. The
inhibitory effects of gammaT and gamma-CEHC stemmed from their inhibition of
COX-2 activity, rather than affecting protein expression or substrate
availability, and appeared to be independent of antioxidant activity. gamma-CEHC
also inhibited PGE(2) synthesis when exposed for 1 h to COX-2-preinduced cells
followed by the addition of arachidonic acid (AA), whereas under similar
conditions, gammaT required an 8- to 24-h incubation period to cause the
inhibition. The inhibitory potency of gammaT and gamma-CEHC was diminished by an
increase in AA concentration, suggesting that they might compete with AA at the
active site of COX-2. We also observed a moderate reduction of nitrite
accumulation and suppression of inducible nitric oxide synthase expression by
gammaT in lipopolysaccharide-treated macrophages. These findings indicate that
gammaT and its major metabolite possess anti-inflammatory activity and that
gammaT at physiological concentrations may be important in human disease
prevention.

Free Radic Biol Med. 2004 Aug 1;37(3):325-38.
Inflammatory mediator and beta-amyloid (25-35)-induced ceramide generation and
iNOS expression are inhibited by vitamin E.
Ayasolla K(1), Khan M, Singh AK, Singh I.
(1)Department of Pediatrics, Medical University of South Carolina, Charleston, SC
29425, USA.
To investigate the putative role of beta-amyloid peptide (A beta) in inducing
oxidative stress damage in Alzheimer disease (AD), we studied the effects of
proinflammatory cytokines and A beta peptide on the induction of inducible nitric
oxide synthase (iNOS). A beta(25-35) upregulated the cytokine (TNF-alpha/IL-1
beta)-induced expression of iNOS and the production of nitric oxide (NO) in
astrocytes, which were inhibited by vitamin E. A beta treatment of C6 glial cells
(together with LPS and IFN-gamma), in addition to inducing iNOS, enhanced the
oxidative stress as measured by increased expression of manganese superoxide
dismutase and an increase in 2,7'-dichlorofluorescein diacetate fluorescence. We
also observed that LPS, IFN-gamma, and A beta(25-35) treatment led to the
activation of the sphingomyelin-ceramide (SM-Cer) cascade with an increase in
cellular ceramide. Inhibition of the SM-Cer cascade either by vitamin E treatment
or by the neutral sphingomyelinase inhibitor 3-O-methyl sphingomyelin also
resulted in alteration of the transcriptional binding activities of C/EBP,
NFkappaB, AP-1, and CREB in C6 glial cells. Hence, these findings suggest a role
for ceramide in iNOS induction and NO production in Abeta-induced AD pathobiology
and provide a possible explanation for the beneficial effects of vitamin E
therapy.

Brain Res. 2008 Feb 8;1193:120-7.
Protective effect of nitric oxide synthase inhibition or antioxidants on brain
oxidative damage caused by intracerebroventricular arginine administration.
Delwing D(1), Delwing D, Bavaresco CS, Wyse AT.
(1)Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde,
Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, CEP
90035-003, Porto Alegre, RS, Brazil.
We have previously demonstrated that acute arginine administration induces
oxidative stress and compromises energy metabolism in rat hippocampus. In the
present study, we initially investigated the effect of intracerebroventricular
infusion of arginine (0.1, 0.5 and 1.5 mM solution) on Na(+),K(+)-ATPase activity
and on some parameters of oxidative stress, namely thiobarbituric acid-reactive
substances (TBA-RS) and total radical-trapping antioxidant parameter (TRAP) in
the hippocampus of rats. Results showed that 1.5 mM arginine solution
significantly increases TBA-RS and reduces Na(+),K(+)-ATPase activity and TRAP in
the rat hippocampus. We also evaluated the influence of the nitric oxide synthase
inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), and antioxidants,
namely alpha-tocopherol plus ascorbic acid, on the effects elicited by arginine
on Na(+),K(+)-ATPase activity, TBA-RS and TRAP. Results showed that treatment
with alpha-tocopherol plus ascorbic acid per se did not alter these parameters
but prevented these effects. Furthermore, intracerebroventricular infusion of
L-NAME prevented the inhibition caused by arginine on Na(+),K(+)-ATPase activity,
as well as the increased of TBA-RS. Our findings indicate that
intracerebroventricular infusion of arginine induces oxidative stress in rat
hippocampus and that the inhibition of Na(+),K(+)-ATPase activity caused by this
amino acid was probably mediated by NO and/or its derivatives ONOO(-) and/or
other free radicals. Finally, we suggest that the administration of antioxidants
should be considered as an adjuvant therapy to specific diets in
hyperargininemia.

Free Radic Biol Med. 2007 Nov 15;43(10):1439-52. .
Cytoprotective properties of alpha-tocopherol are related to gene regulation in
cultured D-galactosamine-treated human hepatocytes.
González R(1), Collado JA, Nell S, Briceño J, Tamayo MJ, Fraga E, Bernardos A,
López-Cillero P, Pascussi JM, Rufián S, Vilarem MJ, De la Mata M, Brigelius-Flohe
R, Maurel P, Muntané J.
(1)Liver Research Unit, Reina Sofía University Hospital, Ciberehd, E-14004
Córdoba, Spain.
Vitamin E (alpha-tocopherol) has demonstrated antioxidant activity and
gene-regulatory properties. d-Galactosamine (D-GalN)-induced cell death is
mediated by nitric oxide in hepatocytes, and it is associated with hepatic
steatosis. The beneficial properties of alpha-tocopherol and their relation to
oxidative stress and gene regulation were assessed in D-GalN-induced cell death.
Hepatocytes were isolated from human liver resections by a collagenase perfusion
technique. alpha-Tocopherol (50 microM) was administered at the advanced stages
(10 h) of D-GalN-induced cell death in cultured hepatocytes. Cell death,
oxidative stress, alpha-tocopherol metabolism, and NF-kappaB-, pregnane X
receptor (PXR)-, and peroxisome proliferator-activated receptor
(PPAR-alpha)-associated gene regulation were estimated in the hepatocytes. D-GalN
increased cell death and alpha-tocopherol metabolism. alpha-Tocopherol exerted a
moderate beneficial effect against apoptosis and necrosis induced by D-GalN.
Induction (rifampicin) or inhibition (ketoconazole) of alpha-tocopherol
metabolism and overexpression of PXR showed that the increase in PXR-related
CYP3A4 expression caused by alpha-tocopherol enhanced cell death in hepatocytes.
Nevertheless, the reduction in NF-kappaB activation and inducible nitric oxide
synthase expression and the enhancement of PPAR-alpha and carnitine palmitoyl
transferase gene expression by alpha-tocopherol may be relevant for cell
survival. In conclusion, the cytoprotective properties of alpha-tocopherol are
mostly related to gene regulation rather than to antioxidant activity in
toxin-induced cell death in hepatocytes.

Lipids Health Dis. 2011 Dec 20;10:239.
Inhibition of nitric oxide in LPS-stimulated macrophages of young and senescent
mice by δ-tocotrienol and quercetin.
Qureshi AA(1), Tan X, Reis JC, Badr MZ, Papasian CJ, Morrison DC, Qureshi N.
(1)Department of Basic Medical Sciences, University of Missouri-Kansas City, 2411
Holmes Street, Kansas City, MO 64108, USA. [email protected]
BACKGROUND: Changes in immune function believed to contribute to a variety of
age-related diseases have been associated with increased production of nitric
oxide (NO). We have recently reported that proteasome inhibitors (dexamethasone,
mevinolin, quercetin, δ-tocotrienol, and riboflavin) can inhibit
lipopolysaccharide (LPS)-induced NO production in vitro by RAW 264.7 cells and by
thioglycolate-elicited peritoneal macrophages derived from four strains of mice
(C57BL/6, BALB/c, LMP7/MECL-1(-/-) and PPAR-α(-/-) knockout mice). The present
study was carried out in order to further explore the potential effects of diet
supplementation with naturally-occurring inhibitors (δ-tocotrienol and quercetin)
on LPS-stimulated production of NO, TNF-α, and other pro-inflammatory cytokines
involved in the ageing process. Young (4-week-old) and senescent mice (42-week
old) were fed control diet with or without quercetin (100 ppm), δ-tocotrienol
(100 ppm), or dexamethasone (10 ppm; included as positive control for suppression
of inflammation) for 4 weeks. At the end of feeding period,
thioglycolate-elicited peritoneal macrophages were collected, stimulated with
LPS, LPS plus interferon-β (IFN-β), or LPS plus interferon-γ (IFN-γ), and
inflammatory responses assessed as measured by production of NO and TNF-α, mRNA
reduction for TNF-α, and iNOS genes, and microarray analysis.
RESULTS: Thioglycolate-elicited peritoneal macrophages prepared after four weeks
of feeding, and then challenged with LPS (10 ng or 100 ng) resulted in increases
of 55% and 73%, respectively in the production of NO of 46-week-old compared to
8-week-old mice fed control diet alone (respective control groups), without
affecting the secretion of TNF-α among these two groups. However, macrophages
obtained after feeding with quercetin, δ-tocotrienol, and dexamethasone
significantly inhibited (30% to 60%; P < 0.02) the LPS-stimulated NO production,
compared to respective control groups. There was a 2-fold increase in the
production of NO, when LPS-stimulated macrophages of quercetin, δ-tocotrienol, or
dexamethasone were also treated with IFN-β or IFN-γ compared to respective
control groups. We also demonstrated that NO levels and iNOS mRNA expression
levels were significantly higher in LPS-stimulated macrophages from senescent
(0.69 vs 0.41; P < 0.05), compared to young mice. In contrast, age did not appear
to impact levels of TNF-α protein or mRNA expression levels (0.38 vs 0.35) in
LPS-stimulated macrophages. The histological analyses of livers of control groups
showed lesions of peliosis and microvesicular steatosis, and treated groups
showed Councilman body, and small or large lymphoplasmacytic clusters.
CONCLUSIONS: The present results demonstrated that quercetin and δ-tocotrienols
inhibit the LPS-induced NO production in vivo. The microarray DNA analyses,
followed by pathway analyses indicated that quercetin or δ-tocotrienol inhibit
several LPS-induced expression of several ageing and pro-inflammatory genes
(IL-1β, IL-1α, IL-6, TNF-α, IL-12, iNOS, VCAM1, ICAM1, COX2, IL-1RA, TRAF1 and
CD40). The NF-κB pathway regulates the production of NO and inhibits the
pro-inflammatory cytokines involved in normal and ageing process. These ex vivo
results confirmed the earlier in vitro findings. The present findings of
inhibition of NO production by quercetin and δ-tocotrienol may be of clinical
significance treating several inflammatory diseases, including ageing process.

 

[David PS]

Near-Infrared Light Regenerates Damage from Traumatic Brain Injury, Latest of Five Studies Show

Dr. Theodore Henderson reports mounting evidence that “neuro-laser” treatment effectively treats traumatic brain injury (TBI) by reversing inflammation, oxidative stress and neurodegeneration FOR…

www.tbi.care

Near-IR light penetrates skull to aid traumatic brain injury

Researchers have found that high-powered NIR light can penetrate the skull to reach the brain and aid in TBI therapy.

www.laserfocusworld.com

@Peatress -My brother-in-law has Parkinson's (chemical injury to the brain?) and he has very positive things to say about infrared light. He has been using a large panel of red LEDs twice daily for about 7 weeks. The image in the article above may be misdirecting in that more lights may be needed. I am beginning to explore red light for Parkinson's here.