Regimen to promote neuroprotection and encourage nerve repair

(plus a compendium of resources and promising adjunctive therapeutic agents for Multiple Sclerosis and other neurological diseases & disorders)

Printable PDF format version

 

Dr. Anthony G. Payne

Steenblock Research Institute

 (949) 248-7034

E-mail: DrAGPayne@yahoo.com

 

 

Suggested regimen to help quell inflammation and promote nerve repair in various neurodegenerative and neuroinflammatory diseases and disorders

 

 

Diet: Paleolithic (“Stone Age”). 30% or more protein (2:1 ratio of omega-3 to omega-6 fatty acid containing fish, game meat, etc., 1:1 Magnesium to Calcium intake, low sodium-high potassium) 70% complex carbohydrates (Fruits and vegetables). No grains, cereals or bovine milk. (Helpful dietary chart can be found below)

 

Use of curry and Tumeric powder in foods is encouraged.

 

 

20 minutes before or 1 hour after meals:

 

 

800 mgs. to 1 gram: N-acetylcysteine

1 gram of Acetyl-L-carnitine

500 mgs. to 1 gram: Taurine

 

 

With meals:

 

500 mgs. to 1.0-1.5 grams time-released Niacinamide

 

50 mgs. Thiamine (B1)

 

50-100 mgs. R-Lipoic Acid

 

50 mgs. Non-toxic NDGA

 

T4 (Thyroid) – Check with primary care physician regarding advisability of using this (MD or DO must monitor T4 hormone level regularly). Abstract concerning rationale for inclusion in references section. 

 

May be of merit - Discuss with primary healthcare provider

 

Velvet Deer Antler extract (Spray or tablets). Follow product label recommendations.

 

Cinnamon Extract Capsules (Counters glutamate neurotoxicity). Follow product manufacturer recommendations. Abstract in reference section.

 

Drink magnesium rich “hard” water as often as possible: http://www.mgwater.com/list5.shtml  . Also make green tea using this type of water (See below)

 

Make and drink organic Japanese green tea 2-3 times daily  http://www.o-cha.com/green-tea/Organic-Matcha-P300-Kaoru-Supreme-pr-16138.html  -. This is one of the best, “Kaoru Supreme” Make using a magnesium rich water (See above for one source). NOTE: Author has no financial or other interest in this firm or any commercial source listed in this free access regimen.

 

Glycerophosphocholine (GPC) – 1 or 2 capsules one (1) hour before or 2 hours following meals.

 

Phosphatidylserine (PS) – 1 softgel 3 x daily or more often.

 

Luteolin: The scientific evidence for the benefits of luteolin for various neurologic challenges is beginning to accrue. One luteolin-rich source is a product called ”Lutimax” --  http://www.lutimax.com/radicals.html

 

Rooibos Tea (Rich in luteolin):

http://www.dragonwater.com/search.tf/tea/rooibos_tea/?z=go_rooibos_tea&gclid=CKq9g-rR6IMCFQMZIgodqzqpLw  - Organic Rooibos Tea

 

L-Theanine  Take 1 capsule with or after each meal and snack and then 2 capsules 30 minutes before retiring at night (Theanine appears to contribute to mood modulation and relaxation-promotion via its ability to increase GABA and dopamine)

 

 

 

 

DIETARY GUIDELINES -- PALEODIET

 

    70 % Per Day 

 

Chlorophyll foods

     Chlorella

     Sprouts

Asparagus

Beets

 

Carob

Cauliflower

Celery

Chard

Cucumber

Green beans

Kale

Leafy lettuce

Mustard greens

Parsnips

Prunes (bedtime)

Radishes

Spinach

String beans

Sweet potatoes

Watercress

Vegetable Juices

  (Green and Yellow)

 

Curcumin/Curry

Cinnamon

Ginger

Ginseng

Fenugreek

Rosemary

Parsley/Cilantro

Sage

Thyme

Natural vanilla flavoring

 

Knox Gelatin

30% Per Day

(Especially the high Protein Meats & such)

Jerusalem Artichoke

Avocado

Brussel Sprouts

Broccoli

Eggplant

Carrots

Carrot Juice (no more than glass)

Blueberries with plain yogurt

Red Grapes with plain yogurt

            (if not allergic)

Grape Juice

 

Onions, garlic

 

Wheat grass juice

 

 

Almonds and filberts (not roasted or salted)

Sunflower seeds

Sesame seeds

Pumpkin seeds

Olives

 

Fish (be careful of mercury content)

    Cod

    Haddock

    Flounder

    Salmon

    Scrod

    Tuna

    Sea Bass

    Bass

    Sardines

    Herring

    Anchovies

Turkey

Chicken

Eggs

Wild Game

0% Per Day

 

Cigarettes/Cigars

 

Beer

Wine

Other Alcoholic drinks

Sodas

Coffee (Caffeinated)

 

Red Meat

 

All grains and cereals

 

Cloves

 

Foods with

     Artificial colors

     Preservatives

     Monosodium glutamate or Vegetable Hydrolyzed Protein      

 

Processed foods with increased salt or sugar

 

Aspartame (Nutrasweet)

 

Fried Foods

 

Water with heavy metals

(fluoride water can increase the toxicity of aluminum)

 

Dairy Products 

 

 

Resources, References, Supporting Material

 

 

 

http://www.stemcelltherapies.org/ms.htm  - This link is to a very comprehensive article on alternative approaches to treating MS (by Dr. David A. Steenblock, Medical Director & CEO, Steenblock Research Institute,  Research & Development Laboratory, 1064 Calle Negocio #B, San Clemente, CA. 92673)

 

http://www.strokedoctor.com/ - Dr. Steenblock’s medical practice website - devoted to brain repair and rehabilitation. Many good research papers and such posted on this website.

 

http://author.emedicine.com/NEURO/topic286.htm - Organophosphates, general.

http://www.safe2use.com/ca-ipm/00-11-12.htm - The Chronic and Delayed Effects of Organophosphate (OP) Poisoning

http://www.lef.org/protocols/prtcl-156.shtml -  Heavy metals toxicity

http://www.webnat.com/ -  Neurodegenerative diseases and conditions: Causes, natural and other treatments, et cetera 

  

Diet, supplements, abstracts, etc.

 

Tumeric (Curcumin)

Curcumin (Diferuloylmethane) is a compound found in the Indian curry spice, tumeric.

It has been discovered that people in India have a very low incidence of neurological diseases and researchers have attempted to find out why this is. They have looked at the spice, tumeric, which was known from traditional Indian medicine as an anti-inflammatory agent effective in wound healing. Research using curcumin, the active ingredient of tumeric, in EAE, a mouse model of multiple sclerosis, has shown that it may be of benefit to people with MS.

Curry spice may fight multiple sclerosis
The Spice of Life - Unlocking the power of curcumin
Piperin Home page
Curcuma longa (turmeric). Monograph.
Curcumin inhibiting of TNF-mediated adhesion of monocytes to endothelial cells
Curcumin inhibiting of macrophage TNF-alpha release
Effect of curcumin and capsaicin on rat macrophages metabolism
Curcumin inhibiting differentiation in human endothelial cells
Curcumin and oxidative activity astrocyte cells
Regulation of IL-1 mediated MMP-9 expression in mesangial cells
Influence of piperine on curcumin in animals and humans
Immunomodulatory activity of curcumin


 

 

 

J Nat Prod. 2002 Sep;65(9):1227-31.

 

 

Discovery of natural products from Curcuma longa that protect cells from beta-amyloid insult: a drug discovery effort against Alzheimer's disease.

Park SY, Kim DS.

Program for Collaborative Research in Pharmaceutical Sciences and Department of Medicinal Chemistry and Pharmacognosy (m/c 877), College of Pharmacy, University of Illinois at Chicago, 60612, USA.

From Curcuma longa, two novel compounds, 4' '-(3' "-methoxy-4' "-hydroxyphenyl)-2' '-oxo-3' '-enebutanyl 3-(3'-methoxy-4'hydroxyphenyl)propenoate (calebin-A, 1) and 1,7-bis(4-hydroxy-3-methoxyphenyl)-1,4,6-heptatrien-3-one (2), and seven known compounds, 1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione (curcumin, 3), 1-(4-hydroxy-3-methoxyphenyl)-7-(4-hydroxyphenyl)-1,6-heptadiene-3,5-dione (demethoxycurcumin, 4), 1,7-bis(4-hydroxyphenyl)-1,6-heptadiene-3,5-dione (bisdemethoxycurcumin, 5), 1-hydroxy-1,7-bis(4-hydroxy-3-methoxyphenyl)-6-heptene-3,5-dione (6), 1,7-bis(4-hydroxyphenyl)-1-heptene-3,5-dione (7), 1,7-bis(4-hydroxyphenyl)-1,4,6-heptatrien-3-one (8), and 1,5-bis(4-hydroxy-3-methoxyphenyl)-1,4-pentadien-3-one (9), were isolated following a bioassay-guided fractionation scheme utilizing an assay to detect protection of PC12 cells from beta-amyloid insult. Compounds 1, 3-5, and 7 were found to more effectively protect PC12 cells from betaA insult (ED(50) = 0.5-10 microg/mL) than Congo red (10) (ED(50) = 37-39 microg/mL).

PMID: 12350137


 

 

 

J Neurosci. 2001 Nov 1;21(21):8370-7.

 

 

The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse.

Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM.

Departments of Medicine and Neurology, University of California, Los Angeles, Los Angeles, California 90095, USA.

Inflammation in Alzheimer's disease (AD) patients is characterized by increased cytokines and activated microglia. Epidemiological studies suggest reduced AD risk associates with long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs). Whereas chronic ibuprofen suppressed inflammation and plaque-related pathology in an Alzheimer transgenic APPSw mouse model (Tg2576), excessive use of NSAIDs targeting cyclooxygenase I can cause gastrointestinal, liver, and renal toxicity. One alternative NSAID is curcumin, derived from the curry spice turmeric. Curcumin has an extensive history as a food additive and herbal medicine in India and is also a potent polyphenolic antioxidant. To evaluate whether it could affect Alzheimer-like pathology in the APPSw mice, we tested a low (160 ppm) and a high dose of dietary curcumin (5000 ppm) on inflammation, oxidative damage, and plaque pathology. Low and high doses of curcumin significantly lowered oxidized proteins and interleukin-1beta, a proinflammatory cytokine elevated in the brains of these mice. With low-dose but not high-dose curcumin treatment, the astrocytic marker GFAP was reduced, and insoluble beta-amyloid (Abeta), soluble Abeta, and plaque burden were significantly decreased by 43-50%. However, levels of amyloid precursor (APP) in the membrane fraction were not reduced. Microgliosis was also suppressed in neuronal layers but not adjacent to plaques. In view of its efficacy and apparent low toxicity, this Indian spice component shows promise for the prevention of Alzheimer's disease.

PMID: 11606625 [PubMed - indexed for MEDLINE]


 

 

J Immunol. 2002 Jun 15;168(12):6506-13.

 

 

Curcumin inhibits experimental allergic encephalomyelitis by blocking IL-12 signaling through Janus kinase-STAT pathway in T lymphocytes.

Natarajan C, Bright JJ.

Division of Neuroimmunology, Department of Neurology, Vanderbilt University Medical Center, Nashville, TN 37212, USA.

Experimental allergic encephalomyelitis (EAE) is a CD4(+) Th1 cell-mediated inflammatory demyelinating autoimmune disease of the CNS that serves as an animal model for multiple sclerosis (MS). IL-12 is a proinflammatory cytokine that plays a crucial role in the induction of neural Ag-specific Th1 differentiation and pathogenesis of CNS demyelination in EAE and MS. Curcumin (1,7-Bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione) is a naturally occurring polyphenolic phytochemical isolated from the rhizome of the medicinal plant Curcuma longa. It has profound anti-inflammatory activity and been traditionally used to treat inflammatory disorders. In this study we have examined the effect and mechanism of action of curcumin on the pathogenesis of CNS demyelination in EAE. In vivo treatment of SJL/J mice with curcumin significantly reduced the duration and clinical severity of active immunization and adoptive transfer EAE. Curcumin inhibited EAE in association with a decrease in IL-12 production from macrophage/microglial cells and differentiation of neural Ag-specific Th1 cells. In vitro treatment of activated T cells with curcumin inhibited IL-12-induced tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT3 and STAT4 transcription factors. The inhibition of Janus kinase-STAT pathway by curcumin resulted in a decrease in IL-12-induced T cell proliferation and Th1 differentiation. These findings highlight the fact that curcumin inhibits EAE by blocking IL-12 signaling in T cells and suggest its use in the treatment of MS and other Th1 cell-mediated inflammatory diseases.

PMID: 12055272 [PubMed - indexed for MEDLINE]


 

 

 

 

NEW ORLEANS (Reuters Health) - Preliminary studies in rats suggest that curcumin, a compound found in the curry spice turmeric, may block the progression of multiple sclerosis (MS).

According to researcher Dr. Chandramohan Natarajan of Vanderbilt University in Nashville, Tennessee, rats with an MS-like illness showed little or no signs of disease symptoms after being injected with curcumin, while animals without the treatment went on to severe paralysis.

"We got a very good inhibition of the disease by treating with curcumin," Natarajan told Reuters Health. He presented the findings here Tuesday at the annual Experimental Biology 2002 conference.

No one knows what causes multiple sclerosis, in which the body's immune system attacks the protective myelin sheath surrounding nerve fibers in the brain and spine. Symptoms of multiple sclerosis include muscle weakness and stiffness, balance and coordination problems, numbness and vision disturbances.

Interest in the potential neuroprotective properties of curcumin rose after studies found very low levels of neurological diseases such as Alzheimer's in elderly Indian populations. Added to this were studies confirming curcumin as a potent anti-inflammatory agent, effective in wound healing. And just last fall, researchers at the University of California, Los Angeles reported that curcumin appeared to slow the progression of Alzheimer's in mice.

In their 30-day study, Natarajan and co-researcher Dr. John Bright gave injections of 50- and 100-microgram doses of curcumin, three times per week, to a group of mice bred to develop a disease called experimental autoimmune encephalomyelitis (EAE)--an autoimmune condition used by researchers as a model for multiple sclerosis because it also results in the slow erosion of myelin. They then watched the rats for signs of MS-like neurological impairment.

By day 15, rats who had not received curcumin developed EAE to such an extent that they displayed complete paralysis of both hind limbs, according to Natarajan.

In contrast, rats given the 50-microgram dose of the curry compound showed only minor symptoms, such as a temporarily stiff tail. And rats given the 100-microgram dose appeared completely unimpaired throughout the 30 days of the study.

The results didn't really surprise Natarajan. "In Asian countries, such as India, China, who are eating more spicy foods, more yellow compounds like curcumin...there are only very, very rare reports of MS," he pointed out. He said the doses the rats received were roughly equivalent in human terms to those found in a typical Indian diet.

Just how curcumin might work to thwart the progression of demyelinization remains unclear. But the Nashville researchers believe it may interrupt the production of IL-12, a protein that plays a key role in signaling immune cells to launch their assault on the myelin sheath.

Natarajan stressed that "we have to do a lot of work on this," including examining other potential mechanisms by which curcumin slows EAE and, potentially, MS.

The work remains preliminary, and MS patients should follow their doctor's advice when it comes to treating the disease. Still, Natarajan said adding a little curry to the diet couldn't hurt. "I think using this spice in their food could be of help," he said.

 

 

http://www.iherb.com/tumeric.html

 

 

 

 

Blue Wavelength light exposure may ameliorate MS

 

Animal Model of Multiple Sclerosis:

   To help in research of multiple sclerosis (MS) researchers utilize an animal model, experimental allergic encephalitis (EAE). EAE is an acute autoimmune demyelination disease, that matches the symptomatology of MS.  Guinea pigs with EAE are reported to have a reduction of serotonin within the central nervous system (CNS), when compared to control subjects. The reduction of serotonin within the CNS leads to an effect on CNS serotonin transmissions in EAE, either at the level of serotonin receptor itself, or at the level of serotonin transmitting neurons (Scott, Cashman, and Spitler, 1982-83). The symptoms of EAE are due to the inhibition of serotonin transmission.
    In animals with EAE, administration of L-5-hydroxytrytophan, a precursor to serotonin, reversed the effects of impaired serotonergic transmission. Suggesting that there might be a blockade of serotonin receptors (Scott, Cashman, and Spitler, 1982-83), which can be overcome by the addition of a drug that increases the CNS serotonin levels. The addition of a precursor of serotonin has such an effect, and then the addition of antidepressant type drugs may  affect the symptoms of EAE in a positive way./SPAN>


http://www.cwu.edu/~chem/courses/chem388488f00/kusche/multiple/animal.htm

 

--------------------------------------------------------------------------------------------------------

Scientific Breakthrough
Blue Light Wavelengths Increase Serotonin

Several very recent studies, most notably research from a team headed by Dr. George Brainard at Thomas Jefferson Medical College in Philadelphia, have identified the specific wavelengths of blue light, 446-477 nm that are crucial in suppressing melatonin production in humans. 1  2  3  4 As Dr. Brainard notes, "This discovery will have an immediate impact on the therapeutic use of light for treating winter depression and circadian disorders."  Melatonin, the neurotransmitter that helps us sleep deeply through the night, is produced from serotonin.  Suppressing melatonin production raises the levels of serotonin in our brains.  This is the key goal of therapeutic bright light treatment.  This neurological pathway entrains our circadian rhythm to be awake during the day and sleep deeply at night.

Four cells in the human retina capture light and form the visual system.  One type, rod cells, regulates night vision.  The other three types, called cone cells, control color vision.  It's known that exposure to light at night can disrupt the body's production of melatonin, which is produced by the pineal gland in the brain and plays a vital role in resetting the body's daily biological clock.

Dr. Brainard and his group showed that the combined three-cone system didn't control the biological effects of light, at least not for melatonin regulation.  But subsequent work led to the surprising discovery that a novel receptor was responsible for the effect.

The study looked at the effects of nine different wavelengths of light, from indigo to orange, on 72 healthy volunteers.  Subjects were brought into the laboratory at midnight, when melatonin is highest.  The subjects' pupils were dilated and then they were blindfolded for two hours.  Blood samples were drawn.  Next, each person was exposed to a specific dose of photons of one light for 90 minutes, and then another blood sample was drawn.  Wavelengths of blue light had the highest potency in causing changes in melatonin levels, he explains.

This new research indicates that there is an as yet unidentified photopigment; most sensitive at theses wavelengths of blue light that controls theses neurological reactions to light.  As another researcher notes, this 'provides the first direct evidence of a non-rod, non-cone photoreceptive system in humans' - one that is activated by blue light between 420-480 nm. 2

We are pleased to announce that this research has been incorporated into the BlueStarTM Light Boxes.  The 10 000 lux, BlueStarTM double tubes have one side that's bright blue (446-477 nm) and one side that's bright white 85 CRI, 5000K.  Clinical use shows that the BlueStarTM Light raises serotonin in 15-30 minutes, instead of the 1-2 hours necessary with bright hi lux light

1         Brainard G, Hanifin J, Gresson J, et al (2001)  Action Spectrum for Melatonin Regulation in Humans:  Evidence for a Novel Circadian Photoreceptor.  Neurosci (16): 6405-6412
2  Thapan K, Arendt J, Skene DJ (2001)  An action spectrum for melatonin suppression:  evidence for a novel non-rod, non-cone photoreceptor system in humans.  J Physiol 535 (pt 1): 261-7
3  Wright HR, Lack LC (2001)  Effect of light wavelength on suppression and phase delay of the melatonin rhythm.  Chronobiol Int 5:801-8
4  Max, M (2001)  Molecular Basis of Phototransduction and Circadian Rhythmicity, notes on current research, Dept. of

2         Physiology and Biophysics of Mount Sinai School of Medicine.

 

 

NIACINAMIDE (Nerve protectant and anti-inflammatory)

 

Clin Exp Immunol. 2003 Jan;131(1):48-52.

 


Nicotinamide is a potent inhibitor of proinflammatory cytokines.

Ungerstedt JS, Blomback M, Soderstrom T.

Coagulation Research, Department of Surgical Sciences, Karolinska Institutet, Stockholm, Sweden. johanna.ungerstedt@ks.se

The present study investigates the modulating effects of nicotinamide on the cytokine response to endotoxin. In an in vitro model of endotoxaemia, human whole blood was stimulated for two hours with endotoxin at 1 ng/ml, achieving high levels of the proinflammatory cytokines IL-1 beta, IL-6, IL-8 and TNF alpha. When coincubating whole blood, endotoxin and the vitamin B3 derivative nicotinamide, all four cytokines measured were inhibited in a dose dependent manner. Inhibition was observed already at a nicotinamide concentration of 2 mmol/l. At a concentration of 40 mmol/l, the IL-1 beta, IL-6 and TNF alpha responses were reduced by more than 95% and the IL-8 levels reduced by 85%. Endotoxin stimulation activates poly(ADP-ribose)polymerase (PARP), a nuclear DNA repair enzyme. It has been hypothesized that the anti-inflammatory properties of nicotinamide are due to PARP inhibition. In the present study, the endotoxin induced PARP activation was dose dependently decreased with 4-40 mmol/l nicotinamide or 4-100 micro mol/l 6(5H) phenanthridinone, a specific PARP inhibitor. 6(5H)phenanthridinone however, failed to inhibit the proinflammatory cytokines. Thus, the mechanism behind the cytokine inhibition in our model seems not to be due to PARP inhibition. In conclusion, the present study could not only confirm previous reports of a down-regulatory effect on TNFalpha, but demonstrates that nicotinamide is a potent modulator of several proinflammatory cytokines. These findings demonstrate that nicotinamide has a potent immunomodulatory effect in vitro, and may have great potential for treatment of human inflammatory disease.

PMID: 12519385 [PubMed - indexed for MEDLINE]


 

Trends Pharmacol Sci. 2003 May;24(5):228-32.