Amyotrophic Lateral Sclerosis Treatments

Animal experiments indicate there are some promising potential treatments for amyotrophic lateral sclerosis. While there’s no true cure for ALS yet, some of these experiments show that new compounds and natural substances can treat symptoms and extend lifespan.

They include:

3-4 diaminopyridine

5-Hydroxytryptophan

5D10

Acetyl-L-Carnitine

Activated Protein C

AEOL 10150

AGS-499

AM-1241

Ammonium tetrathiomolybdate

Angiogenin

Arimoclomol

Ascorbate

Bee Venom

Caffeic Acid Phenethyl Ester

Cannabinol

Caprylic Triglyceride

Celastrol

CK-2017357

Clenbuterol

Colivelin

Creatine

Cyclosporine

D-Penicillamine

Dasatinib

Davunetide

Delta(9)-tetrahydrocannabinol

Dexpramipexole

Diallyl Trisulfide

Dichloroacetate

Dihydrotestosterone

Dimebon

DL-3-n-butylphthalide

DP-109

DP-460

Edaravone

EGb761 (Gingko Biloba Extract)

ENKAD

Epigallocatechin-3-gallate (EGCG)

Exendin-4

Fasudil

Folic Acid

Galactooligosaccharide

Gemals

Ginseng Root

GPI-1046

Granulocyte Colony Stimulating Factor

GSK-3 inhibitor VIII

Heat Shock Protein 70

Hepatocyte Growth Factor

HLA20

Iron Porphyrin

Ivermectin

Jiawei Sijunzi (JWSJZ)

L-745,870

L-arginine

Lead

Lenalidomide

Lipoic Acid

M30

Manganese Porphyrin

Melatonin

Memantine

Methionine Sulfoximine

Milk Whey Proteins

N-acetyl-L-cysteine

Nortriptyline

Olesoxime

Oxidized Galectin-1

P7C3A20

Pegfilgrastim

Phenylbutyrate

Pioglitazone

Polyamine-Modified Catalase

PRE-084

Progesterone

Pyruvate

Rasagiline

Recombinant Human Erythropoietin

Recombinant Human Insulinlike Growth Factor-I (rhIGF-I)

Resveratrol

Riluzole

Ro 28-2653

RPR 119990

S-adenosyl Methionine

S[+]-Apomorphine

Scolopendra Subspinipes Mutilans

Semapimod

SK-PC-B70M

Sodium Phenylbutyrate

Suppressor Factor

Talampanel

TAT-modified Bcl-X(L)

Tempol

Tianeptine

Trichostatin A

Trientine

TRO19622

Uridine

Vascular Endothelial Growth Factor

Vincristine

Vitamin D3

Vitamin E

VK-28

Wen-Pi-Tang

ZK 187638

References:

A dopamine receptor antagonist L-745,870 suppresses microglia activation in spinal cord and mitigates the progression in ALS model mice. http://www.ncbi.nlm.nih.gov/pubmed/18423451

A double-blind study of the effectiveness of cyclosporine in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/3281637

A phase II trial of talampanel in subjects with amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19961264

A pilot trial of memantine and riluzole in ALS: correlation to CSF biomarkers. http://www.ncbi.nlm.nih.gov/pubmed/20839903

Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells. http://www.ncbi.nlm.nih.gov/pubmed/19841542

Additive neuroprotective effects of a histone deacetylase inhibitor and a catalytic antioxidant in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16289867

AM1241, a cannabinoid CB2 receptor selective compound, delays disease progression in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16781706

Ammonium tetrathiomolybdate delays onset, prolongs survival, and slows progression of disease in a mouse model for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18617166

Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. http://www.ncbi.nlm.nih.gov/pubmed/15204022

An ALS mouse model with a permeable blood-brain barrier benefits from systemic cyclosporine A treatment. http://www.ncbi.nlm.nih.gov/pubmed/14756802

An attempt to inhibit the course of amyotrophic lateral sclerosis (ALS) by suppressor factor. http://www.ncbi.nlm.nih.gov/pubmed/8993772

Autophagy activation and neuroprotection by progesterone in the G93A-SOD1 transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23891729

Bee venom attenuates neuroinflammatory events and extends survival in amyotrophic lateral sclerosis models. http://www.ncbi.nlm.nih.gov/pubmed/20950451

Beneficial effect of ginseng root in SOD-1 (G93A) transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/11090864

Benefit of a combined treatment with trientine and ascorbate in familial amyotrophic lateral sclerosis model mice. http://www.ncbi.nlm.nih.gov/pubmed/10327155

Benefit of tianeptine and morphine in a transgenic model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16546757

c-Abl inhibition delays motor neuron degeneration in the G93A mouse, an animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23049975

Caffeic acid phenethyl ester extends survival of a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22206942

Cannabinol delays symptom onset in SOD1 (G93A) transgenic mice without affecting survival. http://www.ncbi.nlm.nih.gov/pubmed/16183560

Caprylic triglyceride as a novel therapeutic approach to effectively improve the performance and attenuate the symptoms due to the motor neuron loss in ALS disease. http://www.ncbi.nlm.nih.gov/pubmed/23145119

Celastrol blocks neuronal cell death and extends life in transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16909005

Chemotherapy delays progression of motor neuron disease in the SOD1 G93A transgenic mouse. http://www.ncbi.nlm.nih.gov/pubmed/15282441

Colivelin prolongs survival of an ALS model mouse. http://www.ncbi.nlm.nih.gov/pubmed/16564029

Combined riluzole and sodium phenylbutyrate therapy in transgenic amyotrophic lateral sclerosis mice. http://www.ncbi.nlm.nih.gov/pubmed/18618304

Control of motoneuron survival by angiogenin. http://www.ncbi.nlm.nih.gov/pubmed/19109488

Death receptor 6 (DR6) antagonist antibody is neuroprotective in the mouse SOD1(G93A) model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/24113175

Dexpramipexole effects on functional decline and survival in subjects with amyotrophic lateral sclerosis in a Phase II study: subgroup analysis of demographic and clinical characteristics. http://www.ncbi.nlm.nih.gov/pubmed/22985432

Dietary supplementation with S-adenosyl methionine delays the onset of motor neuron pathology in a murine model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19757209

Dietary vitamin D3 supplementation at 10× the adequate intake improves functional capacity in the G93A transgenic mouse model of ALS, a pilot study. http://www.ncbi.nlm.nih.gov/pubmed/22591278

Dihydrotestosterone ameliorates degeneration in muscle, axons and motoneurons and improves motor function in amyotrophic lateral sclerosis model mice. http://www.ncbi.nlm.nih.gov/pubmed/22606355

Dimebon slows progression of proteinopathy in γ-synuclein transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/22179976

DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22056419

Effect of nutritional supplementation with milk whey proteins in amyotrophic lateral sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/20464297

Effect of recombinant human insulin-like growth factor-I on progression of ALS. A placebo-controlled study. The North America ALS/IGF-I Study Group. http://www.ncbi.nlm.nih.gov/pubmed/9409357

Effect of sex on lifespan, disease progression, and the response to methionine sulfoximine in the SOD1 G93A mouse model for ALS. http://www.ncbi.nlm.nih.gov/pubmed/23217569

Effects of 3-4 diaminopyridine (DAP) in motor neuron diseases. http://www.ncbi.nlm.nih.gov/pubmed/21321491

Effects of an inhibitor of poly(ADP-ribose) polymerase, desmethylselegiline, trientine, and lipoic acid in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/11259130

Exendin-4 ameliorates motor neuron degeneration in cellular and animal models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22384126

Exogenous delivery of heat shock protein 70 increases lifespan in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18045911

Fasudil, a rho kinase inhibitor, limits motor neuron loss in experimental models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23763343

Folic acid protects motor neurons against the increased homocysteine, inflammation and apoptosis in SOD1 G93A transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/18436268

Galactooligosaccharide improves the animal survival and alleviates motor neuron death in SOD1G93A mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23673277

Gemals, a new drug candidate, extends lifespan and improves electromyographic parameters in a rat model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18428000

Glutamate AMPA receptors change in motor neurons of SOD1G93A transgenic mice and their inhibition by a noncompetitive antagonist ameliorates the progression of amytrophic lateral sclerosis-like disease. http://www.ncbi.nlm.nih.gov/pubmed/16323214

Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21711557

Granulocyte-colony stimulating factor improves outcome in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18835867

Identification and characterization of cholest-4-en-3-one, oxime (TRO19622), a novel drug candidate for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17496168

Inhibition of glycogen synthase kinase-3 suppresses the onset of symptoms and disease progression of G93A-SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17433298

Inhibition of p38 mitogen activated protein kinase activation and mutant SOD1(G93A)-induced motor neuron death. http://www.ncbi.nlm.nih.gov/pubmed/17346981

Intake of polyunsaturated fatty acids and vitamin E reduces the risk of developing amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16648143

Intracerebroventricular infusion of monoclonal antibody or its derived Fab fragment against misfolded forms of SOD1 mutant delays mortality in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/20345765

Intrathecal cyclosporin prolongs survival of late-stage ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/11251210

Intrathecal delivery of hepatocyte growth factor from amyotrophic lateral sclerosis onset suppresses disease progression in rat amyotrophic lateral sclerosis model. http://www.ncbi.nlm.nih.gov/pubmed/17984685

Investigation of the therapeutic effects of edaravone, a free radical scavenger, on amyotrophic lateral sclerosis (Phase II study). http://www.ncbi.nlm.nih.gov/pubmed/17127563

Iron porphyrin treatment extends survival in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/12641736

Ivermectin inhibits AMPA receptor-mediated excitotoxicity in cultured motor neurons and extends the life span of a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17045808

Late stage treatment with arimoclomol delays disease progression and prevents protein aggregation in the SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/18673445

Lead exposure stimulates VEGF expression in the spinal cord and extends survival in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/19914377

Lenalidomide (Revlimid) administration at symptom onset is neuroprotective in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19733563

Life span extension and reduced neuronal death after weekly intraventricular cyclosporin injections in the G93A transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15255263

Manganese porphyrin given at symptom onset markedly extends survival of ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/16049935

Mechano-growth factor, an IGF-I splice variant, rescues motoneurons and improves muscle function in SOD1(G93A) mice. http://www.ncbi.nlm.nih.gov/pubmed/19038252

Melatonin inhibits the caspase-1/cytochrome c/caspase-3 cell death pathway, inhibits MT1 receptor loss and delays disease progression in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23537713

Memantine prolongs survival in an amyotrophic lateral sclerosis mouse model. http://www.ncbi.nlm.nih.gov/pubmed/16262676

Methionine sulfoximine, an inhibitor of glutamine synthetase, lowers brain glutamine and glutamate in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/20060132

Modulation of astrocytic mitochondrial function by dichloroacetate improves survival and motor performance in inherited amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22509356

Motor neuronal protection by L-arginine prolongs survival of mutant SOD1 (G93A) ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/19427829

MRS study of the effects of minocycline on markers of neuronal and microglial integrity in ALS. http://www.ncbi.nlm.nih.gov/pubmed/20832222

Muscle-derived but not centrally derived transgene GDNF is neuroprotective in G93A-SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17034790

N-acetyl-L-cysteine improves survival and preserves motor performance in an animal model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/10943709

NAP (davunetide) modifies disease progression in a mouse model of severe neurodegeneration: protection against impairments in axonal transport. http://www.ncbi.nlm.nih.gov/pubmed/23631872

Neurochemical correlates of differential neuroprotection by long-term dietary creatine supplementation. http://www.ncbi.nlm.nih.gov/pubmed/16140286

Neuroprotective and neuritogenic activities of novel multimodal iron-chelating drugs in motor-neuron-like NSC-34 cells and transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19638399

Neuroprotective effect of oxidized galectin-1 in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15899257

Neuroprotective effects of (-)-epigallocatechin-3-gallate in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17021948

Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/10086395

Neuroprotective effects of diallyl trisulfide in SOD1-G93A transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21147075

Neuroprotective effects of the Sigma-1 receptor (S1R) agonist PRE-084, in a mouse model of motor neuron disease not linked to SOD1 mutation. http://www.ncbi.nlm.nih.gov/pubmed/24141020

Neuroprotective efficacy of aminopropyl carbazoles in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23027932

Nortriptyline delays disease onset in models of chronic neurodegeneration. http://www.ncbi.nlm.nih.gov/pubmed/17686041

Novel telomerase-increasing compound in mouse brain delays the onset of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22351600

Olesoxime delays muscle denervation, astrogliosis, microglial activation and motoneuron death in an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/22369784

Open Randomized Clinical Trial on JWSJZ Decoction for the Treatment of ALS Patients. http://www.ncbi.nlm.nih.gov/pubmed/24093046

Peroxisome proliferator-activated receptor-gamma agonist extends survival in transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15649489

Preliminary investigation of effect of granulocyte colony stimulating factor on amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19922135

Prevention of motor neuron degeneration by novel iron chelators in SOD1(G93A) transgenic mice of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21346313

Pyruvate slows disease progression in a G93A SOD1 mutant transgenic mouse model. http://www.ncbi.nlm.nih.gov/pubmed/17174029

Randomized double-blind placebo-controlled trial of acetyl-L-carnitine for ALS. http://www.ncbi.nlm.nih.gov/pubmed/23421600

Rasagiline alone and in combination with riluzole prolongs survival in an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/15372249

Recombinant human erythropoietin suppresses symptom onset and progression of G93A-SOD1 mouse model of ALS by preventing motor neuron death and inflammation. http://www.ncbi.nlm.nih.gov/pubmed/17439481

Reduced oxidative damage in ALS by high-dose enteral melatonin treatment. http://www.ncbi.nlm.nih.gov/pubmed/17014688

Regenerative therapies for amyotrophic lateral sclerosis using hepatocyte growth factor. http://www.ncbi.nlm.nih.gov/pubmed/22277532

Resveratrol upregulated heat shock proteins and extended the survival of G93A-SOD1 mice. http://www.ncbi.nlm.nih.gov/pubmed/23000195

RPR 119990, a novel alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid antagonist: synthesis, pharmacological properties, and activity in an animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11561094

S[+] Apomorphine is a CNS penetrating activator of the Nrf2-ARE pathway with activity in mouse and patient fibroblast models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23608463

Safety, tolerability and pharmacodynamics of a skeletal muscle activator in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22591195

Scolopendra subspinipes mutilans attenuates neuroinflammation in symptomatic hSOD1G93A mice. http://www.ncbi.nlm.nih.gov/pubmed/24168240

Selective up-regulation of the glial Na+-dependent glutamate transporter GLT1 by a neuroimmunophilin ligand results in neuroprotection. http://www.ncbi.nlm.nih.gov/pubmed/16274998

Sigma-1R agonist improves motor function and motoneuron survival in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/22935988

SK-PC-B70M alleviates neurologic symptoms in G93A-SOD1 amyotrophic lateral sclerosis mice. http://www.ncbi.nlm.nih.gov/pubmed/20971081

Tempol moderately extends survival in a hSOD1(G93A) ALS rat model by inhibiting neuronal cell loss, oxidative damage and levels of non-native hSOD1(G93A) forms. http://www.ncbi.nlm.nih.gov/pubmed/23405225

The CB2 cannabinoid agonist AM-1241 prolongs survival in a transgenic mouse model of amyotrophic lateral sclerosis when initiated at symptom onset. http://www.ncbi.nlm.nih.gov/pubmed/17241118

The Chinese prescription Wen-Pi-Tang extract delays disease onset in amyotrophic lateral sclerosis model mice while attenuating the activation of glial cells in the spinal cord. http://www.ncbi.nlm.nih.gov/pubmed/19252282

The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/9240414

The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice. http://www.ncbi.nlm.nih.gov/pubmed/16356650

The lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17630988

The matrix metalloproteinases inhibitor Ro 28-2653 [correction of Ro 26-2853] extends survival in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/16516196

The oral antidiabetic pioglitazone protects from neurodegeneration and amyotrophic lateral sclerosis-like symptoms in superoxide dismutase-G93A transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/16120782

The serotonin precursor 5-hydroxytryptophan delays neuromuscular disease in murine familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/14527871

Therapeutic benefit of polyamine-modified catalase as a scavenger of hydrogen peroxide and nitric oxide in familial amyotrophic lateral sclerosis transgenics. http://www.ncbi.nlm.nih.gov/pubmed/11117554

Therapeutic benefits of intrathecal protein therapy in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18543336

Therapeutic effects of clenbuterol in a murine model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16388902

Therapeutic effects of dl-3-n-butylphthalide in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22800896

Therapeutic efficacy of EGb761 (Gingko biloba extract) in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11665866

Treatment of amyotrophic lateral sclerosis with ribonucleotides. http://www.ncbi.nlm.nih.gov/pubmed/1266475

Treatment with arimoclomol, a coinducer of heat shock proteins, delays disease progression in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/15034571

Treatment with edaravone, initiated at symptom onset, slows motor decline and decreases SOD1 deposition in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/18718468

Treatment with trichostatin A initiated after disease onset delays disease progression and increases survival in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21712032

Uridine ameliorates the pathological phenotype in transgenic G93A-ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/20565334

Vascular endothelial growth factor prolongs survival in a transgenic mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/15389897

VEGF delivery with retrogradely transported lentivector prolongs survival in a mouse ALS model. http://www.ncbi.nlm.nih.gov/pubmed/15164063

Vitamin D deficiency and its supplementation in patients with amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23815870

Vitamin E intake and risk of amyotrophic lateral sclerosis: a pooled analysis of data from 5 prospective cohort studies. http://www.ncbi.nlm.nih.gov/pubmed/21335424

Vitamin E intake and risk of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15529299

Vitamin E serum levels and controlled supplementation and risk of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23286756

Amyotrophic Lateral Sclerosis Gene Therapy

Experiments in lab animals indicate gene therapy could extend lifespan in amyotrophic lateral sclerosis.

References:

AAV4-mediated expression of IGF-1 and VEGF within cellular components of the ventricular system improves survival outcome in familial ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/20859261

CNS-targeted viral delivery of G-CSF in an animal model for ALS: improved efficacy and preservation of the neuromuscular unit. http://www.ncbi.nlm.nih.gov/pubmed/21139572

Gene therapy of murine motor neuron disease using adenoviral vectors for neurotrophic factors. http://www.ncbi.nlm.nih.gov/pubmed/9095177

Increased survival and function of SOD1 mice after glial cell-derived neurotrophic factor gene therapy. http://www.ncbi.nlm.nih.gov/pubmed/12067438

Intraparenchymal spinal cord delivery of adeno-associated virus IGF-1 is protective in the SOD1G93A model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17963733

Intraspinal cord delivery of IGF-I mediated by adeno-associated virus 2 is neuroprotective in a rat model of familial ALS. http://www.ncbi.nlm.nih.gov/pubmed/19135533

Nerve injection of viral vectors efficiently transfers transgenes into motor neurons and delivers RNAi therapy against ALS. http://www.ncbi.nlm.nih.gov/pubmed/19344276

Neuroprotective effects of glial cell line-derived neurotrophic factor mediated by an adeno-associated virus vector in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/12177190

Rescue of amyotrophic lateral sclerosis phenotype in a mouse model by intravenous AAV9-ADAR2 delivery to motor neurons. http://www.ncbi.nlm.nih.gov/pubmed/24115583

Retrograde viral delivery of IGF-1 prolongs survival in a mouse ALS model. http://www.ncbi.nlm.nih.gov/pubmed/12907804

Therapeutic AAV9-mediated Suppression of Mutant SOD1 Slows Disease Progression and Extends Survival in Models of Inherited ALS. http://www.ncbi.nlm.nih.gov/pubmed/24008656

Viral delivery of antioxidant genes as a therapeutic strategy in experimental models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23732987

Virus-delivered small RNA silencing sustains strength in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15852369

Widespread spinal cord transduction by intrathecal injection of rAAV delivers efficacious RNAi therapy for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/24108104

Cell Therapy ALS Treatments

Cell transplants, including stem cell transplants, have shown some success in treating amyotrophic lateral sclerosis symptoms in lab animal experiments. There are even a few human experiments that have slowed the progression of the disease somewhat.

References:

A novel cell transplantation protocol and its application to an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/18691571

Autologous mesenchymal stem cells: clinical applications in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16808883

Bone marrow stem cell transplantation in amyotrophic lateral sclerosis: technical aspects and preliminary results from a clinical trial. http://www.ncbi.nlm.nih.gov/pubmed/21381286

Chimerization of astroglial population in the lumbar spinal cord after mesenchymal stem cell transplantation prolongs survival in a rat model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19267424

Combined immunosuppressive agents or CD4 antibodies prolong survival of human neural stem cell grafts and improve disease outcomes in amyotrophic lateral sclerosis transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/16644922

Direct muscle delivery of GDNF with human mesenchymal stem cells improves motor neuron survival and function in a rat model of familial ALS. http://www.ncbi.nlm.nih.gov/pubmed/18797452

Dose-dependent efficacy of ALS-human mesenchymal stem cells transplantation into cisterna magna in SOD1-G93A ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/19879334

Feasibility, safety, and preliminary proof of principles of autologous neural stem cell treatment combined with T-cell vaccination for ALS patients. http://www.ncbi.nlm.nih.gov/pubmed/22507681

Fetal olfactory ensheathing cells transplantation in amyotrophic lateral sclerosis patients: a controlled pilot study. http://www.ncbi.nlm.nih.gov/pubmed/18673377

Human mesenchymal stem cell transplantation extends survival, improves motor performance and decreases neuroinflammation in mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18586098

Human mesenchymal stromal cells ameliorate the phenotype of SOD1-G93A ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/17786603

Human umbilical cord blood treatment in a mouse model of ALS: optimization of cell dose. http://www.ncbi.nlm.nih.gov/pubmed/18575617

Intra-bone marrow-bone marrow transplantation slows disease progression and prolongs survival in G93A mutant SOD1 transgenic mice, an animal model mouse for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19686706

Intracerebroventricular injection of encapsulated human mesenchymal cells producing glucagon-like peptide 1 prolongs survival in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/22745655

Intraspinal injection of human umbilical cord blood-derived cells is neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22122965

Intrathecal transplantation of human neural stem cells overexpressing VEGF provide behavioral improvement, disease onset delay and survival extension in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/19626053

Intravenous mesenchymal stem cells improve survival and motor function in experimental amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22481270

Mesenchymal stromal cells prolong the lifespan in a rat model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21736505

Minimally invasive transplantation of iPSC-derived ALDHhiSSCloVLA4+ neural stem cells effectively improves the phenotype of an amyotrophic lateral sclerosis model. http://www.ncbi.nlm.nih.gov/pubmed/24006477

MR spectroscopy evaluation and short-term outcome of olfactory ensheathing cells transplantation in amyotrophic lateral sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/17305006

Multiple administrations of human marrow stromal cells through cerebrospinal fluid prolong survival in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19333801

Multiple intravenous administrations of human umbilical cord blood cells benefit in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/22319620

Neural stem cells LewisX+ CXCR4+ modify disease progression in an amyotrophic lateral sclerosis model. http://www.ncbi.nlm.nih.gov/pubmed/17439986

Positive effect of transplantation of hNT neurons (NTera 2/D1 cell-line) in a model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11922659

Safety and immunological effects of mesenchymal stem cell transplantation in patients with multiple sclerosis and amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/20937945

Short-term outcome of olfactory ensheathing cells transplantation for treatment of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17933231

Stem cell transplantation in amyotrophic lateral sclerosis patients: methodological approach, safety, and feasibility. http://www.ncbi.nlm.nih.gov/pubmed/23356668

Stem cell treatment in Amyotrophic Lateral Sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17582439

Stem-cell transplantation into the frontal motor cortex in amyotrophic lateral sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/19191058

Systemic transplantation of c-kit+ cells exerts a therapeutic effect in a model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/20650960

Systemic treatment with adipose-derived mesenchymal stem cells ameliorates clinical and pathological features in the amyotrophic lateral sclerosis murine model. http://www.ncbi.nlm.nih.gov/pubmed/23727509

Transient recovery in a rat model of familial amyotrophic lateral sclerosis after transplantation of motor neurons derived from mouse embryonic stem cells. http://www.ncbi.nlm.nih.gov/pubmed/19660174

Transplantation of human adipose tissue-derived stem cells delays clinical onset and prolongs life span in ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/24070071

Treatment of amyotrophic lateral sclerosis patients by autologous bone marrow-derived hematopoietic stem cell transplantation: a 1-year follow-up. http://www.ncbi.nlm.nih.gov/pubmed/19012065

Somatotype Heritability

Multiple studies, including twin studies, have estimated the heritability of body type or somatotype. The various estimates of heritability from these studies include:

88% to 97%: somatotype

86%: mesomorphy in men

82%: mesomorrphy in women

82%: endomorphy in girls

81%: ectomorphy in girls

80%: mesomorphy in boys

79%: mesomorphy in girls

76% to 89%: endormorphy in girls

70%: ectomorphy in women

68%: mesomorphy

66%: ectomorphy in men

57% to 76%: ectomorphy in girls

56%: ectomorphy

56%: endomorphy

55%: endomorphy

54%: ectomorphy

52%: mesomorphy

50%: endomorphy

46%: ectomorphy

45%: endomorphy in boys

44%: ectomorphy in boys

42%: mesomorphy

36% to 57%: mesomorphy in girls

References:

Evidence for higher heritability of somatotype compared to body mass index in female twins. http://www.ncbi.nlm.nih.gov/pubmed/17283387

Familial resemblance for physique: heritabilities for somatotype components. http://informahealthcare.com/doi/abs/10.1080/030144600419305

Genetic study on somatotype of child and adolescent twins in Han nationality. http://www.ncbi.nlm.nih.gov/pubmed/17313747

Heritability estimates of somatotype components based upon familial data. http://www.ncbi.nlm.nih.gov/pubmed/7358399

Heritability of somatotype components from early adolescence into young adulthood: a multivariate analysis on a longitudinal twin study. http://www.ncbi.nlm.nih.gov/pubmed/12881140

Heritability of somatotype components: a multivariate analysis. http://www.ncbi.nlm.nih.gov/pubmed/17342076

Heritability of the somatotype components in Biscay families. http://www.ncbi.nlm.nih.gov/pubmed/17570368

Twin resemblance in somatotype and comparisons with other twin studies. http://www.ncbi.nlm.nih.gov/pubmed/8026815

Self Compassion Meditation

Research on self compassion shows it’s much more effective than self-esteem. It’s even more powerful than mindfulness. This is an example of a self compassion meditation exercise:

1. Begin focusing on your breathing.

2. Begin to slow down your breathing by extending the duration of inhalation and exhalation.

3. Think of the idea that making mistakes in life is natural. Even people who seem to have it all still make mistakes.

4. Think of how humanity is united by people pursuing similar goals in life and having similar emotions.

5. Express compassion towards yourself in the same way you would express compassion towards a close friend or someone you love and care for. If you don’t have anyone like that in your life, imagine what those feelings might feel like directed towards yourself.

Microbiome Experiment Results

For the last month I’ve been eating mostly dark chocolate, kefir, whey, chicken, berries, and sometimes green tea. The dark chocolate and green tea acted as prebiotics. The kefir had twelve different strains of probiotic bacteria in it. The whey and berries have shown success in intestinal repair in experiments. The chicken was a neutral source of protein.

A sample meal plan looked like:

Breakfast: 85% cocoa dark chocolate, green tea

Lunch: kefir, chicken

Snack: protein shake made of whey, kefir, and berries

Dinner: chicken

Here are some results of this self-experiment based on the four primary indicators mentioned in my post Microbiome Experiment Update:

1. Does this reduce body fat, especially torso fat?

I still have more fat to lose but I’m beginning to feel like a svelte jungle cat. This high protein diet of kefir and chicken has helped reduce my appetite. Having a specific list of foods to eat has helped prevent food binges. I’m not eating four hamburger patties with cheese and following that up with a big bag of corn chips like I used to do. This eating plan has reduced my intake of calories, carbohydrates, and omega-6 fats. A study involving mice shows that eating probiotics can lead to a “glow of health” and better appearance, even in aged animals. This alone is a good reason to keep eating fermented foods.

2. Does this reduce digestive pain?

Eating dark chocolate in the morning makes me feel queasy. On the plus side, that helps me suppress my appetite. The downside is that nausea doesn’t feel very enjoyable. I only eat it in the morning because I don’t want it to keep me awake or cause acid reflux at night. This is a high protein / moderate carb / low fat diet overall and I’ve noticed less digestive pain than when I was eating a high fat diet. A high intake of dietary fat is associated with dyspepsia, gastroesophageal reflux, or irritable bowel symptoms in some people with gastrointestinal problems. I wonder if meditating before and after mealtimes could reduce stress-related digestive problems, especially when eating meals high in fat.

3. Does this reduce psychological stress?

The brain-gut axis is involved in stress responses, but I feel like I still need pharmaceuticals to treat fear and anxiety. The microbiome may impact the GABA system in the brain, but in my experience changing the microbiome isn’t as fast or as effective as using benzodiazepines for treating anxiety. Food can affect mood. Every diet ranging from carnivorous to vegan has testimonials from people who claim a particular diet cured their depression or anxiety. Maybe it worked for them, but those people need to realize that diet alone may not be enough to fully treat patients with emotional problems and functional abdominal pain dating back to childhood, even though it may be helpful in reducing some symptoms.

I had some cheat meals that I regretted that may have negatively impacted this experiment. This experiment would have been easier to do if my life had less stress, instead of living in fear every day like I do. The microbiome may have more powerful effects on the brain during development and probiotics may be less effective in reducing anxiety once a person reaches adulthood, but that’s just my hypothesis.

4. Does this maintain strength?

The high level of protein and sufficient carbs are effective for maintaining strength and energy. I had the same amount of strength when lifting weights in the gym as I did on my previous high fat high carb diet. Protein is also helpful for redistributing body composition away from body fat and towards muscle.

The following metrics would be useful to measure if anyone wants to conduct a formal clinical study involving multiple participants:

1. Accurate measurement of body composition before and after the experiment

2. Questionnaires to measure irritable bowel symptoms and abdominal pain

3. Self-report inventories to measure mood and stress

4. DNA sequencing to analyze the human microbiome before and after

Obesity Heritability

These studies estimate heritability of body mass index and obesity. These findings come from multiple studies, including twin studies. They estimate the variation in a trait attributable to genetic factors (as opposed to shared environmental or unique environmental factors). These heritability estimates for body mass index are very high. There’s still no such thing as free will. Choice doesn’t exist and people aren’t responsible for their actions.

Heritability Estimates:

94%: BMI among pre-menopausal women

89%: BMI

88%: somatotype in females

86%: obesity in females

84%: BMI in males

82%: childhood BMI

82%: BMI attributable to additive genetic effects

82%: BMI in females

82%: genetic component of regional fat percentages

80%: BMI in males

80%: interindividual variation of BMI

79%: BMI in twins reared apart

79%: BMI in males

79%: BMI in females

78%: BMI in females

78%: BMI at age 11

78%: BMI

81%: weight in males

77%: current body weight

77%: BMI

77%: waist circumference

75%: BMI

75% to 86%: BMI

75% to 80%: phenotypic variation in percent body fat

75% to 78%: BMI

73%: body surface area

73%: skinfolds in males

73%: obesity

73%: weight unrelated to height in females

72%: BMI in males

71%: female waist circumference

71%: maximum BMI

70%: BMI in males

70%: variance in abdominal fat

70%: trend in adult weight gain

68%: weight

66%: BMI in males

64%: variance in obesity in males

63% to 69%: middle age BMI

61% to 87%: BMI among 11 to 12 year olds

61%: waist circumference among post-menopausal women

61%: metabolic syndrome

60% to 70%: BMI and obesity

60%: emotional eating

59% to 70%: BMI

56% to 73%: body composition

References:

A genetic analysis of relative weight among 4,020 twin pairs, with an emphasis on sex effects. http://www.ncbi.nlm.nih.gov/pubmed/7957015

A population-based twin study on sleep duration and body composition. http://www.ncbi.nlm.nih.gov/pubmed/21869757

A QTL genome scan of the metabolic syndrome and its component traits. http://www.ncbi.nlm.nih.gov/pubmed/14975164

A twin study of human obesity. http://www.ncbi.nlm.nih.gov/pubmed/3712713

A twin study of sleep duration and body mass index. http://www.ncbi.nlm.nih.gov/pubmed/20191932

Body weight in the Finnish Twin Cohort. http://www.ncbi.nlm.nih.gov/pubmed/2286148

Childhood obesity: genetic and environmental overlap with normal-range BMI. http://www.ncbi.nlm.nih.gov/pubmed/18421262

Distribution and heritability of BMI in Finnish adolescents aged 16y and 17y: a study of 4884 twins and 2509 singletons. http://www.ncbi.nlm.nih.gov/pubmed/10078843

Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment. http://www.ncbi.nlm.nih.gov/pubmed/18258631

Evidence for higher heritability of somatotype compared to body mass index in female twins. http://www.ncbi.nlm.nih.gov/pubmed/17283387

Evidence for independent genetic influences on fat mass and body mass index in a pediatric twin sample. http://www.ncbi.nlm.nih.gov/pubmed/10390261

Evidence of genetic influence on central body fat in middle-aged twins. http://www.ncbi.nlm.nih.gov/pubmed/2767669

Evidence of shared genetic effects between pre- and postobesity epidemic BMI levels. http://www.ncbi.nlm.nih.gov/pubmed/19876002

Finding the missing heritability in pediatric obesity: the contribution of genome-wide complex trait analysis. http://www.ncbi.nlm.nih.gov/pubmed/23528754

Genetic and environmental contributions to BMI in adolescent and young adult women. http://www.ncbi.nlm.nih.gov/pubmed/19165159

Genetic and environmental contributions to obesity and binge eating. http://www.ncbi.nlm.nih.gov/pubmed/12655626

Genetic and environmental correlations between obesity and body fat distribution in adult male twins. http://www.ncbi.nlm.nih.gov/pubmed/8026816

Genetic and environmental influences on adiponectin, leptin, and BMI among adolescents in Taiwan: a multivariate twin/sibling analysis. http://www.ncbi.nlm.nih.gov/pubmed/18828732

Genetic and environmental influences on BMI from late childhood to adolescence are modified by parental education. http://www.ncbi.nlm.nih.gov/pubmed/21996670

Genetic and environmental influences on eating behavior: the Swedish Young Male Twins Study. http://www.ncbi.nlm.nih.gov/pubmed/15755823

Genetic and environmental influences on insomnia, daytime sleepiness, and obesity in twins. http://www.ncbi.nlm.nih.gov/pubmed/16774154

Genetic effects on obesity assessed by bivariate genome scan: the Mexican-American coronary artery disease study. http://www.ncbi.nlm.nih.gov/pubmed/16899800

Genetic factors in self-reported snoring and excessive daytime sleepiness: a twin study. http://www.ncbi.nlm.nih.gov/pubmed/11587976

Genetic influences on adult weight gain and maximum body mass index in male twins. http://www.ncbi.nlm.nih.gov/pubmed/7942773

Genetic influences on central abdominal fat: a twin study. http://www.ncbi.nlm.nih.gov/pubmed/8856394

Genetic influences on growth traits of BMI: a longitudinal study of adult twins. http://www.ncbi.nlm.nih.gov/pubmed/18239571

Heritability of determinants of the metabolic syndrome among healthy Arabs of the Oman family study. http://www.ncbi.nlm.nih.gov/pubmed/17372303

Heritability of eating behavior assessed using the DEBQ (Dutch Eating Behavior Questionnaire) and weight-related traits: the Healthy Twin Study. http://www.ncbi.nlm.nih.gov/pubmed/19876000

Heritability of plasma leptin levels: a twin study. http://www.ncbi.nlm.nih.gov/pubmed/10100090

Increasing genetic variance of body mass index during the Swedish obesity epidemic. http://www.ncbi.nlm.nih.gov/pubmed/22087252

Increasing heritability of BMI and stronger associations with the FTO gene over childhood. http://www.ncbi.nlm.nih.gov/pubmed/18846049

Linkage analysis of obesity phenotypes in pre- and post-menopausal women from a United States mid-western population. http://www.ncbi.nlm.nih.gov/pubmed/21062459

No linkage to obesity in candidate regions of chromosome 2 and 10 in a selected sample of Swedish twins. http://www.ncbi.nlm.nih.gov/pubmed/12724003

Physical activity reduces the influence of genetic effects on BMI and waist circumference: a study in young adult twins. http://www.ncbi.nlm.nih.gov/pubmed/19048013

Stable genes and changing environments: body mass index across adolescence and young adulthood. http://www.ncbi.nlm.nih.gov/pubmed/20087641

The genetics of middle-age spread in middle-class males. http://www.ncbi.nlm.nih.gov/pubmed/15607010

The heritability of body mass index among an international sample of monozygotic twins reared apart. http://www.ncbi.nlm.nih.gov/pubmed/8782724

Total and regional fat distribution is strongly influenced by genetic factors in young and elderly twins. http://www.ncbi.nlm.nih.gov/pubmed/16421348