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Supplements and Drugs for ALS

als pterostilbene cape

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#1 tham

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Posted 14 January 2013 - 11:06 PM

Memantine prolongs survival in an amyotrophic lateral sclerosis mouse model.


Combined lithium and valproate treatment delays disease onset, reduces neurological
deficits and prolongs survival in an amyotrophic lateral sclerosis mouse model.


Sodium phenylbutyrate prolongs survival and regulates expression of anti-apoptotic
genes in transgenic amyotrophic lateral sclerosis mice.


Phase 2 study of sodium phenylbutyrate in ALS.


Combined riluzole and sodium phenylbutyrate therapy in transgenic a
myotrophic lateral sclerosis mice.


Resveratrol, esculetin, CAPE.

CAPE is found in propolis. The New Zealand manuka product, Bio 30,
is a popular source of CAPE. Yvonne Foong, the Malaysian NF2 girl, has
been taking it for some time and she mentioned it is helping to suppress her tumors.


An in vitro screening cascade to identify neuroprotective antioxidants in ALS.

As expected -

" ..... although the in vitro studies have mostly been successful, they often require
high doses of resveratrol and in vivo studies have shown rapid metabolism and
failed to detect resveratrol in the CNS. Taken together, this suggested that
resveratrol is unlikely to be effective in vivo. "


As noted in the blueberries thread, pterostilbene way outperforms resveratrol when
it comes to bioavailabity, far longer half-life, and penetrating the blood brain barrier,
so it would likely be a good alternative.



Edited by tham, 14 January 2013 - 11:15 PM.

#2 tham

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Posted 15 January 2013 - 01:25 PM

As speculated, octacosanol has benefit in ALS.

"ALS Support Regimen"


However, it is not advised to go on BCAAs and L-threonine due to
unexpected adverse effects.

" The estimated decline in FVC was about 2.5 times greater in the BCAA
and L-threonine groups as compared to placebo. "


" There was an excess mortality in subjects randomized to
active treatment (24 BCAA, 13 placebo) "


Creatine would be preferable to BCAAs.

Neuroprotective effects of creatine.


Despite failures in later trials, coenzyme Q10 is still worth trying.


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#3 tham

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Posted 15 January 2013 - 11:35 PM

3nB, from celery.

Natural Factors's celery appears to be the only one standardized for 3nB.


Therapeutic effects of dl-3-n-butylphthalide in a transgenic mouse model of
amyotrophic lateral sclerosis.


DL-3-n-butylphthalide extends survival by attenuating glial activation in a
mouse model of amyotrophic lateral sclerosis.


The clinical analysis of Dl-3-budylphthalinde for cognitive function in chronic
cerebral circulation insufficiency




Blocking IL-1beta to slow down progression of ALS ?


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#4 tham

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Posted 17 January 2013 - 11:20 AM

Corrected link for the study on Co Q10 above.


Mitochondrial approaches for neuroprotection


Magnetic Resonance Spectroscopy of Regional Brain Metabolite Markers
in FALS Mice and the Effects of Dietary Creatine Supplementation


#5 tham

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Posted 17 January 2013 - 11:29 AM

Supplements which block IL-1beta :

Caffeic acid / CAPE

Fish oil
Resveratrol / pterostilbene
Ellagic acid

Ursolic acid
Olive oil / extracts
White wine


Nettle leaf, urtica dioca.



Drugs :



Pentoxifylline, however, was disappointing, despite the fact that it blocks TNF alpha,
IL-1beta and IL-6.

Pentoxifylline in ALS: a double-blind, randomized, multicenter, placebo-controlled trial.


#6 tham

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Posted 17 January 2013 - 10:39 PM

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

" There were significantly higher numbers of motor neurons in the lumbar spinal
cord of mice on a caprylic triglyceride diet than those on control diet (23.96
vs. 14.61) and the treatment returned the motor neuron count to that found in
WT mice of the same age. "

" ..... transgenic animals fed caprylic triglyceride showed significant improvement
in the clinical signs of ALS and in motor neuron survival in the spinal cord. The
improvement of motor performance in caprylic triglyceride-treated animals was
accompanied by significantly more motor neurons preserved in the spinal cord at
the end stage of disease. These findings are similar to our previously reported
findings in G93A transgenic mice fed a ketogenic diet as well as the R6/2 1J
Huntington's disease model. "

" ..... animals treated with caprylic triglyceride did not have a prolonged life span as
compared to the control group, possibly due to the fact that the treatment did not
result in increased serum triglyceride/cholesterol level. "


" Coconut Oil Reverses Amyotrophic Lateral Sclerosis "


" ALS Patient two year update on coconut oil and magnesium chloride "


Patients with elevated triglyceride and cholesterol serum levels have a
prolonged survival in amyotrophic lateral sclerosis.

" We found a median prolonged life expectancy by 14 months for patients with
serum triglyceride levels above the median of 1.47 mmol/l. (130 mg/dl). "


Lower serum lipid levels are related to respiratory impairment in patients with ALS.


Dyslipidemia is a protective factor in amyotrophic lateral sclerosis.

" Correlation studies demonstrated that bearing an abnormally elevated LDL/HDL ratio
significantly increased survival by more than 12 months. "


#7 Logic

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Posted 18 January 2013 - 10:52 AM

Low dose Naltrexone may be worth looking into



#8 tham

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Posted 18 January 2013 - 03:34 PM

Low dose naltrexone doesn't seem very impressive with these patients.


Thalidomide was also disappointing, but the derivative, lenalidomide,
appears more promising, though it costs a bomb.

Efficacy of thalidomide for the treatment of amyotrophic lateral sclerosis:
a phase II open label clinical trial.


Thalidomide causes sinus bradycardia in ALS.


Lenalidomide (Revlimid) administration at symptom onset is neuroprotective in a
mouse model of amyotrophic lateral sclerosis.


Thalidomide and lenalidomide extend survival in a transgenic mouse
model of amyotrophic lateral sclerosis.


TNF-alpha inhibition as a treatment strategy for neurodegenerative
disorders: new drug candidates and targets.


Says here generic lenalidomide from India costs some $30 per 25 mg capsule.

The originals costs in the region of several hundred to a thousand dollars each ?


#9 tham

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Posted 18 January 2013 - 04:13 PM

From the same researchers who studied caprylic acid.

A ketogenic diet as a potential novel therapeutic intervention
in amyotrophic lateral sclerosis.

" KD fed mice lost 50% of baseline motor performance 25 days later than
disease controls. KD animals weighed 4.6 g more than disease control
animals at study endpoint; the interaction between diet and change in
weight was significant (p = 0.047). In spinal cord sections obtained at
the study endpoint, there were more motor neurons in KD fed animals. "


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#10 tham

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Posted 20 January 2013 - 04:22 AM

This Chinese hospital seems to be having good results treating ALS.




Edited by tham, 20 January 2013 - 04:23 AM.

#11 tham

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Posted 21 January 2013 - 12:25 AM

This person, David Anderson, went to the Zhongfang hospital for treament.
He appeared to have stabilized or improved somewhat initially. However
he stayed for too short a time, just three months from Jan to March 2011,
and his condition appeared to have deteriorated after that.


#12 tham

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Posted 26 January 2013 - 10:05 AM

Escelutin, one of the three screened in the earlier study.

An in vitro screening cascade to identify neuroprotective antioxidants in ALS.


Escelutin is a metabolite of escin, or aescin, the flavonoid found in horse chestnut,
or aesculus hippocastanum. Escin is commonly found in hemorrhoid creams and
formulas for hemorrhoids and varicose veins, as well as creams/gels for bruises and
hematomas, since horse chestnut improves venous insufficiency.

I'm no biochemist, but I believe the cascade is :

Escin > Esculin > Esculetin

You can't find esculetin as a supplement. However, a check shows that there
are manufacturers in China, though they supply it only in bulk.


#13 tham

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Posted 28 January 2013 - 09:35 AM

Whey protein.










CDP choline.






#14 tham

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Posted 28 January 2013 - 10:13 AM

This would emphasize that 5-HTP and SAMe should be the first supplements to
be included in any ALS protocol.

The serotonin precursor 5-hydroxytryptophan delays neuromuscular
disease in murine familial amyotrophic lateral sclerosis.

" 5-HT may be pivotal to the pathogenesis and therapy of ALS.
Furthermore, cerebrospinal fluid levels of tryptophan, a precursor of 5-HT, are
decreased in patients with ALS and plasma concentrations of tryptophan are also
decreased with the lowest levels found in the most severely affected patients. "

" Furthermore, 5-HT is a precursor of melatonin, which inhibits glutamate release
and glutamate-induced neurotoxicity.

" Thus, progressive degeneration of 5-HT neurons affecting motoneuron activity
constitutes the prime mover of the disease and its progression and treatment
of ALS needs to be focused primarily on boosting 5-HT functions. "

" .... the 5-HT precursor 5-hydroxytryptophan (5-HTP) improved locomotor function
and survival of transgenic SOD1 G93A mice, an animal model of ALS.


Platelet Serotonin Level Predicts Survival in Amyotrophic Lateral Sclerosis

" Platelet serotonin levels were significantly decreased in ALS patients. Platelet serotonin
levels did not correlate with disease duration but were positively correlated with survival
of the patients. Univariate Cox model analysis showed a 57% decreased risk of death for
patients with platelet serotonin levels in the normal range relative to patients with
abnormally low platelet serotonin. This protective effect remained significant after
adjustment with age, gender or site of onset in multivariate analysis. "

" The positive correlation between platelet serotonin levels and survival strongly
suggests that serotonin influences the course of ALS disease. "

i) Platelet serotonin levels are significantly decreased in ALS patients relative to
matched controls, and

(ii) Platelet serotonin level is a significant predictor of survival independent of age.

" Number of neurologic and psychiatric conditions, including Alzheimer's disease,
are associated with decreases of the serotonergic system either centrally or in
platelets or both
. A similar decrease in serotonin has been described in frontotemporal
dementia, which is now thought to form a continuum with ALS

" A more attractive hypothesis is a relationship between serotonin and energy
metabolism. Serotonin modulates energy homeostasis through complex and
still incompletely characterized mechanisms. "

" A large number of ALS patients as well as transgenic ALS mice show increased
energy expenditure, a phenotype which appears analogous to the effects of a
chronic depletion in brain-derived serotonin.


The serotonin precursor 5-hydroxytryptophan delays neuromuscular
disease in murine familial amyotrophic lateral sclerosis.


Amyotrophic lateral sclerosis: changes of noradrenergic and
serotonergic transmitter systems in the spinal cord.

" Since lack of the facilitatory monoaminergic (serotonin, noradrenaline, dopamine) influence
would necessitate an increase in the excitatory (glutamate, NMDA) potentially neurotoxic
glutamatergic input onto the motoneurones, we hypothesize that this could contribute to the
progressive loss of spinal motoneurones in amyotrophic lateral sclerosis.


Degeneration of serotonergic neurons in amyotrophic
lateral sclerosis: a link to spasticity


" Two supplements are recommended, 5-HTP and SAMe. The SAMe is an amino acid
which boosts serotonin and dopamine levels. It is considered as effective as prescribed
medications. The 5-HTP serves as an anti-depressant as it is a support for the
antidepressant neuro-transmitter, serotonin.

Dosage: Daily; 200-400 mg 5-HTP [divided] and 400-800 mg of the SAMe [divided]. "


Edited by tham, 28 January 2013 - 10:29 AM.

#15 tham

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Posted 27 May 2013 - 01:46 PM

" Chronic bacterial and viral infections that invade the brain have been found
at high incidence in ALS patients ..... 85% of ALS patients (and 100% of Gulf War
veterans with ALS
) have bacterial infections caused by Mycoplasma species
.... neurotrophic viruses such as the Echo-7 enteroviruses are found in most
ALS patients
, and these viruses could cause cell death to infected cells. "

http://www.immed.org...e diseases.html

Experimental Clinical Study on ALS Infections High Frequency of Systemic
Mycoplasmal Infections in Gulf War Veterans and Civilians with Amyotrophic
Lateral Sclerosis (ALS)

" Mycoplasmas have also been documented to be able to penetrate into the CNS
and cause neurological signs. In addition to bacterial infections, chronic illness
patients also have viral infections. "

" In ALS patients enteroviruses (EV) have been found. EV are small, encapsulated
RNA viruses that have been associated with acute syndromes such as upper respiratory
infections, exanthmas, myocarditis, pleuritis, pancreatitis and aseptic meningitis. "

" In addition, EV are neurotropic and can persist in the CNS. Several scenarios
can be envisaged by which a CNS virus infection could cause, at least in part, the
pathology observed in ALS. "

" Recent studies indicate that cell death following virus infection is often apoptotic and
that neurons, unlike most other cells, are relatively resistant to apoptosis following
virus infection.
This can result in virus persistence, which may or may not be
productive and has been shown to be capable of causing neuronal dysfunction and
eventually death
. "

" Most recently, a study from France showed that EV RNA was present from spinal
cord samples from 15/17 ALS patients. Our data supports the finding of EV
sequences in ALS patient's blood along with mycoplasma sequences
. "

" Also, in 22/25 civilians from USA and England we have found mycoplasmal
infections, most were positive for M. fermentans ; "

" The possible reason that not all researchers have found EV in ALS patients
is that very sensitive and specific methods must be used, and inhibitors of the
PCR reaction must be removed
. "

" Mycoplasmas can hide intra-cellularly, unlike common bacteria which typically
exist inter-cellularly. They cause no inflammatory response so the sed-rate/ESR
diagnostic assay will show negative.
Mycoplasmas can evade detection by conventional
laboratory diagnostic assays that attempt to culture these pathogens and they
escape the immune system by antigenic surface variation and molecular mimicry
. "

" As mycoplasmas do not trigger an elevated white blood cell count, systemic
mycoplasma infection will not show on a routine complete blood count (CBC) used
to determine elevated white blood cells typically associated with a bacterial infection
. "

" Uninformed physicians may diagnose virus as there is no elevated white blood cell
count and antibody tests can result negative in early stages of infection.
Viral infection
can't be helped by antimicrobials but if the true problem is mycoplasmal infection this
can be treated with long-term antibiotic therapy. "


#16 tham

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Posted 27 May 2013 - 09:02 PM

" Mycoplasmas require specialized environments to be cultured. They grow well
at high-altitude/low-pressure conditions and will otherwise culture false-negative.
Only polymerase chain reaction (PCR) testing, otherwise known as dna-amplification
or dna-probe is sensitive enough to ascertain mycoplasma infections reliably
. A
positive test confirms the presence of live mycoplasma genome and active infection. "

" As well as testing for Mycoplasma infection it is advisable to also test for
Rickettsiae, Chlamydia, IL2 and IL6. "

" Mycoplasmas can cause numerous and various pathogenic mechanisms including
extragenital systemic infection, production of super antigens, abnormal stimulation of
cytokines such as interleukin-2, generation of toxic oxygen radicals contributing to
oxidative stress observed in infected individuals (antioxidants can help), development
of lesions in the heart, liver, kidneys, and other organs, induction of apoptosis
(programmed cell death), aphthous ulcerations, thrombocytopenia, central nervous
system disease
, problems with cell-mediated immunity, and numerous other
destructive actions. "

" Mycoplasmas can target the host white blood cells (lymphocytes/WBC) for intracellular
infection, and these cells have the unique ability to cross the blood-brain barrier over into
the spinal fluid and thereby carry infection into the host central nervous system (CNS).
Once inside the CNS, mycoplasmas have been reported to activate the CNS
hypothalamus/pituitary/adrenal axis
. "

" Mycoplasmas interact with the lymphoreticular system as they are immunomodulating
pathogens that can compromise cellular immunity (T-lymphocytes). T-Suppressors (T8)
will move towards a high index when infected with mycoplasma hominis and T-Killers
(T3) will decrease due to mycoplasmosis. Natural killer cell function deteriorates as a
result of extended systemic mycoplasma infection.

" The antibody response may not be measurable during systemic mycoplasma infection
until a patient is nearing death
. This is because mycoplasmas can evade detection by
the immune system
(and thereby cause a characteristically chronic illness) through
various mechanisms including antigenic surface variation and molecular mimicry. "

" Some mycoplasmas are being detected with unusual DNA sequences, such as the
HIV-1 envelope gene which codes for a surface glycoprotein, gp120, involved in
pathogen attachment and entry into cells. "

If this is the case, then EGCG, which blocks gp120, would be the supplement to take :


" The onset of mycoplasma infection can be insidious and/or localized depending on
the particular mycoplasma subtype and isolate involved. "

* The chronic clinical picture can include central nervous system disease .... "

* A typical symptom of systemic mycoplasma infection, resulting from abnormal stimulation
of cytokines, involves a chronic red discoloration of the anterior pharyngeal pillars. Stand in
front of a mirror with your mouth open wide. Point a flash-light into the mirror so that the
beam reflects back into your pharynx. On either side of your throat, behind the molars and
in front of the tonsils, the crescents may be an intense crimson color along the margins
of both pharyngeal pillars.
In patients without tonsils, the crimson crescents would appear
further back. "

* Overcoming systemic mycoplasma infection will depend on the characteristics of the
specific mycoplasma involved, and many cases will respond to combined antibiotic/steroid
treatment, naturopathic treatment and avoidance of stress and certain foods. "

* Where a mycoplasma pathogen targets host white blood cells for infection, the disease
can initiate a vicious cycle of immunological dysregulation where the lymphocytes actually
start replicating and attacking themselves for being infected with the immunomodulating
mycoplasmas. In order to break the vicious cycle combined antibiotic/steroid treatment
protocols can be used. "

" Chloramphenicol is a preferred antibiotics for treatment of systemic mycoplasma
infections. Other antibiotics that have demonstrated efficacy against extragenital
mycoplasma infections include doxycycline, minocycline, zithromax (azithromycin),
rifampin (rifampicin, the TB drug), gentamicin, the lincosamides, trovafloxacin (
for M. hominis) and sparfloxacin
. "

However, I would not prefer to use chloramphenicol due to a risk of aplastic anemia.
One of second/third generation quinolones such as ciprofloxacin and levofloxacin,
or macrolides like azithromycin, would be preferred.

" Mycoplasma shares similar capabilities to viruses in that it can recode DNA and even
alter its own characteristics,
which is why it is so compatible with viral proteins. "

" Penicillins are contraindicated and will actually exacerbate the clinical picture since
mycoplasmas have no cell-wall
. "

" In addition to their role between mycoplasma infection and the endocrine system,
some steroids suppress the production of white blood cells and thereby starve
some mycoplasmas
. "

" Cholesterol and the amino acid arginine (commonly found in chocolate) stimulate growth
of mycoplasmas
and should be avoided, although Mycoplasma hominis characteristically
produces arginine so avoidance of arginine rich foods may not help in this case. "

The following common antibiotic protocols, all 6-week cycles repeated several times,
are mentioned :

Doxycycline, 200 mg a day
Ciprofloxacin, 1,500 mg a day
Azithromycin, 500 mg a day


#17 tham

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Posted 27 May 2013 - 09:58 PM

Determination of systemic infections due to Mycoplasma in patients
with clinically defined amyotrophic lateral sclerosis.

" This indicates that the risk of suffering from ALS, if the PCR test for
Mycoplasma sp. is positive, is 8:1
. "


Lyme disease serology in amyotrophic lateral sclerosis.

" Lyme disease was rare in 414 patients with ALS and is not likely to be causative. "


Garenoxacin, the Japanese fourth generation quinolone, is highly active, with a
high safety profile, against mycoplasmas. However, it had been withdrawn from
the US and European markets due to licensing problems.


" Subsequent oral challenge tests for garenoxacin, which showed negative skin
test results, confirmed that garenoxacin was well tolerated. "


" GRN did not produce class adverse effects of fluoroquinolones such as QTc
prolongation, blood glucose abnormality or severe liver damage.


Gemifloxacin, developed by LG, the Korean group.


Inhibitory and bactericidal activities of gemifloxacin and other antimicrobials
against Mycoplasma pneumoniae.


In vitro activity of gemifloxacin (SB 265805; LB20304a) against human mycoplasmas.



" .... sharing the highest activity with garenoxacin and gemifloxacin against mycoplasmas.
Moxifloxacin killed the 30 mycoplasma isolates tested at a concentration </=1 mg/L,
except those resistant to fluoroquinolone. "


In Vitro Activities of the Newer Quinolones Garenoxacin, Gatifloxacin,
and Gemifloxacin against Human Mycoplasmas.


Thus, third/fourth generation quinolones against mycoplasmas, in order of choice :

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#18 tham

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Posted 30 May 2013 - 01:21 PM

The full text of Garth Nicolson's study above.

High Frequency of Systemic Mycoplasmal Infections in Gulf War
Veterans and Civilians with Amyotrophic Lateral Sclerosis .

http://mx1.ocimc.com...CN-ALS 2002.pdf

#19 steenblock

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Posted 23 June 2013 - 04:16 PM

great review of supplements and drugs for ALS!!! Thank you!! Here is my response to a patient with ALS. I use also a few of these supplements you mention here as well.

Hi, I have a youtube video that explains my current thinking as to the cause of ALS. In a nutshell it is related to a combination of factors. 1) gut dysbiosis including yeast, heavy metal poisoning, and clostridia 2)any other infection that upregulates TNF-alpha and gamma interferon 3)a spinal nerve impingement and Degenerative joint disease in that same area of the spine 3)orally acquired prions? This last one is harder to define but the majority of ALS patients do have it and this makes the most sense as to its migration up and down the spine.
Treatment is 1) treatment of the bacteria, yeast and heavy metals 2) treatment of the inflammation of the spinal nerve area -in your case probably your cervical spine ct scan shows DJD and perhaps spinal stenosis at C4-C5. I usually treat this with direct injections of stem cells into the affected spine. 3)intravenous stem cells. Generally with this program you are much much better within 2-3 weeks. Look at the video, look at your CT exam. I recommend a CDSA (comprehensive stool test) from Doctor's Data, a quantitative urine organic analysis from the Great Plains Lab, and a heavy metal challenge test using DMSA with a 6 hour urine sample sent to Doctor's data. If you are choking and aspirating I recommend we treat first and work on all of the causes later rather than before. If you are in no danger of dying from aspiration or respiratory failure than we should get these tests done ASAP. I also have a ketogenic diet on my website you should be on and you should eat every two-three hours and avoid all sugars since hypoglycemia (from eating sugars) causes the compressed spinal nerve to generate more Tumor necrosis factor-alpha and thus worsens your condition.
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#20 tham

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Posted 04 November 2013 - 12:53 PM

Randomized double-blind placebo-controlled trial of acetyl-L-carnitine for ALS.

'' Median survival was 45 months (ALC) and 22 months (placebo). ''


Garlic's Diallyl trisulfide.

Neuroprotective potential of phase II enzyme inducer diallyl trisulfide.


Neuroprotective effects of diallyl trisulfide in SOD1-G93A transgenic
mouse model of amyotrophic lateral sclerosis.



The effect of epigallocatechin gallate on suppressing
disease progression of ALS model mice.


Neuroprotective effects of (-)-epigallocatechin-3-gallate in a
transgenic mouse model of amyotrophic lateral sclerosis.


Additive neuroprotective effects of creatine and cyclooxygenase 2
inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis.

'' The combination of creatine with COX-2 inhibitors produced additive
neuroprotective effects and extended survival by approximately 30%. ''


Celecoxib/creatine superior to minocycline/creatine.

A novel, efficient, randomized selection trial comparing
combinations of drug therapy for ALS.


Dietary vitamin D3 supplementation at 10× the adequate intake improves
functional capacity in the G93A transgenic mouse model of ALS, a pilot study.


Vitamin D(3) at 50x AI attenuates the decline in paw grip endurance, but not
disease outcomes, in the G93A mouse model of ALS, and is toxic in females.

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#21 tham

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Posted 04 November 2013 - 01:26 PM



ALS more common in men than women due to protective effects of esterogen.

Neuroprotective effects of estradiol on motoneurons
in a model of rat spinal cord embryonic explants.


Effects of estrogen on lifespan and motor functions
in female hSOD1 G93A transgenic mice.

'' E2 (estradiol) treatment rescued the lifespans in overiectomized females. ''


Ovariectomy and 17beta-estradiol modulate disease
progression of a mouse model of ALS.

'' Treatment with estrogens has been shown to be neuroprotective
in models of several neurodegenerative diseases. ''


Protection of cultured spinal motor neurons by estradiol.

'' The dose of estradiols required for motor neuron protection was greatly reduced
by co-administration with glutathione. The results of this study shows that estradiol
protects spinal motor neurons from excitotoxic insults in vitro, and may have
application as a treatment for ALS. ''



Edited by tham, 04 November 2013 - 02:09 PM.

#22 tham

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Posted 04 November 2013 - 02:04 PM



Autophagy activation and neuroprotection by progesterone in the G93A-SOD1
transgenic mouse model of amyotrophic lateral sclerosis.

'' ..... the progression of motor dysfunction was significantly delayed in the
PG-treated group compared with the vehicle control group. The average lifespan
was also prolonged in the PG-injected group. Histological examinations revealed
that PG treatment substantially reduced the death of spinal motoneurons at 14weeks
of age with a concomitant decrease in mutant SOD1 levels.''


Steroid hormones and neurotrophism: relationship to nerve injury.

'' The brain and spinal cord, injured either by disease or by experimentally induced
trauma, is responsive in a reparative manner to exogenous and/or endogenous
gonadal steroid hormones.

The mechanism underlying this therapeutic role of steroids on damaged neurons is
not known but has been postulated to involve direct action of steroid hormones or
target neurons. It has been hypothesized that two diseases, Alzheimer's and ALS,
may be related to steroid hormone/receptor deficiencies.
In this regard, Appel (1981)
has suggested that putative "neurotrophic hormones" acting at the synapse may be
critical in maintaining the neural networks affected in ALS, Alzheimer's disease, and
parkinsonism. Extending that hypothesis to include direct action of such putative
hormones within the cell body and at the level of the genome, the evidence presented
in this discussion would argue that possible candidates could be gonadal steroids. ''


Cellular basis of steroid neuroprotection in the wobbler mouse,
a genetic model of motoneuron disease.

'' In this regard, degenerative diseases may constitute potential targets of these
hormones, based on the fact that the spinal cord expresses in a regional and
cell-specific fashion, receptors for androgens. progesterone, adrenal steroids,
and estrogens. ''



Edited by tham, 04 November 2013 - 02:06 PM.

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#23 Omega 3 Snake Oil

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Posted 24 September 2018 - 03:10 AM

I have Lyme with ALS-like symptoms. A recent MIPS/MEPS breathing test shows 50% loss of breathing strength, and I've had worsening sleep apnea since 2016 (severe insomnia and muscle twitching since 2012 when I believe I was first infected). I've had a lot of reactions to drugs/supplements/foods, some of which have worsened my breathing/twitching/cramping. I'll list some of them here.

Also, I have confirmed mold toxicity and suspected copper toxicity (I say suspected partly based on tests that show low copper and low ceruloplasmin, which I understand can be caused by having toxicity of exogenous copper that in turn causes low bioavailable copper and thus low cp)

Alpha lipoic acid: A single 50mg dose last year left me a lot worse. The next day, and for weeks afterward I was severely constipated. My breathing got worse, weaker. My left hand cramped up. Ever since taking this one dose, I've found I can no longer tolerate certain herbals I used to do fine with, including Japanese Knotweed, which is high in reservatrol. Note that ALA and resv. both chelate copper. 

Ionic zinc: Same as ALA, only it lasted about a day then got better. Took 10mg one time in 2016. 

molybdenum: Took a NAC/molybdenum supplement for a couple of weeks. During that time, my neuromuscular stuff worsened similar to ALA and zinc above, but it happened much slowed, so I didn't notice at first. Moly chelates copper, I've heard. 

DMSO: same as moly. 

Nystatin: similar to all above. I took 5ml three times a week to help detox mold. After one week I was worse off. I imagine there was metals hiding in my gut and killing yeast released them. 

Mitosynergy bioavailable copper: Tried a bottle of 0.1mg caps and didn't feel anything. Then I took 1mg of the raw powder and when I tried to sleep that night I had severe brain zaps and depressed breathing. Honestly thought I wouldn't wake up. 


fermented foods, esp kombucha: Makes me feel like my brain is on fire; severe insomnia, muscle cramping, racing mind. Makes my zopiclone (which works on GABA receptors) not work at all. Glutamate issue, it seems. 

L-Glutamine powder: Same as fermented foods. 

Whey butter: Same as ferments and glutamine.

Whey protein: Somewhat similar to glutamine but not as bad. Still I've cut it out. Now I get protein from eggs and meat. 

So, all these seem to affect either copper/zinc balance or glutamate/GABA balance. I imagine there's a death of motor neurons happening here. 

Another thing that hurt me, worse than maybe anything else, was the antibiotic macrobid. My apnea and cramping weren't that bad until I took that. 


Things that help:

CBD oil: 50mg twice a day, orally.

My other herbs and supplement stack (cod liver oil, PQQ/CoQ10, vinpocetine, curcumin, vit A, hydroxyl and adenosyl B12, and a bunch of others, too many to list here)

Nanolyzed zeolite spray: Sketchy science but I swear it does something. Claims to safely detox all metals. 

Autoimmune paleo diet (modified to allow eggs and a bit of plain yogurt) with 16:8 intermittent fasting

coffee enemas and castor oil packs


LLLT/red LED light therapy (I went to a clinic for this which seemed to help. I stopped due to high cost. Then I bought a 830nm unit for at home use. Also got a Vielight 810 intranasal light)


Also tagged with one or more of these keywords: als, pterostilbene, cape

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