Hi, Since the end of last year I have been suffering with very bad neuropathic pain and muscle spasm's. Last Friday I got some ZMA, it's a bodybuilding supplement containing: Zinc Sulphate 240mg, Chelated Zinc 40mg, Chelated Magnesium 426mg and, Vitamin B6 24mg, I have been taking these along with 4000iu Vitamin D3 and my spasm's have stopped, my leg muscle feel looser and I've reduced by pain medication Amitriptyline 100mg by 50%, I have been using Magnesium Chloride oil for a while but I think the combination above work together for better absorption. I have been using other medication like Lyrica together with Amitriptyline but I was still getting pain and it turned me into a zombie! I am also having trouble sleeping and I take 30mg Baclofen with 50mg Amitiptyline before bed to help me sleep. I think the less medication we take the better!
Best wishes
Steve
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StevenSims
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Thanks for describing your experiences with ZMA. Can you describe for everyone's benefit what led you to try this? In particular, what clinical or other evidence may exist that people could read before trying this treatment?
Although there seem to have been real benefits for you, it could be that the supplements have side-effects on others that are worth knowing about. As you know, I am very keen for all AMN-ers to have access to all the evidence that may be out there.
Nevertheless, I am delighted that you have found some benefit, and that you have taken some action rather than sit back and suffer!
Since my holidays to Cyprus I've been racking my brain? what's different over there? I believe it's vitamin d from the sun and there is salt in the water, which contains magnesium, swimming, washing ect. I've been trying supplements but it's been trial and error, doctors have no knowledge of supplements as they are trained with pharmaceuticals so there is limited advice from them.
We are all different and also there are different mutations of the gene, as my symptoms are completely different to others, like spasm's in my arms, legs, breathing and bad neuropathic pain.
Both zinc and magnesium are essential minerals, required for hundreds of vital life functions. Zinc allows your body's immune function to work properly, providing support for your thymus gland and white blood cells. In a related capacity, it also helps your body heal properly from wounds. A 2011 study published in Cochrane Reviews found evidence that zinc may also help reduce the severity of cold symptoms.
Zinc is a trace mineral, so its recommended daily amount of 15mg or men and 12 mg for women may seem quite low when compared to other minerals.
Magnesium plays a major role in nerve and muscle function, essential for over 300 body processes. It helps your body metabolize food so that you have energy to carry out your everyday tasks. Its support of metabolism continues in its support of insulin production and use by your body. It is essential for bone formation as well as heartbeat regulation.
Side Effects of Taking Zinc and Magnesium
Generally, both minerals are safe to take. In fact, you may find supplements which include both along with calcium as a combination supplement to support good bone and teeth formation as well as prevent osteoporosis.
Hi Steve....I am a Female carrier and have had problems with joint pain muscle cramps and nerve pain. I have been taking a high strength magnesium and Zinc now for years and know that when i run out all my aches and pain come back two fold so I second what you are saying. I wasn't aware of the benefits for AMN but told my brother to try it who has AMN and now reading what you have said about your experience with both mag and zinc there is something to be said about this and that it is well worth everyone giving it a trial run. I know I am a much happier person taking them, And for women Magnesium also has the benefit for female hormones etc.
Hi, Vitamin D uses up Magnesium for absorption so I've reduced my intake to 2000iu per day for the last couple of days and I'm getting the same benefit.
I know if I stop taking these in 24hours my pain gets worse and spasm's come back! I think the combination I take work together because each mineral helps each other for better absorption.
Myself, my sister and Mam have used 5,000iu of vitamin D3 daily after reading about it through your post on here a while ago. Initially I found it improved my (slight) spasms and reduced knee pain somewhat. However, I feel the benefits have decreased so I've now bought some ZMA off ebay to give that a whirl.
It only cost £15 for 120 capsules so it isn't a fortune and I'll post my personal findings in due course. K
It's been 2 and a half weeks since me and my Mam gave ZMA a go. My Mam noticed a difference almost straight away, but more with her movement, saying she felt less stiff.
I didn't notice any difference so I cut down slightly on the AdCal I take alongside the steroids for adrenal problems. Calcium doesn't mix well with ZMA and again I am getting a bit less knee pain but I am still getting a few spasms.
I'm glad your mother is getting benefit, it might be worth you stopping the vitamin d for while to get your magnesium levels back up? vitamin d uses it for absorption. I started taking them together since 20th April, I now only take 10mg of Amitriptyline and I'm having hardly any pain now! and still no spasm's!
Here's some interesting reading about Zinc and ALD
Taken from myelin.org
Zinc
Superoxide dismutase (SOD) is a metallo-protein and is the first enzyme, which acts
as a scavenger of superoxide radicals, catalyzing them to form oxygen and hydrogen
peroxide. This potent antioxidant relies on cofactors to carry out its free radical
scavenging function; zinc is one of the essential components required for it to act.
Fischer and Glass (2010) demonstrated that a loss of SOD predisposed dorsal root
ganglia axons to degeneration due to a lack of protection from oxidative stress. Their
study demonstrated that SOD is “required for dorsal root ganglia axon survival”
(Fischer and Glass, 2010 pg. 255).
Bao et al (2010) explored the anti-inflammatory effects of zinc by administering
45mg/day (as zinc gluconate) to subjects aged 56-83 years for six months. This was
compared to a placebo group receiving nothing. Although this study aimed to
demonstrate the atheroprotective action of zinc, the mechanisms by which zinc brings
about this effect is also relevant to the underlying pathologies of neuro-degeneration
occuring in ALD. The beneficial effects of zinc were seen to significantly decrease Creactive protein (CRP), IL-6, IL-1ß and reduce TNF-a production, in addition to other
inflammatory markers which typically abound in ALD. Bao et al (2010) confirmed
that a deficiency of zinc would increase oxidative stress.
Additionally, ROS production arising from a zinc deficiency has the ability to initiate
nuclear transcription factor kB (NF-kB)-activation of pro-inflammatory genes.
Therefore the data presented demonstrates the potential benefits of zinc in a neuroinflammatory condition like ALD, as the inflammatory mediators indicated in this
study are also seen excessively in ALD.
Peroxisome proliferator activated receptor-alpha (PPAR-a) activation relies on zinc.
Peroxisome proliferator activated receptor-alpha regulates lipid metabolism and fatty Kimberly)Kushner)227921)
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acid beta-oxidation (Bouwens et al, 2008), the characteristic mechanism which is
rendered ineffective in ALD patients. Reiterer et al (2004) adds that PPARs regulate
glucose homeostasis, cell proliferation, cell differentiation and also modulates the
inflammatory response. Bouwens et al (2008) concluded that genes which up-regulate
beta-oxidation are dependant upon PPAR-a activation, and are therefore crucial in
ALD. Bao et al (2010) have demonstrated that PPAR-a activation plays a role in
inflammation by showing that its activation causes a down-regulation of proinflammatory cytokines. Reiterer G et al (2004) also explored PPAR-a in relation to
inflammatory mediators. They reported an increased TNF-a induced inflammatory
response in zinc deficient cells. Further, that when zinc was added back into these
cells, PPAR-a activation caused a down-regulation of NF-kB and activation protein-1
(AP-1). Their study demonstrated that adequate amounts of zinc are required for the
anti-inflammatory effect of PPAR-a to take place. The significant factor at this point
is that activation of PPAR-a, is a zinc dependant reaction, and this is illustrated below
(Bao et al, 2010 pg. 1639): Kimberly)Kushner)227921)
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It is evident that the deficiency of zinc will lead to increased ROS, subsequently
activating NF-kB and up-regulating the production of inflammatory cytokines, CRP,
and inflammatory enzymes (Cycloxygenase-2 [COX-2], and inducible nitric oxide
synthase [iNOS]).
The production of superoxide radicals occurs naturally as a part of the complexes of
the electron transport chain. If SOD enzymes do not quench these free radicals, they
have the ability to undergo chemical reactions and produce other highly toxic free
radicals such as hydroxyl radicals (Fischer and Glass 2010).
In mice lacking SOD, neuro-degeneration and motor neuropathies were evident. The
neurons also exhibited increased apoptosis under ischemic, excitotoxic and trauma
scenarios (Fischer and Glass, 2010 pg. 256). Additionally, the effect of a potent
herbicide, diquat, on axonal health was exacerbated by a SOD deficiency. Therefore,
The deficiency of SOD demonstrated increased axonal toxicity.
Song et al (2009) observed that zinc status was a major contributor towards DNA
damage, and that some DNA damage may be reversible after zinc repletion. Due to
the role of zinc in maintaining DNA integrity, in their study, Song et al (2009, pg.
327) reported that a low zinc intake will increase the breakage of DNA strands either
due to oxidative stress and/or disruptions to DNA repair pathways. A key finding in
their study was that physical manifestations of a zinc deficiency became apparent
before a decline of plasma zinc levels. This clearly indicates the importance of zinc in
maintaining DNA stability and therefore its role in genetic homeostasis.
Copper zinc superoxide dismutase (CuZnSOD) activity was seen to reduce when zinc
levels in subjects were deplete (Song et al 2009, Mariana et al 2006), however
CuZnSOD levels were seen to rise as soon as zinc was replete. Furthermore a key
damaging mechanism in ALD, lipid peroxidation, has been shown to increase in rats
that were zinc deficient (Song et al 2009).
Zinc will increase antioxidant capacity; decrease CRP, inflammatory cytokines and
overall oxidative stress markers after six months supplementation, as demonstrated by Kimberly)Kushner)227921)
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Bao et al (2010). Zinc will also decrease the generation of TNF-a, IL-1ß, NF-kB and
up-regulate PPAR-a. All these mechanisms of zinc are implicated in ALD and would
Steve- Thanks for your valuable input. I have been researching ALD and AMN, but had not made the connection between PPARa abd Zinc. I will tell my friend who has AMN to start taking ZMA and see if his symptoms start to improve.
So far I have developed a two pronged attack for AMN therapy:-
Part 1 is the use of mustard seed oil, a cheaper version of Lorenzo's oil. The blood elevation of the erucic acid component diverts the hepatic cells' elongase ELOVL3 into only elongating monounsaturates, instead of dividing its attention between saturates and monounsaturates. This appears to greatly slow down the process of saturated VLCFA elongation, and the elongated monounsaturates are readily taken care of by peroxisome disposal.
Part 2 is recruitment of PPARa activation of the ABCD2 (ALDR) gene, using phytanic acid (a potent PPARa ligand) as the adjuvant. The liganded pair then join with RXR as a heterodimer to form an activated complex, which settles on the PRE of the ABCD2 gene, creating a permanently bonded factory for ABCD2 transporter production.
It appears that nobody has thought of this idea before, and the ABCD2 gene is notoriously diffcult to activate. This mechanism uses the fact that phytanic acid does not need to form a thioester before activating PPARa (unlike the straight chain fatty acids, all of whom have little or no effect on PPARa activation unless bound as thioesters).
This strategy is however a two-edged sword, as phytanic acid, once liganded to PPARa, cannot be broken (extremely resistant to proteolytic degradation). Therefore if too much phytanic acid is used all at once, one can get an overactivation of ALDR genes, creating too many ABCD2 transporters. This can be dangerous to say the least.
AN EXAMPLE FROM PERSONAL EXPERIENCE:
By accident I gave my right hand contact dermatitis a year ago, playing with phytanic acid that I had concentrated down, and inadvertently spilled on my hand. What I hadn't realised was that when concentrated phytanic acid (as phytol) penetrates the epidermis, it ligands to the PPARa molecules in the differentiating keratinocytes at the epidermal basement level. This created liganded PPARa/RXR heterodimers which promptly migrated to the nucleus and activated the ALDR gene in most of the hand's keratinocytes. This resulted in production of both ABCD1 AND ABCD2 transporters in the same tissue (I don't have AMN), and concomitent sudden depletion of saturated VLCFA from the tissue. The result was a breakdown of the lamellar structure due to loss of ceramides, and widespread apoptosis, permeability barrier disruption and tissue fragility, all the hallmarks of a severe form of dermatitis called dishydrosis.
Fortunately I was able to rectify the situation over a period of months, using homemade concoctions (i.e: not hydrocortisone cream). The hand has now regenerated its tissue and permeability barrier, but I still have to apply creams on a regular basis to prevent flare ups.
With AMN there should be no problem, as the opposite holds true, as the ALDP gene is non-functional, and any help from ALDR gene is a bonus. Therefore any way you can get ABCD2 activation happening is a good thing, provided extreme caution is adhered to.
My friend who has AMN has been taking phytanic acid as phytol in "green smoothies" for months, and his blood VLCFA have dropped dramatically. In due course we will find if this has carried over to a drop in tissue VLCFA levels, and a decline in symptoms as well.
(For more info about this therapy please refer to my posts on this homepage).
I will talk to my friend about what you said regarding zinc and its requirement in full functioning of superoxide dismutase, and its ability to influence PPARa. Zinc therapy could result in even stronger results, and the robust upregulation of SOD should also act to reduce the ROS destroying the neuronal tissue, as you said.
Don't stop the drugs! Speak to your doctor first to taper slowly off them but if they are working for you and if you can manage the side effects then keep taking them?
Not stopping cold turkey. No drugs at bedtime = no sleep for me.
I'll give the supplements a good go and see if I can ramp down on the Benzo's.
Took some Lyrica last night. First time. Groovy medicine, I enjoyed that. That definitely stops all spasms.
I'll start a main thread later where we can all list our medications/supplements. Could well be a help to somebody. My neurologist will prescribe just about anything I ask for.
I have a long list of what works/doesn't/helps a bit.
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