ZMA + VITAMIN D3 = NO SPASM'S + LESS PAIN!

Hi Steve

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!

All the best

Chris

Hi Chris,

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.

Here's some info:

newsmax.com/FastFeatures/Ma...

articlesbase.com/supplement...

livestrong.com/article/3501...

Benefits of Zinc and Magnesium

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.

Thanks

Steve

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.

Leonie

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.

Best wishes

Steve

Hi Keith,

I definately think they are worth a try! I'd be interested to hear how you get on with them.

All the best

Steve

Hi Keith,

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!

All the best

Steve

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

pose a beneficial effect in treatment.

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.

Thanks again, Rob.

I'm bumping this thread. This information is golden.

My muscle spasms occur if I lie down. So, that's usually bedtime, but if I attempt an afternoon nap, they'll kick in after about 5 minutes.

That means no afternoon naps for me.

If I am very tired, ill, hungover or just run down, my legs spasm at any time. Standing up, sat down.

Stomach spasms as well, but to a much lesser extent.

Usually my right leg, sometimes both.

If I am constipated, then my left leg spasms.

Before I discovered Benzodiazopines, my legs would kick up a good metre into the air.

Benzo's lessen the spasms, Gabapentin and Lyrica kill them completely.

I shall give your regimen a go, Steven. Have to stop with the drugs.

Hi,

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?

All the best