220 replies to this topic

[Lufega]

This is an amazing regimen. There are things on this list that I never heard of. I bet it costs a ton. I didn't read through the rest of the replies, just marveling at that list and schedule ...

I've cut down significantly on a lot of supplements from my original list. I was getting some strange effects and some were probably countering others. I found that replacing some minerals I'm deficient in ad increasing my antioxidant intake has really made a difference for me.

[rwac]

edit: There was also this post where I was bashing manganese. http://www.imminst.o...&...st&p=299526 At the time, I was using so many other things, it took me a while to determine the cause. I narrowed it down to eleuthero, forskolin and a few other things. Stopping these ended this problem. All I know is that I feel great right now. I'm out there, I'm dating, I'm social, I want to do things again, I have more energy to do things. It's awsome. I should note, I gave Mn to a friend who is diabetic because it aids the pancreas in insulin production. He also told me he felt more energized and less fatigued.

Hey Lufega, Manganese seems to be great. It's normalizing my blood glucose levels, along with the increased energy ...
This is at 10mg/day

Edited by rwac, 01 September 2009 - 05:46 AM.

[Lufega]

Which brand are you using? This is probably why:

http://en.wikipedia....ate_carboxylase

Manganese is needed by Pyruvate carboxylase. PC plays a crucial role in gluconeogenesis and lipogenesis, in the biosynthesis of neurotransmitters, and in glucose-induced insulin secretion by pancreatic islets.

PC is expressed in a tissue-specific manner, with its activity found to be highest in the liver and kidney (gluconeogenic tissues),

Role in gluconeogenesis

During gluconeogenesis, pyruvate carboxylase is involved in the synthesis of phosphoenolpyruvate from pyruvate. Pyruvate is first converted by pyruvate carboxylase to oxaloacetate (OAA) in the mitochondrion requiring hydrolysis of one molecule of ATP. The OAA is then decarboxylated and simultaneously phosphorylated, which is catalyzed by phosphoenolpyruvate carboxykinase (PEPCK) to produce PEP in the cytosol. Very high levels of PC activity, together with high activities of other gluconeogenic enzymes including PEPCK, fructose-1,6-bisphosphatase and glucose-6-phosphatase in liver and kidney cortex, suggest that a primary role of PC is to participate in gluconeogenesis in these organs. During fasting or starvation when endogenous glucose is required for certain tissues (brain, white blood cells and kidney medulla), expression of PC and other gluconeogenic enzymes is elevated.[8] In rats and mice, fasting promotes hepatic glucose production sustained by an increased pyruvate flux, and increases in PC activity and protein. Similar to other gluconeogenic enzymes, PC is positively regulated by glucagon and glucocorticoids while negatively regulated by insulin.[3]

Aside from the role of PC in gluconeogenesis, PC serves an anaplerotic role (an enzyme catalyzed reaction that can replenish the supply of intermediates in the citric acid cycle) for the tricarboxylic acid cycle (essential to provide oxaloacetate), when intermediates are removed for different biosynthetic purposes.

A deficiency of pyruvate carboxylase can cause lactic acidosis as a result of lactate build up.[9] Normally, excess pyruvate is shunted into gluconeogenesis via conversion of pyruvate into oxaloacetate, but because of the enzyme deficiency, excess pyruvate is converted into lactate instead. As a key role of gluconeogenesis is in the maintenance of blood sugar, deficiency of pyruvate carboxylase can also lead to hypoglycemia.

So maybe insufficient quantities of cofactors, like Mn, can also lead to hypoglycemia? Since using Mn, I have had NO hypoglycemia problems, even when I go hours without eating. Eventually, I'll try to figure out why I have an increased need for Mn. Consumption? Lyme disease?

As far as your energy levels, Mn is needed for neurotransmitter synthesis, although this wiki- doesn't state which ones (I know dopamine is one) and also "Pyruvate carboxylase... catalyzes the irreversible carboxylation of pyruvate to form oxaloacetate (OAA)........It is an important anaplerotic reaction that provides oxaloacetate precursor for the citric acid cycle.

Edited by Lufega, 02 September 2009 - 01:17 AM.

[rwac]

Which brand are you using? This is probably why:

I take half of the Carlson chelated manganese tablet.
I have hyperglycemia, so it might have more to do with an insulin deficiency.

Edited by rwac, 02 September 2009 - 01:20 AM.

[Lufega]

Which brand are you using? This is probably why:

I take half of the Carlson chelated manganese tablet.
I have hyperglycemia, so it might have more to do with an insulin deficiency.

Any chance you can test your fasting glucose so we can get a before and after look?

[rwac]

Any chance you can test your fasting glucose so we can get a before and after look?

The arrow indicates where I added in the 10 mg manganese. Not 100% sure of the date, but I've been using it for the last few days. I'll need a week or so to know for sure, whether it will stay down or not.

Additionally, any sort of analysis would be much appreciated.

Attached Thumbnails

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Edited by rwac, 02 September 2009 - 02:39 AM.

[Lufega]

Everytime I use manganese my essential tremor becomes a little worse. This is only transient and it goes away on the off days. GABA problems are implicated in essential tremors. It seems like manganese lowers GABA in the striatum. Paradoxically though, I do not feel more anxious when I use Mn. I actually feel LESS anxious. So it seems that other neurotransmitters are implicated in anxiety disorders.

Neurologists prescribe GABA analogs to treat tremors but these lower glutamate. I'm afraid this would dumb me down.

Also, I'm noticing that my gynecomastia, which is not due to hormonal problems, is slowly picking up with Mn use. Interesting..

[Lufega]

rwac,

That is very interesting. Notice how the drop was more prominent with Mn use that whatever you were doing b/w may and july that caused a slow, but steady decrease. Wouldn't it be crazy if Mn was the solution for hyperglycemia?

[FunkOdyssey]

Everytime I use manganese my essential tremor becomes a little worse. This is only transient and it goes away on the off days. GABA problems are implicated in essential tremors. It seems like manganese lowers GABA in the striatum. Paradoxically though, I do not feel more anxious when I use Mn. I actually feel LESS anxious. So it seems that other neurotransmitters are implicated in anxiety disorders.

Neurologists prescribe GABA analogs to treat tremors but these lower glutamate. I'm afraid this would dumb me down.

Also, I'm noticing that my gynecomastia, which is not due to hormonal problems, is slowly picking up with Mn use. Interesting..

You are aware tremors are a symptom of manganese toxicity?

[Lufega]

Everytime I use manganese my essential tremor becomes a little worse. This is only transient and it goes away on the off days. GABA problems are implicated in essential tremors. It seems like manganese lowers GABA in the striatum. Paradoxically though, I do not feel more anxious when I use Mn. I actually feel LESS anxious. So it seems that other neurotransmitters are implicated in anxiety disorders.

Neurologists prescribe GABA analogs to treat tremors but these lower glutamate. I'm afraid this would dumb me down.

Also, I'm noticing that my gynecomastia, which is not due to hormonal problems, is slowly picking up with Mn use. Interesting..

You are aware tremors are a symptom of manganese toxicity?

Yep, fully aware. However, if my case was due to toxicity, they would linger on even days after stopping Mn. I first noticed the tremors when I was 19. Essential tremor runs in my family. My grandfather, father, aunt and brothers and sister all have it.

I've never tackled the tremor issue directly. From what I read, it seems to be caused by lack of B1 and Mag, which I'm deficient in. These seem to be needed to make GABA. I already supplement with these along with glutamine. One supp. i've never bothered to use is B6. It comes up everywhere, making it easier for the body to use magnesium, facilitating the production of neurotransmitters, etc. So I'm adding both p5p and pyridoxamine and we'll see how it goes.

I really don't think Mn is as dangerous as they make it seems. This whole toxicity issue is a lame effort at misdirection. Just as we see with other nutrients.

http://whfoods.com/g...iciencysymptoms

What are toxicity symptoms for manganese?

Most cases of manganese toxicity are seen in industrial workers who are exposed to manganese dust. These workers develop nervous system problems similar to Parkinson's disease.

Although symptoms of manganese toxicity do not typically appear even at high levels of dietary intake, in severe cases of excessive manganese consumption individuals can develop a syndrome called "manganese madness," characterized by hallucinations, violent acts, and irritability. Overconsumption of manganese is also associated with impotency. Manganese toxicity is most likely to occur in people with chronic liver disease, as the liver plays an important role in eliminating excess manganese from the body.

I am seeing so many changes since I started Mn. More muscle mass, social anxiety totally gone. Dysautonomia symptoms much improved. Better skin elasticity and plumpness. People are commenting on how much better I'm looking recently. My voice has deepened back to my teenage years status. So it must be having an effect on my hormones, which were all out of tune.

I'm also hoping it will help my musical joints. All them snap, crackle and pop.

Edited by Lufega, 04 September 2009 - 05:46 AM.

[Lufega]

If I do develop some motor problems, this will be the first place to know. In my years of trying "everything!", this seems to be working towards correcting many problems at once. Just to be safe though, I switched to twinlabs Mn gluconate, 10 mg. This didn't do crap. Seems like the chelated forms are better absorbed. Found a 10 mg bisglycinate chelate by bluebonnet. Will try that next. At this dose, I'm within the UL. I'll admit, 20 mg feels too strong.

I also wonder if this will have any effect on my alpha-1-antytripsin deficiency. I posted a study that showed low levels of SOD in A1AT def. patients. Glisodin helped at first, the numbers were coming up, but it stopped working. I was going to increase the dose from 100mg to 500 mg (lef endothelial defense) but since Mn-SOD is the principal antioxidant, I'm willing to bet it'll work better than glisodin. Plus, it's soo much cheaper.

When you put it all together, I have too many signs and symptoms that simply call for more manganese.

[Lufega]

Ive been seeing an endocrinologist to figure out why my serum calcium is high. He has had no luck identifying the cause.

From Manganese in health and disease By Dorothy J. Klimis-Tavantzis

"After 12 months, rats fed diet low in manganese showed higher levels of serum calcium and phosphorous.."

[Lufega]

I have new lab test results. After adding LEF silymarin, my liver enzimes are down to normal. That was just taking 1 a day for a couple weeks. Serum calcium is also down to normal...finally! I guess adding manganese did the trick like it said in the statement in my last post.

Alpha-1- antitrypsin is still low. This means there's still more oxidative stress than my body can handle. I'm going to raise glisodin to 200 mg and retest at a later date.

Alfa 1 Antitripsina.........mg/dL....... 71.80 *[ ] 97.00 161.00

Ammonia is still higher than I'd like it to be. I'm hoping manganese will take care of this over time.

Amonio......................ug/mL....... 0.74 [ *] 0.17 0.80

I'll will also update my stack tomorrow.

Edited by Lufega, 10 September 2009 - 01:43 AM.

[Healthy56]

Here's my hair mineral analysis and additional lab results:




-Lipase 70 u/l range (23-300)
-Leukocytes are positive in urine (1+)
-PROLACTIN 11.5 ng/dl range 5.3 - 22.1
-PSA is normal
- PM serum cortisol 4.34 ug/dl range 2-10
-AM serum cortisol 14.7 ug/dl range 5.5 - 20
-TSH 1.98 uUi/ml range 0.27 - 4.20
-T3 1.23 ng/ml range 0.8 - 2.02
-T4 9.72 ug/dl range 5.1 - 14.1
-T4 free 1.44 ng/dl range 0.93 - 1.71

-My cholesterol and LDL are also a little higher than I'd like them to be.
cholesterol 170 range <200
LDL 114 range <130
HDL 46 range >35
triglycerides 52 range <200

Liver enzymes were normal high when tested 5 months ago. Will retest to see where they stand.
ALT (SGPT) 48 IU/L 0-55 01
AST (SGOT) 35 IU/L 0-40 01


-magnesium (serum, not as accurate) 1.8 mg/dl range 1.6 - 3.0
------------------------------------
4eva,

I suspected pyroluria before and it's on my list of differentials. How can I test for this? My hematocrit is sometimes surprisingly low and I had anemia once before, per lab results. I also suspect a zinc deficiency. The hair minerals showed results within range, on the lower extreme but that's after I've been supplementing with zinc for almost one year so there's an obvious deficiency there. I stopped to allow copper levels to increase but maybe I should add it again, taken at a different time. I will add additional B6 along with magnesium, thanks for the suggestion. My potassium levels were high in the hair analysis but blood test showed levels within range.

k10,

I have not checked PTH levels but will do soon. I'll should have results by tomorrow. Any other suggestions? I was using different types of adrenal extracts but I don't think they did any good. I was also using licorice for a while and I did feel better while on it but I was unsure of the long term effects of it. I stopped a few weeks back but maybe my low testosterone levels are due to the licorice. I don't know if isocort is available here and I did plan on starting it but since my serum results are within range, I don' t know if it's advisable. I want to test saliva cortisol but that's not available here. Maybe I can have it shipped down, I don' t know. There is a relationship b/w low adrenal function and bad connective tissue quality. My thryroid results seems also normal but oddly enough, I tend to have a low basal body temperature always below 98 degrees. That's an indication of adrenal problems.

I had the fillings removed maybe 5 or 6 months ago at the same time. I was waiting the 4 months period as suggested by andy cutlers to allow mercury to reach a level of homeostasis. I should have begun two months ago but I'm soooo lazy right now and it requires dosing every 3 hours. It's pending...

At this point, I am very confused, very. So I am seeking out for help, advice, suggestions or anything that can point me in any direction. So I appreciate any input! I will post all my Sx once I get them organized.

nameless,

Before I started supplementing I had a very low level of functionality. I started using MSM to combat joint pain. Then, after reading a LEF magazine, I added curcumin and Rhodiola rosea and my functionality increased significantly. My stack has evolved prominently since. I generally feel better with my supplements but I'm aware and have already experience that some have deletirious effects. For example, I removed eleuthero because it was making me anxious and I suspect ashwaghanda was doing the same. Also, I was using high dose forskolin (abou 40 mg or more) and that turned me into a raging lunatic so I toned down the dose. As far as interaction, I'm hoping you guys can help me as I am at a total loss right now. I don't plan of keeping this regimen, it's too much. I was remove things as they run now and just keep the essentials. I was also using cholinergics to boost cognitive function but that reduces AV conduction and could have contributed to my heart problems. I did this knowingly.... IN addition, I was using 20 mg of propranolol to control anxiety and tremors. I was rotating though the ER and surgery and I needed to be in control of myself. I'm sure this also worsened my problems, acutely.
----

I have so many symptoms which impede with my level of functionality and I've been trying to treat each of them independently. The result of that is the amount of supplements I have. Whatever is wrong with me is very interesting. Whenever I suspect, and I'm sure of a diagnosis, testing will show that nothing is wrong. That was the case with my arthritis. I had pain and tenderness in every joint in my body but all my inflammatory markers are normal. Also, my terrible problem with dry eyes, I suspected sjogren's, but again, all is normal.

Some adaptogens, like Eleuthero, Ashwaghanda and possibly even Rhodiola (that one is my favorite) can cause the OPPOSITE effect of what we think they do. They can cause jittery, anxious feelings. I would be VERY suspect of any 500 MG Rhodiola (as in jarrow, and NOW brands) because that is just WAY too much of a dose. I'm taking two caps a day of a Rhodiola that is labeled at 150 mg and I am not jittery. When I tried to double this, to 600 MG a day, I could feel the anxiousness coming in. So - what I'm suggesting is that Rhodiola isn't one of those "buy the most mg for your money" kind of products. Go with the Siberian. Go with full spectrum - who the hell cares about how much of two ingredients its got, as long as its got ALL of them. The Verde Botanica brand I use (and would recommend) is labeled "Contains 13 of the 28 active ingredients of the plant.) Also has a package insert with the history of the plant which is very interesting.

[rwac]

Lufega,

I was talking to my LLMD about supplemental Manganese.

He didn't like it very much, he thinks it feeds the Lyme.

I think this might be sufficient reason for some caution, or to stop entirely...

[Lufega]

Lufega,

I was talking to my LLMD about supplemental Manganese.

He didn't like it very much, he thinks it feeds the Lyme.

I think this might be sufficient reason for some caution, or to stop entirely...

That idea alone, is always on the back of my mind. I am still unsure if I have lyme or if all my problems are due to an old EBV infection. You have lyme if I recall correctly, how do you feel??? I wish there was a lactoferrin-type substance, but for manganese

My musical/painful joints are doing all sorts of crazy things, since I started Mn. Almost feels they there's remodeling taking place.

Edited by Lufega, 16 September 2009 - 04:56 AM.

[rwac]

That idea alone, is always on the back of my mind. I am still unsure if I have lyme or if all my problems are due to an old EBV infection. You have lyme if I recall correctly, how do you feel??? I wish there was a lactoferrin-type substance, but for manganese

My musical/painful joints are doing all sorts of crazy things, since I started Mn. Almost feels they there's remodeling taking place.

I feel I'm gently going downhill, after I stopped an antibiotic. Going back on it soon.
Didn't you have some sort of herx from Doxy ?

It's great that you're noting improvements. I suggest you keep an eye out and stop taking it when the improvements slow significantly.

Hmm, at what point are you doing more long term harm than short term good ?

Edited by rwac, 16 September 2009 - 01:00 PM.

[Lufega]

http://books.google....m...;q=&f=false

Scroll to the top where it talks about manganese. This book and many others always state that oral/dietary manganese is safe. The only way Mn is toxic is when you breathe it in, working in metallurgy and such. Also, if you have liver failure and your biliary system doesn't work. I really can't find any references linking diet to any problems, under normal circumstances. Mn is a heavily misunderstood mineral.

The way I see it, ENOUGH Mn is needed for proper dopamine, acetylcholine, hyaluronic acid production as well as a host of other things. TOO much Mn (like too much iron, phosphorus, etc.) will mess everything up. The same way MSG overstimulates glutamate receptors and mess everything up. But you still need sufficient Mn from your diet to keep things working. Seeing how we are supplementing with just about everything because food today is lacking so many nutrients, I think Mn deserves more attention. The key here is figuring out how much is enough.

40% of dietary Mn is absorbed by the gut..slowly.

http://books.google....-...ity&f=false

Another source says it varies b/w 1-25%
http://books.google....-...ity&f=false

Edited by Lufega, 16 September 2009 - 05:24 PM.

[nameless]

If you suspect Lyme, I'd be wary of adding manganese in doses above RDA. Have you done the Chron-o-meter thing, to check for manganese intake from diet too? Useful way to check for other mineral intakes also. Actually, even if you don't have Lyme, I'd be wary. Only reason probably to supplement in large doses is if in fact you are deficient.

Extra manganese + musical joints doesn't sound right to me.

Edited by nameless, 16 September 2009 - 05:43 PM.

[Lufega]

From the Nutrition Almanac By John D. Kirschmann, Nutrition Search, Inc

manganese is found in the highest concentration in the bones with the remaining concentration in the kidneys, liver, pancreas, pituitary gland and adrenal glands. Small amounts are also in the intestinal mucosa and other tissues. Little is stored, with the most being 12 to 20 mg at one time. The body does not store this mineral well. Normally, people excrete about 4 mg each day, which must be replaced. Excretion occurs via the feces, much of it in the form of choline complex in the bile.

Manganese in the amounts present in food and from normal supplemental amounts is one of the least toxic of minerals.

Then they go on to talk about excessive intake from manganese dust in mine workers, destroying dopamine neurons. So the RDA is set a 2-2.5 mg per day but our bodies secrete 4 mg per day? Something's off here.

[Lufega]

If you suspect Lyme, I'd be wary of adding manganese in doses above RDA. Have you done the Chron-o-meter thing, to check for manganese intake from diet too? Useful way to check for other mineral intakes also. Actually, even if you don't have Lyme, I'd be wary. Only reason probably to supplement in large doses is if in fact you are deficient.

Extra manganese + musicial joints doesn't sound right to me.

Ive had the joint problems years before I added Mn. They seem to be improving. They don't produce that "clack" sound quite as bad.

I wanted to update my stack but first, I want to reduce the number of supps I use to things that i've determined essential. I will remove any other ones that don't produce a specific observable effect, as they run out. I'm doing this for cost savings and to figure out exactly what's working and what isn't. As it is, I have significantly removed many items from my original list.

Definite keepers are magnesium, taurine, relora, lithium, pyridoxamine and/or P5P, B1, Maca, glutamine, manganese, Methylene Blue, vitamin D and sylimarin. I take antioxidants like NAC, ALA, glisodin but I will evaluate these further.

Edited by Lufega, 16 September 2009 - 05:54 PM.

[nameless]

I won't say it isn't helping, as for all I know it could be.

But if Lyme, symptoms can change. I know my neck 'crackles', hip hurts, etc. but as to what degree, that can change week to week, month to month. The improvement could be a coincidence or due to something else you take, too.

Just keep an eye on things. If your symptoms get worse at some point, it's probably best to drop the manganese.

Edited by nameless, 16 September 2009 - 06:05 PM.

[rwac]

Lufega

To be a little clearer, I haven't been noticing much from the Manganese recently, because of other stronger effects. I will try again with the Manganese, once I'm done fiddling with the abx.

[Lufega]

Effect of manganese supplementation and source on carcass traits, meat quality, and lipid oxidation in broilers.
Lu L, Luo XG, Ji C, Liu B, Yu SX.

Mineral Nutrition Research Division, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, PR China.

An experiment was conducted using a total of 336 one-day-old, Arbor Acres commercial male broilers to investigate the effect of dietary Mn supplementation on carcass traits, meat quality, lipid oxidation, relative enzyme activities in abdominal fat and meat, and Mn-containing superoxide dismutase (MnSOD) mRNA level in meat. Broilers were randomly allotted by BW to 1 of 8 replicate cages (6 chicks per cage) for each of 7 treatments in a completely randomized design involving a 2 x 3 factorial + 1 arrangement of treatments. Dietary treatments included the corn-soybean meal-based diet (control) and the basal diet supplemented with 100 or 200 mg of Mn/kg as MnSO(4) x H(2)O, Mn AA A with a chelation strength of 26.3 formation quotient (8.34% Mn), or Mn AA B with a chelation strength of 45.3 formation quotient (6.48% Mn). Birds fed supplemental Mn had lower (P < 0.10) percentages of abdominal fat, lipoprotein lipase (LPL), and malate dehydrogenase activities and greater (P < 0.07) hormone-sensitive lipase activities in abdominal fat than birds fed a control diet. Birds fed supplemental Mn from Mn AA A or Mn AA B had lower (P < 0.05) LPL activities in abdominal fat than those fed supplemental MnSO(4) x H(2)O. Birds fed supplemental Mn had lower (P < 0.03) malondialdehyde content in leg muscle and greater (P < 0.02) MnSOD activities and MnSOD mRNA level in breast or leg muscle than those fed the control diet. Birds fed supplemental Mn from Mn AA A had a greater (P < 0.02) MnSOD mRNA level in leg muscle than those fed supplemental MnSO(4) x H(2)O. Results from this study indicated that organic Mn was more available than inorganic Mn for decreasing LPL activity in abdominal fat of broilers, and dietary Mn might reduce abdominal adipose deposition by decreasing LPL and malate dehydrogenase activities or increasing hormone-sensitive lipase activity in abdominal adipose tissue. The results also indicated that dietary Mn upregulated muscle MnSOD gene expression pretranslationally in association with increased MnSOD activity, which might explain the decrease of malondialdehyde content in leg muscle.

[Lufega]

Definition: A trace element with atomic symbol Mn, atomic number 25, and atomic weight 54.94. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver. (From AMA Drug Evaluations Annual 1992, p2035)

[Lufega]

Hyaluronic acid is low in patients with alpha-1-antitrypsin induced emphysema. It is also low in Mitral Valve prolapse. These are two problems I have. I have Dysautonomia, a dysfunction of the ANS which is part of the CNS. I posted a study that suggested HA can repair the CNS.

http://emedicine.med...295686-followup

Other trials are testing hyaluronic acid as individuals with emphysema have been noted to have reduced levels of hyaluronic acid in their lungs.

I'm starting to see a pattern here. HA is made in the fibroblast using the enzyme Hyaluronic acid synthase. HAS uses either magnesium or manganese (Interestingly, manganese ion maximally stimulated HAS activity; in contrast, the streptococcal and the mammalian HASs prefer magnesium ion. ) as a cofactor. It seems that Glucosamine availability appears to be rate-limiting for hyaluronic acid synthesis. So I need to improve the HA status in my body. How do I do this? Do I supplement with HA pills for the rest of my life? Can I increase the use the precursors like glucosamine (N-acetylglucosamine looks like a better candidate) and this will solve my problem? Or is the problem simply caused by an intractable magnesium deficiency that will not improve even after years of using oral supplements?? All my research always comes back to magnesium. When I was investigating oxidative stress and antioxidants, in the end, I posted a study that showed low magnesium status as a cause for increase oxidative stress.

This is very frustrating. Maybe boosting HA will reset everything. Supplements can stimulate fibroblast production of HA.

Exogenous N-acetylglucosamine increases hyaluronan production in cultured human dermal fibroblasts.
Tu CX, Zhang RX, Zhang XJ, Huang T.

Department of Dermatology, The Second Affiliated Hospital of Dalian Medical University, 467 Zhongshan Road, 116027 Dalian, People's Republic of China. tucx2003@163.com

Application of hyaluronan (HA) containing cosmetic products to the skin is reported to moisturize and restore elasticity thereby achieving an antiwrinkle effect. In the skin, HA can be synthesized by dermal fibroblasts and N-acetylglucosamine (NAG) is a precursor for HA biosynthesis in the body. To study the effects of exogenous NAG on HA production in human dermal fibroblasts, HA production and HA-synthesizing enzymes 1, 2 and 3 mRNA expression in cultured human dermal fibroblasts were measured by ELISA and RT-PCR, respectively. The results showed that NAG promoted HA production while had no effect on the expression of HA-synthesizing enzymes 1, 2 and 3 mRNA in human dermal fibroblasts.

In addition, HA production can be affected by thyroid function. Recently, it was discovered that none of the commercial Salts sold in stores contained NO iodine. Nothing. Nada. The thrills of living in the third world...


The following supplements come to mind: Magnesium, manganese, zinc, Iodine, Aloe vera, NAG, gelatin(?) and maybe an amino acid combo (glycine, lysine, proline, leucine).

This is the new direction I will take.

Edited by Lufega, 19 September 2009 - 04:57 AM.

[Lufega]

Manganese deficiency and toxicity: are high or low dietary amounts of manganese cause for concern?

Finley JW, Davis CD.
United States Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, ND 58202-9034, USA.
Manganese is an essential trace element that is required for the activity of several enzymes. Manganese is also quite toxic when ingested in large amounts, such as the inhalation of Mn-laden dust by miners. This review examines Mn intake by way of the food supply and poses the question: Is there reason to be concerned with Mn toxicity or deficiency in free-living populations in North America? Although much remains to be learned of the functions of Mn, at present there are only a few vaguely described cases of Mn deficiency in the medical literature. Given the heterogeneity of the North American food supply, it is difficult to see the possibility of more than greatly isolated and unique instances of Mn deficiency. However, low Mn-dependent superoxide dismutase activity may be associated with cancer susceptibility, and deserves further study. There may be reasons, however, to be concerned about Mn toxicity under some very specialized conditions. Increasing numbers of young people are adopting a vegetarian lifestyle which may greatly increase Mn intake. Iron deficiency may increase Mn absorption and further increase the body-burden of Mn, especially in vegetarians. Mn is eliminated primarily through the bile, and hepatic dysfunction could depress Mn excretion and further contribute to the body burden. Would such a combination of events predispose substantial numbers of people to chronic Mn toxicity? At present, there is no definite proof of this occurring, but given the state of knowledge at the present time, more studies with longer time-frames and more sensitive methods of analysis are needed.

[rwac]

http://jn.nutrition....ract/114/8/1438

Effect of Manganese Deficiency on Insulin Secretion and Carbohydrate Homeostasis in Rats<h2></h2> Deborah L. Baly, Donald L. Curry^*, Carl L. Keen and Lucille S. Hurley

Departments of Nutrition ^* Departments of Nutrition Physiological Sciences, University of California, Davis, CA 95616



The effects of manganese (Mn) deficiency on carbohydrate metabolism in the Sprague-Dawley rat were investigated. Oral glucose tolerance tests were performed on offspring from Mn-sufficient female rats fed 45 µg Mn per gram diet (C-C), offspring from Mn-deficient female rats fed 1 µg Mn per gram diet (D1-D1) and rats not exposed to Mn deficiency in utero but fed D1 diet from weaning to maturity (D1). Mn-deficient rats, D1 and D1-D1, had significantly lower concentrations of Mn in liver, kidney, heart and pancreas than controls. D1-D1 rats responded with a diabetic type of glucose tolerance curve when given oral glucose. Insulin levels of D1-D1 rats were not commensurate with their high glucose levels. Measurements made by using an isolated perfused-pancreas preparation indicate that insulin output due to release of stored hormone was 76% of control levels in D1-D1 rats. This suggests either lower insulin stores or impaired release of insulin in D1-D1 rats. Second phase insulin release was also significantly lower in D1-D1 rats than in controls. Pancreatic insulin content was 63% of control levels in D1-D1 rats, further supporting the idea of lower insulin stores in Mn-deficient rats. No differences in plasma glucose levels were observed between D1 rats and controls after an oral-glucose load. These findings indicate that dietary Mn deficiency can result in impaired insulin secretion producing impaired carbohydrate metabolism; however, the timing of the deficiency may be a critical factor in the expression of this abnormality.

[Lufega]

rwac,

Would the full article state what the best time to intervene is? I have a friend who is diabetic post steroid use. I got him on 10 mg manganese gluconate and he lost all this stubborn body fat he had which I attribute to a decrease in fasting blood glucose. I'm waiting for his glycemia to confirm.

[Lufega]

Boom! I can finally explain all of my signs and symptoms (except the alpha 1 antitrypsin deficiency) in terms of dysautonomia (autonomic neuropathy). These include all my connective tissue problems and might also explain the multiple mineral deficiencies. Now I'm getting somewhere..

[Heart and autonomic nervous system in connective tissue disorders]

[Article in Italian]

Laganà B, Gentile R, Vella C, Giovani A, Tubani L, Mastrocola C, Baratta L, Bonomo L.
Dipartimento di Medicina Clinica, Università La Sapienza, Roma.
Heart rate variability (HRV) is a suitable diagnostic tool in identifying patients with autonomic nervous system (ANS) disorders even in pre-clinical stage. We have enrolled in this study all patients with large variety of connective tissue disorders, given the possibility of an involvement of ANS in these diseases. The study population consisted in eighty-five patients (68 females and 17 males), 35 of whom affected by systemic lupus erythematosus, 16 by rheumatoid arthritis, 14 by Sjögren syndrome, 12 by progressive systemic sclerosis, 3 by Behçet syndrome and 5 by antiphospholipid antibodies syndrome. The mean age ranged between 33.7 of patients with lupus erythematosus and 51.8 of those with Sjögren syndrome. As control, we enrolled healthy subjects of different age, divided into two groups, to rule out the aging as potential source of considered parameters alteration. The autonomic function has been evaluated by 24 hours ambulatory monitoring, using a Zymed 1210 Scanner with Zymed 3.74-PC 1990 software. We have considered: in the time domain, the standard deviation of the RR intervals average (SDNN) and the percentage of RR adjacent intervals differing each other more than 50 msec (pNN50); in the frequency domain, the low (LF) and high (HF) frequencies, the LF/HF ratio, and the total power (RT). The HRV parameters resulted abnormal in every type of the connective tissue diseases considered: particularly SDNN, pNN50, LF, HF and RT (p < or = 0.01). In conclusion: the results of our study suggest that autonomic neuropathy may be present in any kind of connective tissue disorders even in preclinical stage.

Dysautonomia basically involves a dysfunction of the cholinergic system. Manganese is needed for both acetylcholine production and connective tissue integrity. However, Mn is not the end of the road, but another link in the chain.