32 replies to this topic

[stephen_b]

Morning with breakfast

• Astaxanthin (NOW 4 mg)
• Bacopa Extract (225 mg)
• Epicor (1 capsule, 500 mg)
• IP6 (1 capsule Jarrow 500 mg)
• LEF Mitochondrial energy optimizer (2 capsules)
• PlusEPA (2 capsules, 1000 mg EPA total)
• Trimethylglycine (1 capsule Kirkman 500 mg)
• Ubiquinol (Jarrow QH-Absorb, 100 mg)
• Vitamin D3 (3000 IU)
• Whey protein shake (Jarrow mix) one serving in orange juice.
• DHEA (LEF 50 mg) every other day
• B12 Jarrow Sublingual methyl-B12 (1 per week)

Mid Morning
3 AOR ortho core, old formula

Mid Afternoon
3 AOR ortho core, old formula

After Supper
LEF Mitochondrial energy optimizer (2 capsules)

Before bedtime
Melatonin (3 mg 1 hour before bed)

Sometime during day

• Resveratrol recipe: Take 1 gram transresveratrol and dissolve in about 15 mL of vodka. Take a tablespoon of LEF soy lecithin, mix with water, and let sit, stirring occasionally. Combine ingredients and chug.
• Curcumin and raw chocolate power recipe: mix 1500 mg curcumin and 1500 mg chocolate powder into about 10 ml olive oil.

Rational for selected supplements:
1. TMG is taken because my level of homocysteine at 11.6 umol/L was higher that the desired 7.2 umol/L for LE purposes.
2. DHEA to try to lower my estradiol of 38 pg/mL for LE purposes.
3. IP6 to chelate iron, since my level was high at 214 ug/dL. I have also been giving blood every two months (will continue for a half year) and have started using IP6 for maintenance.

I'm a 43-year-old male, 5'8'', 145 pounds (BMI of about 22). I try to eat a lower carbohydrate diet with lots of colorful veggies. Running is my main form of exercise. I have little family history of heart disease, but cancer does run in my family, especially on the side of the men. I'd like to raise my current HDL of 41 mg/dL.

I'm by no means an expert, but have put this list together guided by the conclusions of people on this forum, so suggestions are welcome!

Stephen

Edited by stephen_b, 26 January 2008 - 11:57 PM.

[balance]

Looks good. I'd add in a good pre&probiotic. I like garden of life's primal defense ultra and combine it with Jarrow inulin FOS powder. Lef's blueberry pomegranate cocoa is a great product that u could add. I'd really recommend u take 4 of the mitochondrial energy optimizer to fully benefit from lipoic acid and especially carnosine. Some bone support like strontium citrate 680mg elemental and/or aor's ortho bone wouldn't hurt.

[stephen_b]

Looks good. I'd add in a good pre&probiotic. I like garden of life's primal defense ultra and combine it with Jarrow inulin FOS powder. Lef's blueberry pomegranate cocoa is a great product that u could add. I'd really recommend u take 4 of the mitochondrial energy optimizer to fully benefit from lipoic acid and especially carnosine. Some bone support like strontium citrate 680mg elemental and/or aor's ortho bone wouldn't hurt.

Thanks for the comments. I actually do take 4 of the mitochondrial energy optimizers, but forgot to add the last two.

Stephen

[krillin]

You may need more TMG. BAC's powder is a cheap way to get it. (And wouldn't DHEA raise estradiol via DHEA -> 5-AD -> estradiol? When Patrick Arnold took 2-3 grams/day DHEA he started getting titties.)

J Nutr. 2006 Jan;136(1):34-8.
Erratum in: J Nutr. 2007 Apr;137(4):1124.
Orally administered betaine has an acute and dose-dependent effect on serum betaine and plasma homocysteine concentrations in healthy humans.
Schwab U, Törrönen A, Meririnne E, Saarinen M, Alfthan G, Aro A, Uusitupa M.
Department of Clinical Nutrition, University of Kuopio, Finland. Ursula.Schwab@uku.fi

Betaine, i.e., trimethylglycine, is linked to homocysteine metabolism. A 3-mo daily betaine supplementation decreased even normal plasma total homocysteine (tHcy) concentrations in humans. The pharmacokinetic characteristics and metabolism of betaine in humans have not been investigated in detail. The aim of this study was to assess the pharmacokinetics of orally administered betaine and its acute effect on plasma tHcy concentrations. Healthy volunteers (n = 10; 3 men, 7 women) with normal body weight (mean +/- SD, 69.5 +/- 17.0 kg), 40.8 +/- 12.4 y old, participated in the study. The betaine doses were 1, 3, and 6 g. The doses were mixed with 150 mL of orange juice and ingested after a 12-h overnight fast by each volunteer according to a randomized double-blind crossover design. Blood samples were drawn for 24 h and a 24-h urine collection was performed. Orally administered betaine had an immediate and dose-dependent effect on serum betaine concentration. Single doses of 3 and 6 g lowered plasma tHcy concentrations (P = 0.019 and P < 0.001, respectively), unlike the 1-g dose. After the highest dose, the concentrations remained low during the 24 h of monitoring. The change in plasma tHcy concentration was linearly associated with betaine dose (P = 0.006) and serum betaine concentration (R2 = 0.17, P = 0.025). The absorption and elimination of betaine were dose dependent. The urinary excretion of betaine seemed to increase with an increasing betaine dose, although a very small proportion of ingested betaine was excreted via urine. In conclusion, a single dose of orally administered betaine had an acute and dose-dependent effect on serum betaine concentration and resulted in lowered plasma tHcy concentrations within 2 h in healthy subjects.

PMID: 16365055

[balance]

I don't see why anyone would want/need to take 2-3 grams of DHEA per day... DHEA in normal doses does not cause any problems regarding estogen metabolism.

[stephen_b]

I haven't updated my regime in a while, so here goes.

Before breakfast

• ALCAR (2 g)

Morning with breakfast

• Benfotiamine (80 mg)
• Curcumin (1 capsule LEF BCM-95 Bio-Curcumin 400 mg)
• Fish oil (1 tbsp. Jarrow Max DHA Liquid)
• Generic BPAP (20 mcg)
• Lithium orotate (120 mg containing 4.9 mg Li)
• Mineral complex NOW Full Spectrum Minerals (2 capsules)
• Niacin (as nicotinic acid 100 mg)
• Source Naturals, Coenzymate B Complex (1 tablet sublingually)
• Sublingual B Complex Jarrow Sublingual methyl-B12 (1 lozenge)
• Ubiquinol (50 mg)
• Vitamin A (5000 IU from fish liver oil)
• Vitamin D3 (7500 IU)
• Vitamin E (Mixed Tocopherols and Tocotrienols 1 Softgel)
• Vitamin K2 as MK-4 (10 mg)

Lunch

• Pyridoxamine (50 mg)
• Niacin (as nicotinic acid 100 mg)

Supper

• Curcumin (LEF BCM-95 Bio-Curcumin 400 mg)
• Mineral complex NOW Full Spectrum Minerals (1 capsule)
• Niacin (as nicotinic acid 100 mg)
• Pyridoxamine (50 mg)
• Ubiquinol (50 mg)

Before bedtime

• Bacopa plus ginko (300 mg)
• Generic ALT-711 (80 mg)
• Melatonin (6 mg)

I do take a few other things on occasion (sublingual NAD, NAC, aminoguanidine, resveratrol, astralagus) too.

StephenB

Edited by stephen_b, 13 April 2009 - 04:30 AM.

[pycnogenol]

[*]Generic ALT-711 (80 mg)

Hi Stephen,

What is the name of the supplier you get the ALT-711 from?

— pycnogenol

Edited by pycnogenol, 13 April 2009 - 12:30 AM.

[niner]

[*]Generic ALT-711 (80 mg)

What is the name of the supplier you get the ALT-711 from?

And what is your sense, if any, of how it's working? Notice anything?

[stephen_b]

pycnogenol, PM me if interested.

niner, I've been taking it since around the first of the year. Typically, the most noticeable effect is a lowering of blood pressure. My blood pressure when I wake up is about 101/60. It hasn't gone down. During the day though it had gotten higher, with numbers like 128/80. It doesn't often get over 117/75 now.

Oh, there's one other thing I've noticed with it. How can I put this ... I am favorably inclined to endorse the conclusions of PMID 16490017.

StephenB

[david ellis]

Stephen,
I am wondering if your Vitamin D intake might have changed your estradiol levels? I suspect it has in my case, driving it down to 15 from 30.

[stephen_b]

Stephen,
I am wondering if your Vitamin D intake might have changed your estradiol levels? I suspect it has in my case, driving it down to 15 from 30.

Well, at a vitamin D intake of 4000 IU my estradiol level was 23 pg/ml a year ago. At 2000 IU estradiol was 38 pg/ml two years ago. I'm getting retested in a couple of weeks, so we'll see. You might be on to something there.

A doc at LEF suggested that 30-60 mg of zinc lowers estradiol.

StephenB

[stephen_b]

BPAP removed -- I don't seem to be able to tolerate it in a daily dose. It does the same thing to me that deprenyl does -- I start hearing my pulse in my ears, especially when I lie down at night.

It would be nice to have something to slow the age related decline of neurons in the brain. I'm considering taking it at wider intervals, lower doses, or substituting methylene blue.

StephenB

[4eva]

Hearing your pulse in your ear when lying down is considered an indication of histadelia.

http://www.naturopat.../nutrition.html

This condition is considered controversial.

Histadelia is the same as MTHFr SNP and undermethylation.

Your high HCY levels would seem to be consistent with a methylation problem.

Some of the supplements you take are not the right forms. The coenzymate B complex, for example, has folic acid and not methylfolate.

[stephen_b]

Hearing your pulse in your ear when lying down is considered an indication of histadelia.

http://www.naturopat.../nutrition.html

This condition is considered controversial.

Histadelia is the same as MTHFr SNP and undermethylation.

Your high HCY levels would seem to be consistent with a methylation problem.

Some of the supplements you take are not the right forms. The coenzymate B complex, for example, has folic acid and not methylfolate.

Thank you for responding. Interestingly, I did actually get a kryptopyrole test, and I was not quite borderline.

My homocysteine levels were 11.6 umol/l on 2007-10 and 13.3 umol/l on 2008-05, which is on the high side. The LEF consult person recommended 7.2 as a target, and suggested TMG, B12, and B6.

I've read that non-vegetarians who are undermethylators might benefit from methylfolate as their methyl donor. I do have sublingual M-B12 and DMG too, and I'm wondering if I do need methyl donor supplementation and if so in what form.

The first two comments for Solgar's Metafolin product at iHerb were interesting:

Sixty percent of people are either heterozygous or homozygous for the MTHFR polymorphism, meaning regular folic acid is not only useless, but potentially harmful because it blocks absorption of the meagre amounts of methyl folate we receive. Methyl folate, as the activated form, completely bypasses this problem. Methyl folate is so important for methylation pathways, and a lack can contribute to depression, elevated homocysteine levels, CFS/ME, fibromyalgia, heart disease, fertility problems, and a host of other degenerative conditions. This product is so important, particularly since most supplements are full of folic acid which as I said above can cause more harm than good. Everyone should be taking this instead.

and

Thank you for the metafolin. This bioactive folic acid is needed because many people can't convert it to the body ready form. I have low ferritin and my doctor recommended metafolin and ferrous succinate.

I do have issues with muscle pain that I keep blaming on a hard mattress, but I'm not sure if that's the issue.

I'm trying to find some supporting studies for that last ferritin claim; my serum ferritin was quite low too at 22 ng/ml, but I haven't found anything yet.

StephenB

[4eva]

If you wanted to supplement for undermethylation or histadelia you should make some other changes.

Niacinamide instead of niacin.
SAMe as the main methyl donor. TMG to help lower HCY.

Calcium and magnesium are important. Vitamin C helps too; it lowers histamine. Zinc, copper and manganese are needed and should be balanced (though not always easy to do).

I think some other form of B6 might be good, p-5-p would be the obvious one. Too much B6 can be a problem though. But restoring dream recall is a good indicator of adequate B6 levels.

I'm not sure what is causing muscle pain and low ferritin but would think it might be something your missing. (Calcium and magnesium are important.)

If I recall correctly, riboflavin helps with metabolising iron. MTHFr need ribo. You take B1 and B3 separately so it might be creating an imbalance to take only some B vitamins in higher doses and not others like ribo.

[stephen_b]

It's interesting how Dr. Walsh's (Pfeiffer Treatment Center) protocol recommends against folate supplementation for under-methylators, but other sources take the opposite position ("The folate puzzle. Part I: The Janus face of folate in cancer medicine", full text linked there):

The biochemical pathways of dietary methionine produce S-adenosylmethionine, which is the universal methyl donor and a precursor for homocysteine. To save methionine for the body, homocysteine can be converted to methionine. This bioreaction shares the reaction process with the folate bioreaction cycle. Thus, dietary folate and methionine are biochemically linked and folate intake may reduce homocysteine levels. This explains why homocysteine is a sensitive marker for folate deficiency and reduced biomethylation.

Interesting Pfeiffer commentary here. Perhaps Dr. Walsh is against regular folic acid but not methylfolate; hopefully I'll get to ask him next month if I see him at a conference I'm attending.

StephenB

Edited by stephen_b, 17 April 2009 - 05:37 AM.

[4eva]

Originally it was recommended that undermethylators or histadelics avoid folic acid (before methylfolate was available).

Histadelics or those with MTHFr SNP have a problem with metabolising folate and it becomes trapped. And this type might show high folate levels on lab results even without supplementation.

And that's why this type needs methylfolate. It bypasses this problem of trapped folate because of undermethylation.

But both folic acid and nicotinic acid raise histamine levels. (The main method the body gets rid of histamine is through methylation.)

[krillin]

Here's an exercise for people to try: compare the cost per methyl group of methylfolate and TMG. You'll find that the only reason to take methylfolate is to bypass the rate-limiting conversion of folic acid to dihydrofolate, and folinic acid does it cheaper. I'll need to see some proof that methylfolate in reasonable doses can treat the MTHFR polymorphism: the biological lifetime of a folic acid molecule is a heck of a lot longer than the lifetime of its methyl group, so bypassing MTHFR just once per molecule won't do you much good. (Besides, that polymorphism can be rendered harmless by single-digit milligram doses of B2.)

[stephen_b]

Hi krillin. Would you expect folinic acid by itself to lower elevated homocysteine levels?

[stephen_b]

LEF has a nice write-up, "When Homocysteine Levels Won’t Come Down". They recommend for those with homocysteine > 7-8 µmol/L, in order

• Folic acid — 1600-3200 mcg
• Vitamin B12 — 1000-2000 mcg
• Vitamin B6 — 250-1000 mg
• TMG — 4000-8000 mg

It says:

Some people fail to convert folic acid to L-methylfolate, which results in them accumulating higher-than-desired levels of homocysteine.

That would seem to apply to me, as my b-complex (I also sometimes take Jarrow B-right) is already at the level recommended for people without elevated homocysteine. The article goes on to recommend L-methylfolate from Source Naturals if the above doesn't do the trick. I was impressed that they recommended a competitor's product.

StephenB

[stephen_b]

"Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C->T polymorphism" (PMID 16380544).

[david ellis]

LEF has a nice write-up, "When Homocysteine Levels Won’t Come Down". They recommend for those with homocysteine > 7-8 µmol/L, in order

• Folic acid — 1600-3200 mcg
• Vitamin B12 — 1000-2000 mcg
• Vitamin B6 — 250-1000 mg
• TMG — 4000-8000 mg

It says:

That would seem to apply to me, as my b-complex (I also sometimes take Jarrow B-right) is already at the level recommended for people without elevated homocysteine. The article goes on to recommend L-methylfolate from Source Naturals if the above doesn't do the trick. I was impressed that they recommended a competitor's product.

StephenB

Steve,
I have been using LEF's protocol since 2005 for homocysteine and I was successful in controlling it, getting tests of 7.9 in '06, 9.9 in '07(lax in my supplementation), and 6.9 umol/L result in '08.

However, in April this year, I tested my levels of amino acids and came up low in histidine(30thpercentile) and threonine(18th percentile), high in the remaining amino acids(75-90th percentile). Low histidine, with high scores in the other amino acids indicates folic acid deficiency.

My doctor suspected MTHFR was responsible, and recommended Bayer's methylfolate, more TMG, and threonine supplementation. I understand the folic acid acid deficiency results in a feeling of anxiety. Which I did have. And the stress of the anxiety lowered my histidine levels. Also the anxiety levels resulted in a high cortisol profile which catabolically reduced my threonine levels.

The feelings of anxiety and depression lifted in a few days. I used to believe that I was responsible for how I felt. A good attitude was my responsibility. It was an eye opener to discover that minor changes in supplementation would make major psycholgical changes.

I am posting here in your thread because I am trying to sort out why apparently I don't have a folic acid deficiency when treating homocysteine levels, but do have a folic acid deficiency that catabolizes my histidine. It does seems that krillin was correct about methyl from TMG would be cheaper and as effective as methylfolate in treating homocysteine. Also it is interesting that Metametrix's suggestion to treat low histidine with more folic acid and low threonine with more TMG also. Soon in the future, I should substitute folic acid for the methlyfolate and find out if it is essential. Maybe the difference is due to being homozygous or hetereozygous for MTHFR. Right now though, I will wait before challenging the success I had.


edit-missing parenthesis

Edited by david ellis, 08 July 2009 - 06:26 PM.

[stephen_b]

I am posting here in your thread because I am trying to sort out why apparently I don't have a folic acid deficiency when treating homocysteine levels, but do have a folic acid deficiency that catabolizes my histidine. It does seems that krillin was correct about methyl from TMG would be cheaper and as effective as methylfolate in treating homocysteine. Also it is interesting that Metametrix's suggestion to treat low histidine with more folic acid and low threonine with more TMG also. Soon in the future, I should substitute folic acid for the methlyfolate and find out if it is essential. Maybe the difference is due to being homozygous or hetereozygous for MTHFR. Right now though, I will wait before challenging the success I had.


edit-missing parenthesis

Sorry about not seeing this sooner. Krillin's point about methylfolate being able to donate a methyl group once and then it's done seems valid, especially since folate is long lived in the body. For pure methyl group donation, TMG seems the way to go.

I had had anxiety in the past but not any more. Could methylfolate have been responsible? Maybe. Another anxiety reducer for me has been low dose naltrexone. I love the stuff. For long term preservation of immune system function, it makes a lot of sense to me.

[1kgcoffee]

What about MSM? You can take very large doses without any worry of toxicity. It's super cheap.

[Sillewater]

I was reading about oxidation and Kupffer cells and came across the fact that glycine inhibits Kupffer cells (has to do with calcium channel) the study is here:

Carcinogenesis. 1999 Jan;20(1):27-33.
Kupffer cell oxidant production is central to the mechanism of peroxisome proliferators.
Rose ML, Rivera CA, Bradford BU, Graves LM, Cattley RC, Schoonhoven R, Swenberg JA, Thurman RG.

Laboratory of Hepatobiology and Toxicology, CB#7365, MEJB, Curriculum in Toxicology, University of North Carolina, Chapel Hill 27599-7365, USA.
Abstract
Increased cell proliferation most likely plays a key role in peroxisome proliferator-induced liver cancer. Recently, Kupffer cells were shown to be responsible for Wy-14,643-induced cell proliferation. However, the mechanism by which peroxisome proliferators activate Kupffer cells is unknown. Since gut-derived endotoxin is a known activator of Kupffer cells, the hypothesis that it is involved was evaluated. Increased cell proliferation and peroxisome induction were unaffected by gut sterilization. Moreover, endotoxin was not detectable in portal blood following treatment with Wy-14,643. Therefore, it is concluded that gut-derived endotoxin is not responsible for Kupffer cell activation. To test the hypothesis that Kupffer cells are activated by Wy-14,643 directly, Kupffer cell superoxide production was measured following treatment in vitro. Wy-14,643 increased superoxide production in a dose-dependent manner (0.1 and 50 microM) with half-maximal stimulation at 2.5 microM. Diethylhexylphthalate (DEHP) and ethylhexanol did not increase superoxide production even at doses 50 times higher than Wy-14,643; however, monoethylhexylphthalate (MEHP) activated superoxide production as effectively as Wy-14,643 with half-maximal stimulation at 5 microM. Treatment with Wy-14,643 for 21 days caused a 2-fold increase in Kupffer cell superoxide production while DEHP did not. Pretreatment of Kupffer cells with staurosporine (0.01-10 pM) completely blocked generation of superoxide demonstrating that protein kinase C is required. Moreover, Wy-14,643 increased Kupffer cell protein kinase C activity 3-fold. Pretreatment of Kupffer cells with the amino acid glycine (0.01-3 mM), which blunts calcium signaling, inhibited Wy-14,643-stimulated superoxide production and increased protein kinase C activity completely. These data are consistent with the hypothesis that potent peroxisome proliferators (Wy-14,643 and MEHP) directly activate Kupffer cell production of oxidants via mechanisms involving protein kinase C. Further, peroxisome proliferator treatments that sustain elevated rates of cell proliferation (e.g. Wy-14,643) activate Kupffer cell superoxide production following long-term dietary treatment supporting the hypothesis that Kupffer cell-derived oxidants are involved in peroxisome proliferator-induced neoplasia.

PMID: 9934846 [PubMed - indexed for MEDLINE]Free Article

There are other studies noting the same thing. Anyways I remember you supplement with glycine. I don't know if that would be a problem in vivo but I thought I should just let you know.

[krillin]

Here's an exercise for people to try: compare the cost per methyl group of methylfolate and TMG. You'll find that the only reason to take methylfolate is to bypass the rate-limiting conversion of folic acid to dihydrofolate, and folinic acid does it cheaper. I'll need to see some proof that methylfolate in reasonable doses can treat the MTHFR polymorphism: the biological lifetime of a folic acid molecule is a heck of a lot longer than the lifetime of its methyl group, so bypassing MTHFR just once per molecule won't do you much good. (Besides, that polymorphism can be rendered harmless by single-digit milligram doses of B2.)

This advice sucks. The folinic acid on the market is racemic. The unnatural d-folinic acid (also called 6R folinic acid) does not interfere with rescue from methotrexate (a dihydrofolate reductase inhibitor) therapy (PMID: 8173189), but it does interfere with the 5-fluorouracil/l-folinic acid anti-cancer effect (PMID: 7483142). Methylene tetrahydrofolate made from l-folinic acid stabilizes the fluorodeoxyuridylate (FdUMP)-thymidylate synthase complex (PMID: 8353102), so that the dUMP -> dTMP reaction doesn't occur and dividing cancer cells end up with faulty DNA. There is thus the possibility that d-folinic acid could interfere with dUMP -> dTMP in normal cells and cause faulty DNA production.

Solgar's Metafolin is chirally pure. LEF's label, however, says "Folate (as 5-Methyltetrahydrofolic acid (5-MTHF), and calculated based upon the biologically Active 6S isomer)", so it appears that they are selling something that is both inferior and more expensive.

TMG is potentially bad, as proposed by Stephen B, although I think the person he quoted garbled the science. I can't find evidence that TMG induces BHMT, but methionine does inhibit methionine synthase. And since there is no BHMT in the brain, TMG does all its methylation outside it and the methionine produced can travel to the brain and inhibit its methionine synthase.

This is a problem because the methionine that is incorporated in phospholipid-methylating D4 receptors (MET313) can get stuck as homocysteine and thus be unable to increase membrane fluidity.

Alternative sources of methyl groups which feed into the B12 pathway and not the TMG pathway are serine, DMG, or glycine. Alternative agents to counteract reductive stress from NADH accumulation from the loss of oxphos in free-radical damaged mitochondria are cholines and carnitines.

[kismet]

TMG is garbage to begin with as it probably raises TC or LDL-C.

[stephen_b]

May 2011 Update

Before breakfast
Beta alanine (1/4 tsp/1g)
Methylene blue (60 mcg)
Rhodiola (100/200 mg)

Breakfast
Cod liver oil (1 softgel 2500 IU)
Curcumin (600 mg)
Niacinamide (100 mg)
Vimmortal multivitamin (1 capsule)
Vitamin D3 (5000 IU)
Vitamin K2-MK4 (1 mg)
Vitamin E full spectrum (1 softgel)

Lunch
Vimmortal multivitamin (1 capsule)

Supper
Vimmortal multivitamin (1 capsule)

Before bedtime
l-Arginine (3 capsules)
Bacopa Extract (1x150mg)
D-Limonene (1 capsule)
Glycine (3 g)
Melatonin (6 mg)
Pycnogenol (100 mg)

Biweekly
Iodide (1 drop 19 mg)

I'm taking a half dose of Vimmortal. I settled on getting folate by eating a cup or two of spinach daily. I generally have two egg yolks (one white) daily, and try to eat beef liver once weekly. I take occasional fish oil, but will probably cut back once my 1/4 grass fed cow is in the freezer. I have been running 40 miles/week, and ran into some soreness issues after letting my vitamin D get below 35 ng/ml (my target is 50 ng/ml).

[e Volution]

ALCAR? IP-6? Methylcobalamin? You're only getting 0.5mg of Lithium with the half dose of Vimmortal + whatever from diet but Lithium looks so safe to me I think it's worth getting an entire mg from supplementation.

Edited by e Volution, 13 May 2011 - 02:53 PM.

[Justchill]

Why did you make these changes stephen? How are you feeling on these supplements?