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here is an interesting table from the following article:
Zinc and copper in multiple sclerosis
Journal of Neurology, Neurosurgery, and Psychiatry 1982;45:691-698
free full text

at first i tried making this chart in html, but after some much-needed advice, here is the previewed, tweaked, now finally somewhat aligned table:
adapted from: Palm and Hallmans. (1992). Zinc and copper in multiple sclerosis.

i had found this table while hunting for biochem diffs btw guys and gals with ms. freaks me out even more now, knowing that my zn was 8.6 at the end of 2007. (sorry 'bout all these edits, table formatting haaard)

ps. normal range is 11.5-18.5, so if you are told your zinc level is "normal", it could well be within the "ms part" of that range.

okay this is the funniest nutrition quote i've ever seen gotta relay

"We hate to say it, but in a zinc-deficient adolescent, sexual excitement and excessive masturbation might precipitate insanity."—Zinc and Other Micro-nutrients (Keats: New Canaan, Conn., 1978), p. 45.

an old but interesting abstract... nutrition, immune function... more dots to connect...

it's been a while since i looked at the cell function of the immune system in detail - any significant holes to be poked in this abstract, with 30 years of hindsight under our belts?

Med Hypotheses. 1979 Sep;5(9):969-85.
The nutritional regulation of T lymphocyte function.

Prostaglandin (PG) E1 plays a major role in the regulation of thymus development and T lymphocyte function and the evidence for this is reviewed. The production of PGE1 is dependent on nutritional factors with linoleic acid, gamma-linolenic acid, pyridoxine, zinc and vitamin C playing key roles.
Inadequate intake of any one of these will lead to inadequate PGE1 formation and defective T lymphocyte function.
Megadoses of any one are likely to be only minimally effective in the absence of adequate intakes of the others.
By careful attention to diet it should be possible to activate T lymphocyte function in the large number of diseases including rheumatoid arthritis, various auto-immune diseases, multiple sclerosis, and cancer in which such function is defective. It is possible that T lymphocytes may require both endogenous and exogenous PGE1 in order to function adequately. It is therefore of particular interest that many cancer cells and virally infected cells are unable to make PGE1 because they cannot convert linoleic acid to gamma-linolenic acid. The direct provision of gamma-linolenic or dihomo-gammalinolenic acids in these situations is worthy of full investigation.

i've recently started to tie together the relatively low levels of both zinc and uric acid in ms patients.

i don't know why i didn't stumble across this sooner, but i didn't. anyway, they're both low in ms patients, and i'm starting to compile research that looks at the relationship between zinc and uric acid. i have posted things here and there but i'm going to start putting it all in one place on this thread.

here's today's tidbit:
[2017 link update] http://bit.ly/2i8g8mp
basically, it compares what zinc deficient diet did to women on or off oral contraceptives.

the uric acid findings

Code: Select all

      UA BEFORE                       UA AFTER ZN DEPLETION
+OCA  4.6 mg/dL  (273.608 µmol/L)     3.6 mg/dL (214.128 µmol/L)
-OCA  4.3 mg/dL  (255.764 µmol/L)     3.6 mg/dL (214.128 µmol/L)
       

214 µmol/L uric acid is around the MS remission average.

the zinc end date (day 36) findings

Code: Select all

	
+OCA  53.4 mg/dL     (8.1702 µmoI/L)
      38   mg/dL     (5.814  µmoI/L)
      62.8 mg/dL     (9.6084 µmoI/L)
      32.8 mg/dL     (5.0184 µmoI/L)
      37.3 mg/dL     (5.7069 µmoI/L)
				
-OCA  68.4 mg/dL     (10.4652 µmoI/L)
      87.2 mg/dL     (13.3416 µmoI/L)
      52.8 mg/dL     (8.0784  µmoI/L)
      78.2 mg/dL     (11.9646 µmoI/L)
      30.8 mg/dL     (4.7124  µmoI/L)

Clinical findings. Reduced resistance to infection (21), diarrhea (22, 23), and dermatological changes (21) occur in severely zinc-deficient animals and humans. These same symptoms were noted in seven of our ten subjects. This high frequency of clinical symptoms is unusual for our metabolic unit and may be related to the zinc-deficient diet. The subject with seborrheic dermatitis (3902) had followed ovo-lacto vegetarian food habits for 3 years

[JL note: only 3 ]

and entered the study with a low-normal serum zinc level, 75.8 /µg/dl. By day 36, her serum zinc had fallen to 32.8 /µg/dl ( table 6 ).

...in the +OCA group, the subject who finished with lowest zinc at 32.8 mg/dL (5.0184 µmoI/L) above was the vegetarian. i thought it was interesting that the zinc deficient diet resulted in greater drops in uric acid and zinc when subjects were taking oral contraceptives.

these subjects had pretty obvious external zinc deficiency signs, but they were clearly well below even the ms zinc average.

an interesting review of zinc and the immune system:

http://jn.nutrition.org/cgi/content/full/133/5/1452S
Zinc-Altered Immune Function
2003 The American Society for Nutritional Sciences
J. Nutr. 133:1452S-1456S
Supplement: 11th International Symposium on Trace Elements in Man and Animals

sample interesting citation:
61. Cakman, I., Kirchner, H. & Rink, L. (1997) Reconstitution of interferon-{alpha} production by zinc-supplementation of leukocyte cultures of elderly individuals. J. Interferon Cytokine Res. 13: 15–20.

so "normal range" 11.5-18.5 µmol/L
ms range for men ~11-15 µmol/L
ms range for women ~10-14 µmol/L

healthy controls average:
-men 18.20 µmol/L (95% CI=17.90-18.36)
-women 18.36 µmol/L (95% CI=18.05-18.66).

Clin Chim Acta. 2006 Nov;373(1-2):132-8.
Serum vitamin A and zinc levels of healthy people in northeast Thailand.
BACKGROUND: Vitamin A and zinc are micronutrients which co-related to diseases afflicting northeast Thais. Vitamin A and zinc concentrations in serum have been studied in healthy northeast Thais between 23 and 75 years. METHODS: Vitamin A was analyzed by HPLC and zinc was determined by flame atomic absorption spectrometry. RESULTS: The average serum vitamin A level of the population (n=744) was 2.30 micromol/l (95% CI=2.25-2.35). Males had significantly higher vitamin A levels than females, i.e. 2.61 micromol/l (95% CI=2.53-2.68 ) vs. 2.03 micromol/l (95% CI=1.98-2.09) (p<0.0001). The vitamin A level of females tended to increase significantly with age (p<0.005), whereas in males levels were relatively constant throughout the age range studied. The average serum zinc level of the population (n=1113) [JL comment: nice n!!!] was 18.20 micromol/l (95% CI=18.05-18.36). There was no significant difference in the zinc levels between males and females, i.e. 18.20 micromol/l (95% CI=17.90-18.36) vs. 18.36 micromol/l (95% CI=18.05-18.66). The zinc level tended to decrease significantly as age increased, particularly in the male population (p<0.05). CONCLUSION: The results from this study provide baseline data of serum vitamin A and zinc levels in healthy northeast Thais.

another vote for serum zinc at 18:

Reductions in red meat and increases in cereals in the diet may compromise the intake and bioavailability of Zn. In this cross-sectional study of 330 premenopausal New Zealand women aged 18--40 years, we have assessed the inter-relationships among dietary intakes (via computer-administered food-frequency questionnaire), biochemical Zn status, and anthropometric indices, and compared our results with earlier data. Fasting serum (12.00 (sd 1.36) micromol/l) and hair Zn (2.71 (sd 0.36) micromol/g) were lower than those for young Dunedin, New Zealand, women in 1973 (non-fasting serum Zn 18.6 (sd 4.6) micromol/l, hair Zn 2.99 (sd 0.35) micromol/g). Further, our mean serum Zn was at the 25th percentile of the US National Health and Nutrition Examination Survey (NHANES) (1976--1980) reference sample for women aged 20--44 years. Meat-poultry-fish contributed only 28 % total Zn in the present study, a level comparable with that from cereals-nuts-legumes (27 %), compared to about 40 % in 1989. Significant negative correlations existed between serum Zn and dietary [phytate]:[Zn] molar ratios (r -0.163, 35 % had diets with [phytate]:[Zn] >15, a level said to compromise Zn status...

and one more vote for zinc at 18:

Blood Concentrations of Selenium, Zinc, Iron, Copper and Calcium in Patients with Hepatocellular Carcinoma
...The results demonstrate that these patients have a lower concentration of selenium (0.18±0.02 μg/ml vs. 0.28±0.06 μg/ml) and zinc (11.2±2.75 μg/ml vs. 18.2± 7.33 μg/ml) than healthy controls (p<0.05)... Thus, hepatocellular carcinoma seems to be associated with the changes in the whole blood concentrations of selenium, zinc, iron, copper and calcium.

[JL EDIT: actually on another thread, NHE raised something pretty valid about this abstract - the units here being μg/ml when the numbers seem to correspond better to findings of 18.2 in other studies using μmol/L. there doesn't appear to be a corresponding author listed on the abstract as far as i can tell][JL EDIT: i have contacted the journal to inquire].

okay how the heck did i miss this - maybe i have posted it elsewhere at some time?? anyway...

Am J Med Sci. 1986 Nov;292(5):289-92.
Oral zinc therapy normalizes serum uric acid level in Wilson's disease patients.
Umeki S, Ohga R, Konishi Y, Yasuda T, Morimoto K, Terao A.
The authors investigated changes in the serum uric acid (s-UrA) level seen in a Wilson's disease patient who had to undergo oral zinc therapy because of the occurrence of D-penicillamine-induced acute sensitivity reactions, including neutrophilic agranulocytosis, thrombocytopenia, and skin eruptions. Although s-UrA levels were low before oral zinc therapy (mean +/- SD, 1.60 +/- 0.20), they increased (mean +/- SD, 2.63 +/- 0.32) to within normal range (2.8-8.0 mg/dl) after therapy. There were no significant changes in the renal tubular reabsorption of UrA during oral zinc therapy. This therapy also produced an improvement of the decreased cholinesterase (ChE) values usually seen in Wilson's disease. These results suggest that oral zinc therapy can normalize UrA metabolism in Wilson's disease by improving liver dysfunction and increasing UrA synthesis.

Well this is a bit of a head scratcher...


Increase of uric acid and purine compounds in biological fluids of multiple sclerosis patients.

Clin Biochem. 2009 Mar 30.
Amorini AM, Petzold A, Tavazzi B, Eikelenboom J, Keir G, Belli A, Giovannoni G, Di Pietro V, Polman C, D'Urso S, Vagnozzi R, Uitdehaag B, Lazzarino G.
Institute of Biochemistry and Clinical Biochemistry, Catholic University of Rome "Sacro Cuore", Rome, Italy.

OBJECTIVES: In this study, the concentrations of uric acid, purine profile and creatinine in samples of cerebrospinal fluid and serum of multiple sclerosis (MS) patients were measured by HPLC and compared with corresponding values recorded in patients without MS (cerebrospinal fluid) and healthy subjects (serum).

DESIGN AND METHODS: All samples were deproteinized with ultrafiltration (which ensures minimal sample manipulation and efficient protein removal) and then assayed for the synchronous HPLC separation of uric acid, hypoxanthine, xanthine, inosine, adenosine, guanosine and creatinine.

RESULTS: Values of all compounds assayed were significantly higher in both biological fluids of MS patients with respect to values measured in controls. In particular, serum hypoxanthine, xanthine, uric acid and sum of oxypurines were, respectively, 3.17, 3.11, 1.23 and 1.27-fold higher in these patients than corresponding values recorded in controls (p<0.001).

CONCLUSIONS: Differently from what previously reported, we here demonstrate that all purine compounds, including uric acid, are elevated in biological fluids of MS patients. Reinforced by the trend observed for creatinine, this corroborates the notion of sustained purine catabolism, possibly due to imbalance in ATP homeostasis, under these pathological conditions. These results cast doubt on the hypothesis that uric acid is depleted in MS because of increased oxidative stress, rather suggesting that this disease causes a generalized increase in purine catabolism. As observed in other pathological states, uric acid, purine compounds and creatinine, can be considered markers of metabolic energy imbalance rather than of reactive oxygen species, even in MS.

http://www.ncbi.nlm.nih.gov/pubmed/19341721

interesting.. quite a bit in there - but to the salient bits:
their healthy controls appear to have UA around 260, and the MS patients up around 315 umol/L.
authors say their HPLC methodology is better than other studies, ie 'colorimetric assay' which appears to be slightly dumbed-down spectrophotometry.
my lab, as far as i can tell, uses 'uricase' methodology to assess UA.
this study compares uricase methodology to HPLC:
broken link updated.... study link (sorry no abstract, only full text preview...)
they find that coffee and tea drinkers get false high uric acid results when using the uricase method. the HPLC method gives a LOWER result because it does not get influenced by subjects' consumption of coffee or tea.
that raises interesting questions, because my past results have been 194 then 188 umol/L using (i think) the uricase method. i am a coffee and tea drinker. if the HPLC method would have found a lower number, that's a far cry from 315.
i have no idea if uricase and colorometric methods are supposed to be the same, something to ponder.

can't find any other studies of HPLC methods for UA in MS. we'll have to wait and see what turns up i guess

dignan wrote:CONCLUSIONS: Differently from what previously reported, we here demonstrate that all purine compounds, including uric acid, are elevated in biological fluids of MS patients. Reinforced by the trend observed for creatinine, this corroborates the notion of sustained purine catabolism, possibly due to imbalance in ATP homeostasis, under these pathological conditions. These results cast doubt on the hypothesis that uric acid is depleted in MS because of increased oxidative stress, rather suggesting that this disease causes a generalized increase in purine catabolism.

I have to admit that I did not read the full text, so my opinion is a little biased towards the "old way" of thinking.

It has been more than one study showing the relation between low uric acid and MS. Reading only the brief details above, I get the feeling that, because of oxidative stress in MS, the body attempts to compensate by producing more uric acid (which they measured in this study) but may consume it more rapidly than it can be produced, and hence the general previous findings of reduced serum UA (see gout and the MS statistical relation and UA increase effects on relapse rates). Just my personal unjustified point of view.

okay the results are starting to come in.

as detailed above and elsewhere here, over the last three years my UA levels have been 194, 188, 194 µmol/L (basically, smack on the "ms average", or worse, in spite of switching from vegan to meat-eating diet).

on the date of that last 194 µmol/L test, i had also asked for zinc and it was 8.6 µmol/L. i overcompensated with the supplements and went to just over 20. i'm aiming for 18.2. (normal range 11.5-18.5)

this month i've had zinc and uric acid tested together. the zinc results are not in yet. but the uric acid is up to 255µmol/L. what a difference!!! i'm aiming for closer to 300 ultimately. (normal range 140-360)

so curious to see those latest zinc results come in now

the zinc came back today, and the copper.
the zinc only went up from 8.6 to 11.6, and even with just that level of increase, the uric acid shot up from 194 to 255! once i get the zinc up a little higher i imagine the uric acid will normalize.
my copper result was high normal, have to get that dealt with. i think a bit more zinc will kill two birds with one stone: get the uric acid up, and bring the copper down.
dignan it's been a while since i was reading that one study, i plan to give it another look soon to see if i can make better sense of it..

For the experts (Jimmy Legs are you out there?)on selenium: do you take an actual supplement or do you eat three brazil nuts daily?? Also, how much zinc do you take? thanks! Indigo