220 replies to this topic

[rwac]

The article just says that reintroduction of Manganese into the diet improves the diabetes/insulin-resistance caused by deficiency. I copied some text, messy because it's a pdf.

A relationship between manganese and
abnormal carbohydrate metabolism was
first suggested by Rubenstein and co-workers
in 1962 (5). They reported the case of a
diabetic patient, resistant to insulin therapy,
who responded to oral doses of manganese
chloride with a consistent drop in blood
glucose levels. Manganese supplementation
was tried because of the ineffectiveness of
high doses of insulin in maintaining normal
blood glucose and the patient's statement
that his diabetic condition could be con
trolled to some extent by an extract of lucerne
(alfalfa, Medicago sativa). Analysis of the
alfalfa extract revealed a high concentration
of manganese In contrast to the effective
ness of manganese, oral supplements of zinc,
magnesium, cobalt or iron had no effect on
the patient's blood sugar levels, indicating a
specific role for manganese in insulin release
or action.

A similar observation was reported by
Shani et al. (6). They found that the sand
rat, whose natural diet is high in manganese,
developed an insulin-resistant diabetes when
fed a commercial rat feed containing rela
tively low levels of manganese. The diabetic
condition was reversed after reintroduction
of the manganese-rich natural diet.

Everson and Shrader (7) reported that
guinea pigs, born to manganese-deficient
dams and fed manganese-deficient diets
from birth to 60 days of age, had abnormal
glucose tolerance curves. Histological exami
nation of the pancreas from these animals
indicated that the deficient animals had
hypertrophied pancreatic islet tissue with
degranulated beta-cells and an increased pro
portion of alpha-cells(8). All of these signs o
manganese deficiency were reversed follow
ing dietary manganese supplementation fo
2 months.

Based on the latter observations, we formulated
the hypothesis that manganese deficiency
might result in altered insulin secretion.
Such an abnormality could explain, at
least partially, the altered glucose metabolism
observed in manganese-deficient animals.
The specific effect of manganese on insulin
metabolism might occur at several
levels, including reduced synthesis and/or
secretion of insulin (in addition to reduced
peripheral insulin sensitivity). In this study,
we have examined the relationship of manganese
deficiency and pancreatic function in rats.

Edited by rwac, 28 September 2009 - 03:02 AM.

[Lufega]

I read this before. Remembered after reading the part about the Sand rats. Makes you think about the treatment approach to diabetes. Glucose levels are so high that the body is exhausted of all its vitamins and minerals. Simple replenishing some of these lost nutrients, restores a bit of homeostasis.

[Lufega]

Hyaluronic acid through a new injectable nerve guide delivery system enhances peripheral nerve regeneration in the rat.

Seckel BR, Jones D, Hekimian KJ, Wang KK, Chakalis DP, Costas PD.

Department of Plastic and Reconstructive Surgery, Lahey Clinic, Burlington, Massachusetts 01805, USA.
The use of non-neural conduits to bridge gaps in peripheral nerves has been noted in the literature for many years. A logical extension of this concept is the introduction of neurotrophic or growth promoting factors into the lumen. We present here an injectable nerve guide that allows percutaneous access to the microenvironment of the regenerating peripheral nerve within the guide's lumen. Hyaluronic acid, a compound associated with decreased scarring and improved fibrin matrix formation, is added sequentially to the regenerating peripheral rat sciatic nerve via this injectable nerve guide. Assessment of nerve regeneration and reinnervation shows better conduction velocity, higher axon counts, and a trend toward earlier myelination with hyaluronic acid compared with saline. This work not only implies hyaluronic acid's role as an agent that aids nerve growth but also describes a new tool that allows percutaneous access to the milieu of a regenerating nerve.

So, HA aids nerve growth? Cool.

[rwac]

Another thing about Manganese.

It seems like even taking 5mg has a significant effect.
But the 2.5mg in my multi-mineral (NOW-amino acid chelate) doesn't seem to have any effect at all.

It's probably not well absorbed.

[Lufega]

Another thing about Manganese.

It seems like even taking 5mg has a significant effect.
But the 2.5mg in my multi-mineral (NOW-amino acid chelate) doesn't seem to have any effect at all.

It's probably not well absorbed.

You split the tab into quarters? This is good news though. I think you'll feel much safer taking the lower doses long term, if it continues to work. I do not use any multi's for that reason..

[Lufega]

Boom! I can finally explain all of my signs and symptoms (except the alpha 1 antitrypsin deficiency) in terms of dysautonomia (autonomic neuropathy)...

Looks like I spoke too soon.

Heart rate variability reflects severity of COPD in PiZ alpha1-antitrypsin deficiency.

Stein PK, Nelson P, Rottman JN, Howard D, Ward SM, Kleiger RE, Senior RM.
Division of Cardiology, Washington University School of Medicine, Barnes-Jewish Hospital, St. Louis, MO 63110, USA.

BACKGROUND: Analysis of heart rate variability (HRV) is a powerful method of assessing severity of conditions affecting the autonomic nervous system. STUDY OBJECTIVE: To determine if HRV is decreased and if HRV reflects severity in COPD. DESIGN: Prospective determination of HRV from 24-h outpatient Holter recordings.PATIENTS: Eighteen individuals with PiZ alpha1-antitrypsin deficiency: 13 with COPD and 5 with normal FEV1. HRV was also determined in 18 matched normal control subjects. Approximately 3 years after the initial recording, all COPD subjects were contacted to determine current status. MEASUREMENTS: Indexes of heart rate (HR) and HRV were compared for groups of patients with and without COPD and their control subjects. RESULTS: Mean and minimum HRs were higher in COPD patients. Virtually all indexes of HRV were significantly decreased in COPD patients. No differences were found in HR or HRV between PiZ individuals with normal FEV1 and their age-and gender-matched control subjects. Patients who had a change in status (ie, death, lung transplant, listed for transplant) had significantly higher daytime HRs, lower values for HRV indexes reflecting mixed sympathetic and parasympathetic modulation of HR, and reduced daytime high-frequency spectral power, an index of cardiac vagal modulation. Significant correlations (r=0.48 to 0.88) were found between FEV1 and these and other indexes of HRV. Most other indexes of HRV also tended to be lower for the group whose status had changed. CONCLUSION: PiZ alpha1-antitrypsin deficiency COPD is associated with abnormal cardiac autonomic modulation. Indexes of HRV appear to reflect severity and may have prognostic value in COPD patients.

Edited by Lufega, 28 September 2009 - 03:44 AM.

[Lufega]

Role of nitric oxide in the regulation of activity of proteinase inhibitors alpha(1)-antitrypsin and alpha(2)-macroglobulin by capsaicin-sensitive nerves.

Spiridonov VK, Tolochko ZS.
Laboratory of Functional Neuromorphology, Institute of Physiology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk, Russia. spiridon@iph.ma.nsc.ru
Regulation of activity of serine proteinase inhibitor a1-antitrypsin and nonspecific proteinase inhibitor alpha(2)-macroglobulin in the blood by nitric oxide was studied in intact rats and animals with damage to capsaicin-sensitive nerves. Nonselective nitric oxide synthase inhibitor L-NAME produced a dose-dependent increase in alpha(1)-antitrypsin activity in intact animals. Neuronal NO synthase inhibitor 7-nitroindazole increased alpha(2)-macroglobulin activity. Deafferentation with capsaicin was followed by a decrease in alpha(1)-antitrypsin activity. Both inhibitors of nitric oxide synthase increased activity of alpha(1)-antitrypsin in capsaicin-receiving rats. Nitric oxide precursor L-arginine had a normalizing effect on reduced activity of alpha(1)-antitrypsin after capsaicin deafferentation. Our results suggest that nitric oxide has a modulatory effect on activity of proteinase inhibitors and is involved in the effector influence of capsaicin-sensitive nerves on alpha(1)-antitrypsin activity.

I've used capsaicin before. This could have complicated things. Arginine is also needed to remove ammonia from the body. My ammonia levels are a bit on the high side (outside upper range) Using arginine might be worth a try. I have a old bottle of arginine/ornithine. I'll start using it ASAP.

Edited by Lufega, 28 September 2009 - 01:15 PM.

[Lufega]

methylselenocysteine upregulates the production of alpha-1-antitrypsin. The abstract doesn't specify the dose, though. So in my arsenal, I have methylselenocysteine, arginine (and manganese as a cofactor), and glisodin. Also the effect glisodin has is minimal but it probably targets part of the problem.

Growth and hepatospecific gene expression of human hepatoma cells in a defined medium.

Darlington GJ, Kelly JH, Buffone GJ.

The production of albumin, alpha-fetoprotein (AFP), and alpha-1 antitrypsin has been compared among human hepatoma cells cultured in medium containing serum, medium containing hormones and growth factors, and a basal medium containing selenium as the only supplement. Growth is sustained in all three media, and the expression of all three proteins was maintained for over 4 mo. in the various media. However, the quantitative production of albumin and AFP were dramatically different in the three media. Two hormones, insulin and triiodothyronine, influenced the level of secreted proteins. Triiodothyronine increases the amount of secreted albumin whereas insulin at 10 micrograms/ml reduced the level of total secreted protein.

Dietary supplementation with selenomethylselenocysteine produces a differential proteomic response.

Mahn AV, Toledo HM, Ruz M.
Department of Chemical Engineering, University of Santiago of Chile, Santiago, Chile. amahn_2000@yahoo.es

Organic forms of selenium offer important health benefits including cancer prevention. Selenium intake has been traditionally quantified as glutathioneperoxidase activity or selenium concentration in blood or tissues. However, these indexes do not reflect organic selenium intake. Effect of dietary supplementation of rats with selenomethylselenocysteine on the blood plasma proteome was investigated in order to detect protein abundance differences between experimental (supranutritional selenium supplementation) and control [minimum selenium dose and sodium selenate instead of selenomethylselenocysteine (SeMSeCys)] groups. Four experimental groups and six control groups consisting of six rats each were fed with base diet supplemented with SeMSeCys or sodium selenate in different concentrations for different periods of time. A proteomic approach, comprising two-dimensional gel electrophoresis and mass spectrometry, was used to assess protein abundance in blood plasma. Statistically significant differences in the abundance of some proteins were detected in all the experimental groups. Four proteins were found to increase their abundance in response to the experimental conditions: apolipoprotein E, haptoglobin and alpha-1-antitrypsin abundance was related to the extent of supplementation period and transthyretin in response to SeMSeCys dose. Apolipoprotein E and transthyretin were not differentially expressed when diets were supplemented with sodium selenate instead of SeMSeCys. We postulate that these proteins are potential biomarkers of chemoprotective selenium intake.

Selenoprotein S/SEPS1 modifies endoplasmic reticulum stress in Z variant alpha1-antitrypsin deficiency.

Kelly E, Greene CM, Carroll TP, McElvaney NG, O'Neill SJ.
Respiratory Research Division, Department of Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland.
Z alpha(1)-antitrypsin (ZAAT) deficiency is a disease associated with emphysematous lung disease and also with liver disease. The liver disease of AAT deficiency is associated with endoplasmic reticulum (ER) stress. SEPS1 is a selenoprotein that, through a chaperone activity, decreases ER stress. To determine the effect of SEPS1 on ER stress in ZAAT deficiency, we measured activity of the grp78 promoter and levels of active ATF6 as markers of the unfolded protein response in HepG2 cells transfected with the mutant form of AAT, a ZAAT transgene. We evaluated levels of NFkappaB activity as a marker of the ER overload response. To determine the effect of selenium supplementation on the function of SEPS1, we investigated glutathione peroxidase activity, grp78 promoter activity, and NFkappaB activity in the presence or absence of selenium. SEPS1 reduced levels of active ATF6. Overexpression of SEPS1 also inhibited grp78 promoter and NFkappaB activity, and this effect was enhanced in the presence of selenium supplementation. This finding demonstrates a role for SEPS1 in ZAAT deficiency and suggests a possible therapeutic potential for selenium supplementation.

Edited by Lufega, 28 September 2009 - 02:57 PM.

[rwac]

I've been taking 200mcg selenomethylselenocysteine for a while now, because I definitely feel worse if I stop. None of the other forms of selenium seem to work.

I suppose one of these proteins is the explanation ?
Do I possibly have an alpha-1-antitrypsin deficiency which I fixed without knowing about it.

[Lufega]

I've been taking 200mcg selenomethylselenocysteine for a while now, because I definitely feel worse if I stop. None of the other forms of selenium seem to work.

I suppose one of these proteins is the explanation ?
Do I possibly have an alpha-1-antitrypsin deficiency which I fixed without knowing about it.

The only way to know is by getting lab work done. Also, I only read the abstract so I don't know what dose is needed to up-regulate production of these proteins. Either way, I have some handy

[Lufega]

I´ve been thinking a lot lately about calorie restriction and intermittent fasting and it´s relationship to increased autophagy. This study shows that this might also help increase alpha 1 antitrypsin production by hepatocytes.

[quote]Chaperone-mediated regulation of hepatic protein secretion by caloric restriction.
Dhahbi JM, Cao SX, Tillman JB, Mote PL, Madore M, Walford RL, Spindler SR.

Department of Biochemistry, University of California, Riverside, Riverside, California 92521, USA.

Calorie restriction (CR) delays age-related physiological changes, reduces cancer incidence, and increases maximum life span in mammals. Here we show that CR decreased the expression of many hepatic molecular chaperones and concomitantly increased the rate and efficiency of serum protein secretion. Hepatocytes from calorie-restricted mice secreted twice as much albumin, 63% more alpha1-antitrypsin, and 250% more of the 31.5-kDa protein 2 h after their synthesis. A number of trivial explanations for these results, such as differential rates of protein synthesis and cell leakage during the assay, were eliminated. These novel results suggest that CR may promote the secretion of serum proteins, thereby promoting serum protein turnover. This may reduce the circulating level of damaging, glycoxidated serum proteins. Copyright 2001 Academic Press./quote]

Question is, would adding two fasting days a week, say Tuesday and Thursday, have this same effect??

[Lufega]

Added 3 grams of Arginine and found that is reduces my hand tremors. That was a nice surprise. Seems like Arginine has some effects of the GABA.

L-arginine potentiates GABA-mediated synaptic transmission by a nitric oxide-independent mechanism in rat dopamine neurons.

Shen KZ, Cox BA, Johnson SW.
Department of Physiology and Pharmacology, Oregon Health Sciences University, Portland 97201, U.S.A.

Effects of L-arginine in the nervous system are often attributed to nitric oxide. Using whole-cell patch pipettes to record membrane currents in voltage-clamp from dopamine neurons in the rat midbrain slice, the present studies found that L-arginine potentiates GABA-dependent membrane currents via a nitric oxide-independent mechanism. L-Arginine (0.3-10 mM) increased the peak amplitude, half-width duration and time constant of decay of GABA(B) receptor-mediated inhibitory postsynaptic currents in a concentration-dependent manner. In the presence of CGP 35348 (300 microM), a GABA(B) receptor antagonist, L-arginine also prolonged the duration of inhibitory postsynaptic currents mediated by GABA(A) receptors, but their amplitudes were reduced. L-Arginine (10 mM) also evoked 17+/-3 pA of outward current (at -60 mV) which was significantly increased in the presence of exogenous GABA (100 microM). Pressure-ejection of GABA from micropipettes produced outward currents mediated by GABA(B) receptors (recorded in bicuculline) or GABA(A) receptors (recorded in CGP 35348); both types of receptor-mediated currents were increased by L-arginine (10 mM). In contrast, outward currents evoked by baclofen, a GABA(B) receptor agonist, were not potentiated by L-arginine. The GABA transport inhibitors NO 711 (1 microM) and nipecotic acid (1 mM) significantly increased the half-width duration and time-constant of decay of GABA(B)-mediated inhibitory postsynaptic currents, thus mimicking effects of L-arginine. However, nitric oxide donors failed to mimic effects of L-arginine on GABA(B) inhibitory postsynaptic currents, and inhibitors of nitric oxide synthesis failed to selectively block the action of L-arginine. These findings suggest that L-arginine potentiates GABA synaptic transmission by a nitric oxide-independent mechanism. Similarities between effects of L-arginine, NO 711 and nipecotic acid suggest that L-arginine inhibits a GABA transporter.

[Lufega]

Started my first day of fast. I was originally going to do 32 hours but instead, I had breakfast this morning. This fast will last until breakfast tomorrow (24 hours). Only supplements I used this morning were lithium and olive leaf.

[Lufega]

Started my first day of fast. I was originally going to do 32 hours but instead, I had breakfast this morning. This fast will last until breakfast tomorrow (24 hours). Only supplements I used this morning were lithium and olive leaf.

I could only go up to 3 pm without food. I really felt HORRIBLE. I'll try it again tomorrow.

[nameless]

If you felt terrible just going to 3 PM, why do you think an entire day will be better? Do you eat a lot of carbs or glucose? I noticed that people who eat high carb, sugary diets tend to feel sickly if they go more than 2-4 hrs without food.

Maybe go for mild CR instead of fasting? I found eating low calorie pretty easy myself... seems I inadvertently do mild CR without even knowing it (until I added up calories).

Edited by nameless, 07 October 2009 - 03:46 AM.

[rwac]

If you felt terrible just going to 3 PM, why do you think an entire day will be better? Do you eat a lot of carbs or glucose? I noticed that people who eat high carb, sugary diets tend to feel sickly if they go more than 2-4 hrs without food.

That's definitely one possibility.

The other possibility is that Autophagy is releasing bacteria hiding out in lysosomes into the blood stream.
Borrelia hides out in within lysosomes, where it's protected from the immune system...

[meursault]

I've posted this in cnorwood's thread, but in case you haven't picked up on it, it appears that other forms of lithium should be used in place of lithium orotate.

[Lufega]

I tried again today and failed. I think a lot of it is psychological. I had breakfast at 8 am and by 3 pm I was dying. Same today. However, I've gone longer without eating, like say, no breakfast or lunch and then dinner at 8 pm and have never felt this bad. I'm going to do at least one 24 hour fast, damn it, so I'll keep trying until I do.

[Lufega]

Sugar and alcohol molecules provide a therapeutic strategy for the serpinopathies that cause dementia and cirrhosis.

Sharp LK, Mallya M, Kinghorn KJ, Wang Z, Crowther DC, Huntington JA, Belorgey D, Lomas DA.
Department of Medicine, University of Cambridge, UK.
Mutations in neuroserpin and alpha1-antitrypsin cause these proteins to form ordered polymers that are retained within the endoplasmic reticulum of neurones and hepatocytes, respectively. The resulting inclusions underlie the dementia familial encephalopathy with neuroserpin inclusion bodies (FENIB) and Z alpha1-antitrypsin-associated cirrhosis. Polymers form by a sequential linkage between the reactive centre loop of one molecule and beta-sheet A of another, and strategies that block polymer formation are likely to be successful in treating the associated disease. We show here that glycerol, the sugar alcohol erythritol, the disaccharide trehalose and its breakdown product glucose reduce the rate of polymerization of wild-type neuroserpin and the Ser49Pro mutant that causes dementia. They also attenuate the polymerization of the Z variant of alpha1-antitrypsin. The effect on polymerization was apparent even when these agents had been removed from the buffer. None of these agents had any detectable effect on the structure or inhibitory activity of neuroserpin or alpha1-antitrypsin. These data demonstrate that sugar and alcohol molecules can reduce the polymerization of serpin mutants that cause disease, possibly by binding to and stabilizing beta-sheet A.

Trehalose can help with the misfolding seen in alpha 1 antitrypsin deficiency. Yes! I can finally make that sweetened chocolate drink and not feel guilty about it!

[Benedictus]

The one's in bold describe me.

The ones.

* Little or no dream recall this improved after using Diamong XPC
* Poor morning appetite and/or tendency to skip breakfast
* Pale skin, poor tanning or burn easy in sun
* Sensitivity to bright light
* Hypersensitive to loud noises
* Reading difficulties (e.g. dyslexia) (only lately)
* Histrionic (dramatic)
* Argumentative/enjoy argument (sooooo me!)
* Mood swings or temper outbursts
* Much higher capability & alertness in the evening, compared to mornings
* Anxiousness
* Preference for spicy or heavily flavored foods
* Abnormal body fat distribution

You do realize these are all quite normal for ANY human being to experience every now and then? Here's my advice:
Go live in one of the National Parks of Thailand for a year or so, abandon your entire intake of anything other than the food they have available for you there. Eat enough vegetables, no meat, not too much fish.
Most of all: Stop being a spoiled pussy.

[Lufega]

Benedictus,

It's all part of understanding myself as a whole. Btw, is it really that important for your ego to point out a simple grammatical error?

I think this thread was written just for you, buddy:

Stop me if I'm wrong, but have the morons taken over?, Is it just me or are there more morons here?

Edited by Lufega, 18 October 2009 - 09:56 PM.

[Kutta]

I think this thread was written just for you, buddy:

Seconded.

BTW, Lufega, this thread is absolutely outstanding. You've put an enormous amount of good research into your case. I came to appreciate even more the hardships and complexity of diagnosis and medicine in general. Also, you and other people here on ImmInst who are putting up amazing fights against various illnesses are a huge inspiration for me.

Edited by Kutta, 19 October 2009 - 08:14 AM.

[Lufega]

I'm taking another look at IF. I was going about it all wrong and this site detailed it nicely. I was actually trying to fast 34+ hours and my scheduling make no sense. This Doc. lays a pretty intelligent schedule which allows you to eat everyday. Thanks to Duke for posting this.

http://www.proteinpo...-better-health/

We set up our cutoff time as 6 PM. On the day we started, we ate until 6 PM, then fasted until 6 PM the next day. On the next day we ate supper right after 6 PM and ate breakfast and lunch (and a few snacks) the next day until 6 PM when we started fasting again.

I'm starting to dislike having to take so many pills everyday. I'll be done with Medical school in one year and this means no more loan money coming in. Additionally, it appears that it will be 1 or 2 years before I'll match for a residency programs so money will be even tighter. I wont be able to afford supplements. Instead, I'll try to adopt a simpler, whole food approach instead of supplementing specific nutrients. Foods like chocolate, Aloe, green tea and Curcumin will be mainstay.

Edited by Lufega, 25 October 2009 - 07:20 AM.

[doctordog]

hey just curious Lufega - i kind of skim-read your thread and noticed a point towards the beginning where you complained about low motivation depression and low copper levels.

i kind of had a stress burn-out a year ago which i haven't had much success treating. the problem is i have OCD, which became dormant, but was replaced by terrible executive dysfunction issues. anything that acts on catecholamine release (green tea extract, s-AMe, tyrosine) provides an instant mood lift, which is why i completely refrain from SSRI's. like you, i even feel like experiments with Lexapro, etc. seemed to push me further into depersonalization.

i have not nearly conducted the amount of testing you've been able to - i never get much further than being labelled a hypochondriac - but one result i noticed was that my blood copper levels were below normal rage (Copper serum: 9 umol/L, with the minimum being 12 or so). i know it's not much, but are blood levels a reliable indicator at all? 4eva mentioned that one might have low blood levels but that's because their copper's simply biounavailable, and they might even be copper toxic? would it be a mistake to go ahead and supplement? my zinc also tested low fwiw.

[Lufega]

hey just curious Lufega - i kind of skim-read your thread and noticed a point towards the beginning where you complained about low motivation depression and low copper levels.

i kind of had a stress burn-out a year ago which i haven't had much success treating. the problem is i have OCD, which became dormant, but was replaced by terrible executive dysfunction issues. anything that acts on catecholamine release (green tea extract, s-AMe, tyrosine) provides an instant mood lift, which is why i completely refrain from SSRI's. like you, i even feel like experiments with Lexapro, etc. seemed to push me further into depersonalization.

i have not nearly conducted the amount of testing you've been able to - i never get much further than being labelled a hypochondriac - but one result i noticed was that my blood copper levels were below normal rage (Copper serum: 9 umol/L, with the minimum being 12 or so). i know it's not much, but are blood levels a reliable indicator at all? 4eva mentioned that one might have low blood levels but that's because their copper's simply biounavailable, and they might even be copper toxic? would it be a mistake to go ahead and supplement? my zinc also tested low fwiw.

I wouldn't supplement right away. Copper can easily become your worst enemy even with modest supplementation. Have you done a hair analysis? Ceruloplasmin? Did you test serum, RBC or whole blood?

[doctordog]

I wouldn't supplement right away. Copper can easily become your worst enemy even with modest supplementation. Have you done a hair analysis? Ceruloplasmin? Did you test serum, RBC or whole blood?

i am not too sure. maybe serum? my GP didn't bring up the result, so maybe it's nothing to worry about. i did have a low white cell count though, which someone here said could be linked to low copper. i only worry because i take other substances - zinc, NAC, vit C - which i know can further antagonize copper.

[Lufega]

Low neutrophils (neutropenia) is linked to low copper. How were your levels?

[doctordog]

Low neutrophils (neutropenia) is linked to low copper. How were your levels?

sorry for the delay; was waiting to get a copy of my results back.

neutrophil seg = 2.12b\l (2.2-7.5)

white cell count = 5.91b\l (4.0-11.0)

copper serum = 9umol\l (13-22)

is that enough evidence to take copper?

[Lufega]

How about ceruloplasmin levels? You can just take copper and see how that makes you feel. Or, you can stop all the antagonists and see if your levels return to normal just with your dietary intake alone.

[doctordog]

How about ceruloplasmin levels? You can just take copper and see how that makes you feel. Or, you can stop all the antagonists and see if your levels return to normal just with your dietary intake alone.

i can't see ceruloplasmin levels on the results sheet ..

i've had zinc deficiency signs for as long as i can remember (white spots under my nails, etc.), and mag and NAC help my anxiety/OCD, so i guess the logical first step is to try copper supplementation ...