General Nutrition/MS Research

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jimmylegs
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case report: Near death by milk of magnesia

Post by jimmylegs » Sat Apr 01, 2017 6:13 am

kinda *looks* like april fool's content, but is not!
Near death by milk of magnesia
https://www.ncbi.nlm.nih.gov/pubmed/28325719
We report a case of hypermagnesemia associated with the use of milk of magnesia in a male patient with end-stage renal disease. After experiencing nausea and vomiting, he developed severe bradycardia and then asystole. Resuscitation efforts were successful; however, he developed atrial fibrillation with severe widening of the QRS and diffuse ST elevation, hypothermia, hypotension and apnoea requiring intubation. Initial diagnoses included ST-elevation myocardial infarction, cardiogenic and/or septic shock and hyperkalaemia. However, serum magnesium was later found to be >4.1 mmol/L (equivalent to >10 mg/dL). He underwent haemodialysis (HD) to remove serum magnesium with remarkable overall improvement. Severe hypermagnesemia can manifest with severe bradycardia and asystole, shock, hypothermia and respiratory failure and can mimic acute coronary syndromes complicated with cardiogenic shock or septic shock. Therefore, clinicians should be aware of this life-threatening condition in patients with significant renal dysfunction. Timely treatment with HD is highly effective and lifesaving.
i remember using MoM, which i had never used previously, in 2006. my gut cramped up so bad i went to the clinic. i remember telling them i thought it was possibly just bad constipation or something, and must have been from the milk of magnesium. RIGHT magnesium constipation that's a thing lol. oh, learning curves.

anyhoo, don't have time atm but will have to revisit and look into the daily elemental mag intake, and renal function test results which coincided with the 4.1+mmol/L level in this particular patient's case.
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2017 study: trends in vit D excess, high Ca, low PTH

Post by jimmylegs » Sat Apr 01, 2017 1:36 pm

The increasing problem of subclinical and overt hypervitaminosis D in India: An institutional experience and review
http://www.sciencedirect.com/science/ar ... 0716302210
Highlights
• A cohort of 5527 patients had an increasing trend for hypervitaminosis D [25-hydroxyvitamin D (25-OHD) >250 nmol/L] from 2011 to 2016 (1.48% to 7.82%).
Of patients with hypervitaminosis D and vitamin D intoxication (25-OHD>375 nmol/L), 46.22% and 62.25%, respectively, had elevated calcium or suppressed parathyroid hormone.
• Children, women, and surgical patients are especially susceptible to hypervitaminosis D,
• There has been a global secular trend of increase in 25-OHD over the past number of years and a disturbing trend of increased hypervitaminosis D in the developing world.
Empiric, unmonitored, prolonged vitamin D supplementation, especially intramuscular, should be discouraged.
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2017 report: maybe those DRIs need some work, ya?

Post by jimmylegs » Tue Apr 04, 2017 8:21 am

breaking news in 2017... smh... getting there slowly but surely!

think redefining 'deficiency' will be one key element going forward (normal ranges they're coming for youuu).

also, getting over the notion that people are getting it, when told to eat x servings of anything per day, without understanding the math OR having any issues with missing those targets flagged per status quo nutritional bloodwork (if ever ordered)...

anyhoo, will need to make time to read this in full
Options for basing Dietary Reference Intakes (DRIs) on chronic disease endpoints: report from a joint US-/Canadian-sponsored working group1
free full text http://ajcn.nutrition.org/content/105/1/249S.full.pdf
"The development of the DRIs has been critical for the successful (near) elimination of diseases of deficiency in Canada and the United States. If the DRI framework could be expanded to more effectively include chronic disease outcomes, the potential impact on public health would be even greater. This report identified the evidence-related and intake-response relation challenges that have hampered the inclusion of chronic disease endpoints in the derivation of DRIs with the use of a traditional framework and approach. The report presents several potential options to address those challenges. The next step will be to make decisions about the feasibility of including chronic disease endpoints in future DRI reviews and to determine which options and/or their adaptations warrant inclusion in guiding principles for basing DRI values on chronic disease endpoints.
Traditional DRIs have always been based on adequacy for the apparently healthy population. However, when DRI values are based on chronic disease endpoints, the target population or populations might be narrower (e.g., individuals with high blood pressure or obesity). Although beyond the scope of this report, further consideration of how to define target populations when DRIs are based on reduction in chronic disease risk may be needed.
The report also highlights several research opportunities that are key to the derivation of future DRIs based on chronic disease endpoints (Table 10). Among the most salient examples of those
opportunities are the need for qualified biomarkers of long-term intakes for a large array of nutritional variables (i.e., nutrients and other food substances), tools specifically designed to assess the quality of evidence required for setting DRIs, and novel statistical and other analytic methods for integrating diverse relations linking specific food components to multiple outcomes of interest."
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2017 study: copper, zinc, and multidrug-resistant infection

Post by jimmylegs » Wed Apr 19, 2017 10:40 am

WOW lowest actual serum zinc levels i have ever seen, yikes.
Assessments of serum copper and zinc concentration, and the Cu/Zn ratio determination in patients with multidrug resistant pulmonary tuberculosis (MDR-TB) in Côte d’Ivoire
full text: http://bit.ly/2oW9bpe
Abstract
Background: In Côte d’Ivoire, multidrug-resistant tuberculosis (MDR-TB) is a serious public health problem with a prevalence estimated at 2.5% in 2006. Zinc and copper are essential Trace element needed to strengthen the immune system and also useful in the fight against tuberculosis. The Cu / Zn ratio is a good indicator of oxidative stress.
The principal aim of this study was to evaluate the serum concentration of some trace element and determine the Cu / Zn ratio in patients with multidrug resistant pulmonary tuberculosis (MDR-TB) before and after second line treatment of TB.
Methods: Blood samples were obtained from 100 MDR-TB patients after confirmation of their status through the microscopic and molecular diagnosis of resistance to Isoniazid and Rifampicin by GeneXpert. The concentration level of zinc and copper were determined using flame air / acetylene atomic absorption spectrometer (AAS) Type Varian Spectr AA-20 Victoria, Australlia.
Results: A significant decrease in zinc levels (P < 0.05) and an increased Cu / Zn ratio (P < 0.05) was observed in MDR-TB patients compared to controls TB free. During treatment a significant reduction in Cu / Zn ratio (P < 0.05) was observed compared to the initial result.
Conclusions: The decrease in serum zinc level and the high Cu / Zn ratio could explain the immune system dysfunction and the high level of oxidative stress in patients with MDR-TB. Therefore the evaluation of the zinc and copper status could represent essential parameters in monitoring of TB second line treatment for better treatment management.
see page 3 of 6 for insanely low se zn levels. thought mine had been bad under 10, but under FIVE?! they don't bother spelling out the serum cu levels in text but you get a sense graphically in fig 2. good graphic showing spectrum of cu/zn ratios from sick to not sick/normal groups also.

from there it appears clear that a solid shot of zinc should sort out the cu/zn ratio quite handily.
"The persistence deficiency in zinc despite 6 months of second-line TB treatment require zinc supplement intake in these MDR-TB in addition to anti-tuberculosis molecules. This supplementation would boost the immune system and restore the balance between the production of free radicals and antioxidants in this MDR-TB. This will enhance the effectiveness of the TB treatment and prevent new resistance to second-line TB drugs."
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2017 study: Diet, serum Cu/Zn ratio and EDSS in RRMS

Post by jimmylegs » Wed Apr 19, 2017 4:43 pm

YASSSSS hey science WELL DONE thanks for this one :D AWESOME.
Dietary habits, concentration of copper, zinc and Cu/Zn ratio in the serum and the ability status of patients with relapsing-remitting multiple sclerosis
http://www.sciencedirect.com/science/ar ... 071730059X
Highlights
•Copper (Cu) and zinc (Zn) , due to their antioxidant activity are important in the case of multiple sclerosis (MS).
•Decreased Zn concentration in serum and higher Cu/Zn ratio may suggest a connection between MS and oxidative stress.
•Various internal and external factors may have an influence on Cu and Zn concentration in serum.
•Higher Cu/Zn ratio in serum may be associated with inferior ability status

Dietary habits and adequate intake of antioxidants, e.g. copper (Cu) and zinc (Zn) in the diet may be one of the environmental factors for the occurrence of multiple sclerosis (MS). The objective of this study was to estimate the influence of dietary habits on the concentration of Cu, Zn in the serum and the impact of Cu/Zn ratio on the ability status of patients with relapsing-remitting MS.

Methods
It was an observational case-control study included 101 individuals with MS and 68 healthy people. Food-frequency questionnaires were used to collect the dietary data. The serum concentration of Cu and Zn was determined by the electrothermal and flame atomic absorption spectrometry method, respectively. Cu/Zn ratio was also calculated and compared with Expanded Disability Status Scale of patients.

Results
The concentration of Zn was significantly lower in the serum of individuals with MS (0.776±0.195 mg/L) than in the control group (0.992±0.315 mg/L). Cu/Zn ratio was higher in the examined patients (1.347±0.806) than in the healthy volunteers (1.012±0.458). The lower ability status (p<0.05) was revealed in patients with abnormal Cu/Zn ratio, particularly, in the cerebellar function, pyramidal tracts and emotional condition.
Selected dietary habits have a significant influence on Cu and Zn concentration in the serum of patients with MS.

Conclusions
Lower serum concentration of Zn and higher Cu/Zn ratio in MS patients can suggest the relationship between MS and oxidative stress. The products that are the source of Zn should be included in the diet, which can improve the clinical condition of people with MS.
take control of your own health
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Re: 2017 study: Diet, serum Cu/Zn ratio and EDSS in RRMS

Post by jimmylegs » Wed Apr 19, 2017 5:46 pm

and let's also note that the ms patients' serum zinc levels would qualify as NORMAL many places... including the lab at my local hospital MS clinic which uses 11.5-18.5 umol/L (0.776 mg/L = 11.87 umol/L) and the lower 'normal' cutoffs from *some* labs i can think of from around here (ie TiMS) are even lower (like single digits lower. (8.57 umol/L) we have a lab here in town like that too; i've had a test done there as well (8.6 umol/L). TERRIBLE).
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SeanReynolds
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Re: 2017 study: copper, zinc, and multidrug-resistant infect

Post by SeanReynolds » Wed Apr 19, 2017 8:58 pm

Very interesting

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Re: 2017 study: copper, zinc, and multidrug-resistant infect

Post by jimmylegs » Thu Apr 20, 2017 3:06 am

yes :) semi-related
Metal ion acquisition in Staphylococcus aureus: overcoming nutritional immunity
https://link.springer.com/article/10.10 ... 011-0294-4

same year i was diagnosed, i used to get a vivid painful and raw rash on my rib cage. i didn't know what was going on. the only thing testing picked up was s. aureus. that was before i figured out some of my nutritional problems. esp where metals closely associated with immune sys function are concerned.
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Re: 2017 study: copper, zinc, and multidrug-resistant infect

Post by jimmylegs » Thu Apr 20, 2017 5:49 am

more: cpn redistributes iron to suit its own needs, zinc status drops while iron increases, cu/zn ratio increases accordingly. topping up with zinc would help keep iron in line.
Chlamydophila pneumoniae changes iron homeostasis in infected tissues
http://www.sciencedirect.com/science/ar ... 2108000313
Many bacteria, including Chlamydophila pneumoniae (C. pneumoniae), are dependent on iron (Fe) for their growth. However, it is not known whether bacterial infections affect gastrointestinal uptake and uptake of trace elements in infected tissues. A human C. pneumoniae strain adapted to C57BL/6J mice was used to study hepcidin gene expression in the liver and divalent metal transporter 1 (DMT1) content in the liver and intestine and whether Fe is concomitantly changed in serum, liver, and intestine. The copper/zinc (Cu/Zn) ratio in the serum was used as a marker for infection. Bacterial DNA, mRNA, and hepcidin were measured by real-time PCR, DMT1 by Western blot, and trace elements by ICP-MS on days 2, 5, and 8 of the infection. C. pneumoniae DNA was found in the liver on all days but the number of viable bacteria peaked on day 8. Hepcidin expression increased on days 2 and 5, whereas DMT1 content in the liver increased on day 8. Fe decreased in serum, increased in the liver but was not changed in the intestine during the disease. In the serum, the Cu/Zn ratio peaked on day 5. The peak of viable bacteria in the liver was associated with increased DMT1 and Fe contents and increased hepcidin expression, but this did not affect intestinal Fe uptake. Thus, growth of C. pneumoniae in tissues parallels a redistribution of Fe to those tissues resulting in a changed body homeostasis of Fe.
so we know increased zinc depletes iron (ferritin) in serum and vice versa. weird that a serum decrease in iron accompanies increase in cu/zn ratio (will need to dig into full text to examine what happened with serum cu and serum zn individually). wonder if more zinc intake would interfere with bacteria-supporting iron redistribution to the liver during infection.

as posted (years) previously, we know low zinc is associated with iron dysregulation and undesirable deposition elsewhere in the body.
http://www.thisisms.com/forum/chronic-c ... tml#p68425
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Studies: From ABX to Zinc for 'decoppering' disease, cancer

Post by jimmylegs » Thu Apr 20, 2017 5:08 pm

i really want to see these lines of investigation moving forward! keep finding myself checking for oral zinc trials in chronic diseases and malignancies in particular.
Paradigm shift in treatment of Wilson's disease: Zinc therapy now treatment of choice 2005
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102454/

Zinc therapy has replaced penicillamine as first-line therapy for Wilson's disease. New guidelines reflect the paradigm shift in treatment that has occurred in recent years. In the old paradigm, Wilson's disease was seen as genetic disorder associated with the accumulation of copper in the liver and in other organs once the liver had become overloaded with copper. When left untreated, the disease was regarded as uniformly fatal. The old treatment guidelines advised, ‘decoppering’ with penicillamine because this chelating agent was considered effective in restoring most patients to health. Before the start of treatment, patients were warned that their symptoms could worsen during the first weeks or months of therapy, so as to prevent them from abandoning penicillamine therapy in dismay. In the new paradigm, Wilson's disease is seen as a hereditary disorder associated with copper intoxication. The essence of symptomatic Wilson's disease is poisoning by free copper in the blood, that is, by copper that is not bound to ceruloplasmin. This form of copper is toxic, whereas accumulated copper and copper that is bound to ceruloplasmin or metallothionein is not. The treatment of symptomatic Wilson's disease is no longer aimed at ‘decoppering’, the removal of accumulated copper, but at the normalization of the free copper concentration in blood, to reverse the copper poisoning. This can be achieved safely and effectively with zinc therapy. Zinc induces metallothionein, a highly effective detoxification protein that binds copper. Oral zinc therapy leads to storage of metallothionein-bound copper in the mucosa of the gut and to the excretion of copper via the stools. New treatment guidelines advise against the use of chelating agents as initial treatment because they may aggravate copper intoxication and cause iatrogenic deterioration.
Anticopper therapy against cancer and diseases of inflammation and fibrosis 2006
http://www.sciencedirect.com/science/ar ... 4605035415

Anticopper drugs that have been developed to treat Wilson's disease, a disease of copper toxicity, include tetrathiomolybdate, zinc, penicillamine, and trientine. Lowering copper levels by a modest amount in non-Wilson's patients with tetrathiomolybdate inhibits angiogenesis, fibrosis and inflammation while avoiding clinical copper deficiency. Through this mechanism tetrathiomolybdate has proven effective in numerous animal models of cancer, retinopathy, fibrosis, and inflammation. Penicillamine has efficacy in rheumatoid arthritis and trientine has efficacy in diabetic neuropathy and diabetic heart disease. If clinical studies support the animal work, anticopper therapy holds promise for therapy of cancer, fibrotic disease and inflammatory and autoimmune diseases.
Zinc: A promising agent in dietary chemoprevention of cancer 2010
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102454/

Proper intake of dietary nutrients is considered crucial for preventing the initiation of events leading to the development of carcinoma. Many dietary compounds have been considered to contribute in cancer prevention including zinc, which plays a pivotal role in host defense against the initiation and promotion of several malignancies. Zinc is an essential element that is integral to many proteins and transcription factors which regulate key cellular functions such as the response to oxidative stress, DNA replication, DNA damage repair, cell cycle progression, and apoptosis. Zinc has been ascribed roles in the metabolism and interaction of malignant cells, particularly in apoptosis. Zinc is involved in structural stabilization and activation of the p53 that appears to be an important component of the apoptotic process and also in activation of certain members of the caspase family of proteases. Zinc exerts a positive beneficial effect against chemically induced preneoplastic progression in rats and provides an effective dietary chemopreventive approach to disease in vulnerable section of population with family history of carcinoma. The present review provides an insight into the research conducted on animals as well as on human subjects for providing the concept that zinc deficiency is an important factor in the development and progression of malignancy and that zinc could be efficacious in the prevention and treatment of several cancers viz., colon, pancreas, oesophageal and head and neck. However, it needs further exploration with regard to other definitive bioassays including protein expression and documentation of specific molecular markers to establish the exact mechanism for zinc-mediated cancer chemoprevention. Preclinical trials need to investigate the genetic and epigenetic pathways of chemoprevention by zinc.
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2017 case:Reversible parkinsonism due to vitamin D toxicity

Post by jimmylegs » Fri Apr 21, 2017 7:54 am

Sir,

A 72-year-old retired man presented to the medical emergency with a history of difficulty in walking, tremors of hands and forgetfulness for the past year. There was associated nausea, loss of appetite, and significant loss of weight in the past 6 months. No history of fever or other constitutional symptoms was present. Family members denied any episodes of seizures or recent trauma. There was no history of falls, visual complaints, and hallucinations in the past. The patient was a known case of hypertension for the past 5 years and was on tablet amlodipine 10 mg once daily. His family members revealed that he was in the habit of taking over the counter vitamins and health supplements from the pharmacy 2 to 3 times a week.

On examination, the patient was conscious but not oriented to time place or person. Mild dehydration was present. Glasgow coma scale was E 4 V 3 M 4. Pulse rate was 86 beats per minute, regular, normal, and character. Blood pressure was 136/82 mm of Hg in the upper limb in supine position.

There was no pallor, icterus, cyanosis, clubbing, lymphadenopathy, or edema. Higher mental functions could not be tested. Resting pin rolling tremor was present. There was hypertonia in all four limbs with cogwheel rigidity. He was moving all four limbs equally. All deep tendon reflexes were exaggerated. Plantars were flexor. The clinical impression was of a parkinsonian disorder, likely primary Parkinson's disease, given the age at initial presentation and the representative neurological findings. The altered mentation was, however, unexplained. Routine investigations revealed a corrected serum calcium of 13.2, a serum phosphorus level of 6.1 other electrolytes were within normal range. Serum parathyroid hormone (PTH) levels were done and were significantly low for age at 4.16 ng/ml. There was no derangement in renal function. Serum Vitamin D3 levels were studied and found to be raised at 142.7 ng/ml. Urinary calcium was found to be significantly raised at 386 mg per 24 h. The possibility of hyperparathyroidism was ruled out as serum PTH was suppressed. On carefully revising the history, family members revealed he had been taking Vitamin D3 sachets 60,000 iu/week for the past 4 years as over the counter vitamin supplements. A diagnosis of Vitamin D toxicity was made. The patient was hydrated adequately and started on loop diuretics. The patient showed clinical improvement over the next week with near complete resolution of symptoms. At discharge, the corrected calcium level was found to be 9, with an ionic component of 5.8. On 6 months follow-up, the patient did not demonstrate any relapse of similar symptoms, his relatives having been appraised of the need to restrict unwarranted nutritional supplementation.

Parkinson's disease has been repeatedly linked in existing literature Vitamin D insufficiency.[1],[2],[3]

Dietary Vitamin D, in addition to endogenous Vitamin D have been found to be inversely associated with the prevalence of Parkinson's disease.[4] Vitamin D has been found to be a potential modulator of neurodegenerative disorders due to the widespread presence of Vitamin D receptors in the human brain along with 1-alpha-hydroxylase, the enzyme responsible for activation of Vitamin D.[3]

There have been reported cases of hypercalcemia secondary to hyperparathyroidism causing parkinsonian symptoms. Our case was a rare event of hypervitaminosis D-induced parkinsonism that may mimic a state similar to hyperparathyroidism. Vitamin D supplementation leading to parkinsonian features in not widely reported in literature.

A meta-analysis to find out the role of Vitamin D and Parkinson's disease concluded that supplementation of the same may have a role in the prevention of Parkinson's disease.[5] However, one must always in life watch for a streak of zealotry in our endeavors, even regarding vitamin supplements supported by evidence.

The over the counter sale of vitamin supplements bears potentials risk of such instances of abuse that may lead to serious medical conditions.[6] In a country like India, where even prescription medicine is routinely dispensed at abandon on no recommendation from the medical community, the regulation of over the counter vitamins is nigh impossible.
take control of your own health
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ask for referrals to preventive health care specialists eg dietitians
don't let suboptimal self care muddy any underlying diagnostic picture!

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2015 study: zinc deficit alters gut microbiome in chicks

Post by jimmylegs » Tue Apr 25, 2017 5:12 am

Chronic Zinc Deficiency Alters Chick Gut Microbiota Composition and Function
full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4690049/

Zinc (Zn) deficiency is a prevalent micronutrient insufficiency. Although the gut is a vital organ for Zn utilization, and Zn deficiency is associated with impaired intestinal permeability and a global decrease in gastrointestinal health, alterations in the gut microbial ecology of the host under conditions of Zn deficiency have yet to be studied. Using the broiler chicken (Gallus gallus) model, the aim of this study was to characterize distinct cecal microbiota shifts induced by chronic dietary Zn depletion. We demonstrate that Zn deficiency induces significant taxonomic alterations and decreases overall species richness and diversity, establishing a microbial profile resembling that of various other pathological states. Through metagenomic analysis, we show that predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways responsible for macro- and micronutrient uptake are significantly depleted under Zn deficiency; along with concomitant decreases in beneficial short chain fatty acids, such depletions may further preclude optimal host Zn availability. We also identify several candidate microbes that may play a significant role in modulating the bioavailability and utilization of dietary Zn during prolonged deficiency. Our results are the first to characterize a unique and dysbiotic cecal microbiota during Zn deficiency, and provide evidence for such microbial perturbations as potential effectors of the Zn deficient phenotype.
...
The diversity of the cecal microbiota in the Zn(+) and Zn(−) groups was assessed through measures of α–diversity, β–diversity, and overall species richness (Figure 2). ... For both measures, the Zn deficient group had significantly lower phylogenetic diversity, indicating a less diverse cecal microbial composition (Figure 2A,B). ... Principal coordinate analysis demonstrated a significant expansion of β-diversity in the Zn deficient group (Figure 2C). Interestingly, the same features of lower α-diversity and richness together with higher β-diversity compared to the control as seen in Zn deficiency are also found in GI microbiota observed during a deficiency of the trace mineral selenium [36], as well as in various pathological states such as Crohn’s disease [37], inflammatory bowel disease [38], opportunistic infections [39], diabetes [40], obesity [41] and others [42].
...
Our data suggest that as a consequence of this remodeling, a Zn (–) microbiota has the potential to perpetuate, and perhaps even aggravate, the Zn deficient condition through the further sequestration of Zn from the host (Figure 8 ). Such a microbiota are not functionally compatible with the physiological needs of the Zn deficient host. In addition, others have observed decreased luminal Zn solubility in the intestines [87], increased GI inflammation and intestinal permeability, and an overall decline in GI health [93,94] under Zn deficiency. Our findings add to this knowledge by suggesting possible mechanisms by which the gut microbiota may contribute to host Zn deficiency. Further research should determine whether the gut microbiome could represent a modifiable risk factor for chronic Zn deficiency.
ugh opportunistic infections.. been there :S BEFORE zinc repletion, that is..
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2017 abstract: low zinc? expect fecal transplant to fail

Post by jimmylegs » Wed Apr 26, 2017 5:04 am

something to consider perhaps;
Zinc Deficiency Predicts Fecal Microbiota Transplant Failure in Recurrent Clostridium Difficile Infection
http://www.gastrojournal.org/article/S0 ... 1421-X/pdf

Overall, 22 patients (23.2%) experienced CDI recurrence within one year post-FMT. Low zinc predicted one-year failure, with 11/40 (27.5%) of low zinc and 7/55 (12.7%) of normal zinc subjects experiencing failure at one year (p=0.04, Kaplan-Meier/Wilcoxon).
oh good old 'normal'. a very low cutoff, .66 mcg/ml.. wonder what percent of subjects with low zinc would have experienced failure after one year if they used a cutoff closer to levels seen repeatedly in purely healthy controls ie 1.20 mcg/ml. hint: all of them :S lol
my other question is, how many would have even needed to consider this procedure at all, if the internal environmental conditions had been right [ie not zn deficient in the first place..] to support a healthy microbiome from the start..
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2016 study: copper/zinc ratio and taste disorders

Post by jimmylegs » Sat Apr 29, 2017 2:46 pm

Validity of the copper/zinc ratio as a diagnostic marker for taste disorders associated with zinc deficiency
http://www.sciencedirect.com/science/ar ... 2X16300669
Although zinc (Zn) deficiency is often suspected in patients with taste disorders, it may be difficult to diagnose Zn deficiency, especially in patients without any clear risk factors. Accordingly, the aim of the present study was to detect possible markers for taste disorders or zinc deficiency. To achieve this aim, we analyzed data obtained from 122 Japanese men who were not using medicines and had no diseases requiring treatment. We evaluated the following factors: awareness of dysgeusia; salty taste recognition threshold (SRT); the serum concentrations of Zn, copper (Cu), iron, alkaline phosphatase, and albumin; and the Cu/Zn ratio. The serum Cu/Zn ratio was positively correlated with the both the SRT and the awareness of dysgeusia. The serum Zn concentration was not correlated with the SRT or the awareness of dysgeusia in univariate analyses. However, in multivariate logistic regression, the serum Zn concentration was associated with the awareness of dysgeusia. In conclusion, the serum Cu/Zn ratio is a good diagnostic marker for taste disorders and the value of 1.1 may be a threshold level for detecting taste disorders.
so now the question is, were they just using such a broad normal range for zinc that they could not pick up an effective zinc deficiency correlation?
also i question this 1.1 threshold, since we have seen elsewhere that a nominally healthy cu/zn ratio should be from 0.7-1.0.
1.1 is more where you want to be for a zinc copper ratio. if we flip cu zn 1.1 and make it a zinc copper ratio, it's only 0.9. not good enough!

had to get into full text for this one:

Table 2
Results of laboratory tests and reference ranges.
Items........Reference range...Value............Minimum value...Maximum value
Zn (ug/dL)...64–111..............88.9 ± 12.8......57...................128
Cu (ug/dL)...70–132..............88.5 ± 14.4......62...................136

too bad they lumped everyone together for this section of their results presentation. i'd much rather have been able to see mean copper and zinc with and without taste disorder, in addition to the ratio analyses.

Cu/Zn ratio.................Awareness of dysgeusia......P-value
................................Presence..........Absence
<1.1.........................18 (21.4%).......66 (78.6%)...0.028
≥1.1.........................16 (42.1%).......22 (57.9%)

i want to know those means in the aware group with cu/zn <1.1. also would like to see the stats on awareness if the cu/zn cutoff was <1.0. 0% ???
ALSO i want to know the zinc levels in those with cu zn ratio above 1.1, who are also aware of taste disorder. can't have everything i guess!
take control of your own health
pursue optimal self care at least as actively as a diagnosis
ask for referrals to preventive health care specialists eg dietitians
don't let suboptimal self care muddy any underlying diagnostic picture!

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jimmylegs
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2015 review: Selenium vs Viral and Bacterial Infection

Post by jimmylegs » Wed May 03, 2017 8:36 am

Dietary Selenium in Adjuvant Therapy of Viral and Bacterial Infections
free full text http://advances.nutrition.org/content/6/1/73.full.pdf
Viral and bacterial infections are often associated with deficiencies in macronutrients and micronutrients, including the essential trace element selenium. In selenium deficiency, benign strains of Coxsackie and influenza viruses can mutate to highly pathogenic strains. Dietary supplementation to provide adequate or supranutritional selenium supply has been proposed to confer health benefits for patients suffering from some viral diseases, most notably with respect to HIV and influenza A virus (IAV) infections. In addition, selenium-containing multimicronutrient supplements improved several clinical and lifestyle variables in patients coinfected with HIV and Mycobacterium tuberculosis. Selenium status may affect the function of cells of both adaptive and innate immunity. Supranutritional selenium promotes proliferation and favors differentiation of naive CD4-positive T lymphocytes toward T helper 1 cells, thus supporting the acute cellular immune response, whereas excessive activation
of the immune system and ensuing host tissue damage are counteracted through directing macrophages toward the M2 phenotype. This review provides an up-to-date overview on selenium in infectious diseases caused by viruses (e.g., HIV, IAV, hepatitis C virus, poliovirus, West Nile virus) and bacteria (e.g., M. tuberculosis, Helicobacter pylori). Data from epidemiologic studies and intervention trials, with selenium alone or in combination with other micronutrients, and animal experiments are discussed against the background of dietary selenium requirements to alter immune functions.

Conclusions and Outlook
A balanced and sufficient supply of macro- and micronutrients is important to support host immune defense and resistance against pathogens. The habitual diet is often not sufficient to meet the increased demands for micronutrients in infectious diseases. Dietary multimicronutrient supplements containing selenium up to 200 μg/d have potential as safe, inexpensive, and widely available adjuvant therapy in viral infections (e.g., HIV, IAV) as well as in coinfections by HIV and M. tuberculosis...
related:
Brazil nuts: an effective way to improve selenium status
https://www.ncbi.nlm.nih.gov/pubmed/18258628
Consumption of 2 Brazil nuts daily is as effective for increasing selenium status and enhancing GPx activity as 100 mug Se as selenomethionine.
so, looks like *preventive* (longer term) = 2 brazil nuts per day.
*therapeutic* (short term) = 4 brazil nuts per day
take control of your own health
pursue optimal self care at least as actively as a diagnosis
ask for referrals to preventive health care specialists eg dietitians
don't let suboptimal self care muddy any underlying diagnostic picture!

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