1. Patients launch $1.27 million crowdfunding campaign for ME/CFS gut microbiome study.
    Check out the website, Facebook and Twitter. Join in donate and spread the word!
Join the National PR Campaign for ME: Power to the Patient (P2tP)
Have you had enough of all the neglect and abuse of ME/CFS patients? Gabby Klein says now is the time for a National PR Campaign for ME/CFS to impress a change. Join the Patient Revolution to restore power to ME patients ...
Discuss the article on the Forums.

Hair Mineral Testing

Discussion in 'Alternative Therapies' started by Dog Person, Mar 10, 2012.

  1. hixxy

    hixxy Woof woof

    Messages:
    724
    Likes:
    107
    Russell Island, Australia
    It would also be convenient for the levels of heavy metals in a HMT to accurately reflect tissue levels, and low levels meaning no toxicity -- as this makes HMT a much more useful test.

    Gotta love wading through so much conflicting information.

    hixxy
     
  2. Little Bluestem

    Little Bluestem Senescent on the Illinois prairie, USA

    Messages:
    2,638
    Likes:
    1,993
    Midwest, USA
    I am a proponent of hair mineral testing. That being said, it is, at best, only one view of the body. It is something to use along with, not instead of, other means of testing.

    When I tested extremely low in tissue potassium(K) for the second time after starting K supplementation, I asked my physician for a blood K test. The blood level was low normal. This meant that the problem is not getting K from my gut to my blood, but from my blood to my tissue.

    Based only on my tissue test, my dietitian (who knows nothing about ME/CFS) told me not to take B12 because it depletes K. Since my K blood level is normal(ish), I probably need B12, and who knows what else, to produce the energy needed to move the K from my blood into my cells. I would not have know that without both tests.
     
  3. hixxy

    hixxy Woof woof

    Messages:
    724
    Likes:
    107
    Russell Island, Australia
    That's like saying you shouldn't spend too much time in the sun because you will deplete yourself of magnesium metabolising the vitamin d. B12 doesn't "deplete" K, it uses K by stimulating the production of red cells (every red cell needs tome K in it).

    Likewise the K isn't getting into your tissues because you have mitochondrial failure and secondary NA/K pump failure because of that. This is normal for CFS/ME. Trying to correct an intracellular K deficiency while you still have mitochondrial failure is very very difficult.

    hixxy
     
  4. brenda

    brenda Senior Member

    Messages:
    1,301
    Likes:
    656
    UK
    from Christine :

    "Claus Henn et al. Environmental Health 2011, 10:97

    http://www.ehjournal.net/content/10/1/97



    Associations of iron metabolism genes with blood manganese levels: a population-based study with validation data from animal models



    Birgit Claus Henn, Johghan Kim, Marianne Wessling-Resnick, Martha Maria Tellez-Rojo, Innocent Jayawardene,

    Adrienne S. Ettinger, Mauricio Hernandez-Alvila, Joel Schwartz, David C. Chrisiani, Howard Hu and Robert O Wright



    In a pilot study of 141 Ohio residents, Haynes et al. observed no significant associatoin of HFE (hematochromatosis) and TF (transferrin) with hair or blood manganese [48]. The relationship between ambient air manganese and hair manganese, however, was significant after adjusting for HFE and TF genotypes, suggesting that manganese absorption varies by genotype. In a separate analysis of the same cohort as the present study, we observed lower hair manganese levels among one month-old infants whose mothers carried the HFE variant genotype (mean (SD) = 1.8 (1.4) mcg/g) compared to wildtype mothers (mean (SD) = 3.2 (4.4) mcg/g) (natural log-transformed hair manganese: B= -.05, 95% CI: - 0.9 to -0.1), which is again consistent with results presented here for material blood manganese.



    It should be noted that ferritin and hemoglobin, peripheral biomarkers of body iron stores, are not the gold standard biomarkers of body iron. Bone marrow iron or liver biopsy, which are considered the gold standards [51,52], were not available.



    In the clinical setting, measuring body iron status accurately is notoriously difficult, and the limitations of serum ferritin and whole blood hemoglobin are well known. Bone marrow iron concentration is considered the gold standard, but is seldom used due to the invasive nature of this measure.



    If the mechanism by which HFE genotype is associated with reduced blood manganese does reflect a change in iron status, transport mechanisms affecting both metals could be involved and reduced manganese levels may reflect altered uptake and distribution due to excess iron stores competing for manganese binding and transport. Loss of HFE function is associated with abnormally low levels of the iron regulatory hormone hepcidin, which results in up-regulation of the basolateral iron exporter ferroportin and net dietary absorption of iron [50]. It remains uncertain whether ferroportin is involved in absorption of dietary manganese across the intestine. While increased ferroportin levels may enhance transfer of iron from the enterocyte to circulation, manganese export out of the enterocyte may be blocked. Alternatively, increased iron loading upon loss of HFE function may affect distribution of manganese between the blood and soft tissue compartments and/or may facilitate excretion of manganese via biliary secretion.



    Author details:

    Department of Environmental Health, Harvard School of Public Health , Boston , MA USA

    Department of Genetics and Complex Diseases, Harvard School of Public Health , Boston , MA USA

    Division of Statistics, Center for Evaluation Research and Surveys, National Institute of Public Health, Cuemavaca, Morelos, Mexico

    Channing Laboratory, Department of Medicine, Brigham and Womens Hospital, Harvard Medical School , Boston , MA , USA

    Center for Perinatal, Pediatric and Environmental Epidemiology, Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut, USA

    Ministry of Health, Mexico City , Mexico

    Department of Environmental Health Sciences, University of Michigan School of Public Health , Ann Arbor , MI , USA

    Department of Emergency Medicine, Childrens Hospital Boston, Boston , MA , USA"
     
  5. Lou

    Lou Senior Member

    Messages:
    496
    Likes:
    314
    southeast US
    Anyone remember post re b complex containing only rda requirement values? Can't seem to find it, thinking maybe I dreamed it.
     
  6. Little Bluestem

    Little Bluestem Senescent on the Illinois prairie, USA

    Messages:
    2,638
    Likes:
    1,993
    Midwest, USA
    I know that, but my dietitian doesn't. That is why I was taking B12 even before Christine confirmed the decision.

    ETA: In fairness to my dietitian, I suppose I should say that I have not seen her since I had the blood potassium test, so she does not know that it was normal.
     
  7. Little Bluestem

    Little Bluestem Senescent on the Illinois prairie, USA

    Messages:
    2,638
    Likes:
    1,993
    Midwest, USA
    I don't recall the post, but I noticed recently that my father has one, so they do exist.
     
  8. brenda

    brenda Senior Member

    Messages:
    1,301
    Likes:
    656
    UK
    Another study backing up MHA.

    http://jn.nutrition.org/content/133/5/203E.full

    114A.Prospective Study of Hair Calcium Concentration as a Predictor of Mortality from Coronary Heart Disease. Jozsef Bacso* and Allan MacPherson.+ *Institute of Nuclear Research, P.O. Box 51, H-4001, Debrecen, Hungary and +SAC, Auchincruive, Ayr, KA6 5HW, Scotland, UK.

    As reported at TEMA 10 hair calcium concentration was shown to be inversely related to CHD and to reliably reflect the known pattern of heart disease risk in the UK. Its usefulness as an individual risk factor has yet to be demonstrated. An opportunity to do this arose when hair samples were obtained from 822 male subjects aged from 2564 years who had been recruited by the Belfast Centre for the WHO co-ordinated MONICA project (multinational monitoring of trends and determinants in cardiovascular disease). These samples which were collected between November 1983 and May 1984 were analyzed by us in 1994. Data on the number of deaths and the causes of mortality over the period from 19832000 were collected and collated during 2001. Over this seventeen-year period 112 subjects died. Almost 75% of the deaths were due either to some form of malignant neoplasm or of cardiovascular disease. Subjects who died of acute myocardial infarction had significantly lower hair calcium concentration (459 2.81 ppm) than the mean concentration of all other subjects (582 0.81 ppm). However the mean concentration of subjects who died of the various forms of malignant neoplasms (428 2.61 ppm) was even lower and also significantly below that of the survivors. Thus low hair calcium concentration would appear to suggest increased risk of death but not to afford a differential prognosis as to the likely cause. A full analysis will be presented showing the effect of the inclusion of other risk factors on these findings.
     
  9. barbc56

    barbc56 Senior Member

    Messages:
    1,530
    Likes:
    938
    This is for a prospective study. Are the above the results of the study as it looks more like a hypothesis for a future study as it's hard to tell from the above. How can I access this study as I can't find in PubMed which makes me think it was never published, but I could be wrong about that. I would like to get access to the full study if I can. I am also going to see what info. I can find.

    There are several things I have highlighted that I feel may reflect the quality of this research

    Thanks.

    Barb C.:>)
     
  10. brenda

    brenda Senior Member

    Messages:
    1,301
    Likes:
    656
    UK
    barbc56

    http://www.sciencedirect.com/science/article/pii/S0048969700004332

    Relationship of hair calciumconcentration to incidence of coronary heart disease

    Allan MacPhersona, Corresponding author contact information,
    Jozsef Bacsb

    a SAC, Auchincruive, Ayr KA6 5HW, Scotland, UK
    b Institute of Nuclear Research, P.O. Box 51, H-4001 Debrecen, Hungary

    Received 23 September 1999. Accepted 20 January 2000. Available online 13 June 2000.

    Abstract
    This study was designed to evaluate whether hair calcium concentration reflects the mortality from coronary heartdisease on a UK-wide basis and to determine the effect if any of environmental factors which might affect calcium metabolism on this relationship. The study was based on our earlier findings of an inverse relationship between haircalciumconcentration and that in the intima of the aorta and the association of high aorta calcium with severe alterations to the vessel walls which was found never to co-exist with haircalciumconcentrations greater than 700 ppm. Hair samples were collected from 4393 males in an ethically approved study in 40 different health districts. These covered the range in known prevalence of heart disease as reflected in the published standardised mortality ratios (SMR). Data on water hardness were obtained from the Water Authorities and on mean annual sunshine hours from the Meteorological Office. Statistical analysis was by regression and multivariate regression techniques. Hair calcium was determined by XRF analysis and the accuracy validated by means of certified reference samples. Significant relationships were found between health district and county SMR and their respective mean hair calcium concentrations accounting for 37 and 55% of their respective variances in SMR. Water hardness and sunshine hours accounted for 39 and 49% of the variance in mortality from CHD. In combination they accounted for 54% of the variance and with the inclusion of hair calcium 65%. South-east England had the highest hair calcium, the hardest water and the most sunshine hours and the lowest mortality from CHD. The converse was true of Scotland. Hair calcium concentration did reflect the risk of CHD on a population basis and was strongly influenced by both the hardness of the water supply and the annual sunshine hours which also independently affected the SMR for CHD."
     
  11. barbc56

    barbc56 Senior Member

    Messages:
    1,530
    Likes:
    938
    THanks so much!! I will take a look at this.

    Barb C.:>)

    ETA

    Darn, I still can't access anything other than the abstract without paying forty some odd dollars. What I want to see are the methods, statistics used, etc. etc. as the abstract doesn't really go into depth.

    Anyone have an idea how to access this without paying an arm and a leg? :confused:
     
  12. brenda

    brenda Senior Member

    Messages:
    1,301
    Likes:
    656
    UK
    Sorry I don`t know.
     
  13. brenda

    brenda Senior Member

    Messages:
    1,301
    Likes:
    656
    UK
    Hairs to Health, Inc. wanted the ME/CFS diagnosed people that submitted hair charts to see the following information. All the charts reviewed indicte a very low level of hair manganese with a very low ability for gluconeogenesis (Ca/Mg ratio). Considering that Yale and Harvard University used hair manganese readings to determine body manganese status, (as previously posted) these hair tests would appear to indicate manganese deficiency. In addition, the liver biopsies preformed on dogs with hair tests indicating low hair manganese, all showed deficient liver stores of manganese. Since manganese is vital for the Krebs energy cycle, this may be one piece in the puzzle of low energy production (see below).
    Handbook of Behavior, Food and Nutrition, Volume 1

    By Victor R. Preedy, Ronald Ross Watson, Colin R. Martin

    Springer, June 29, 2011



    As a critical component of dozens of proteins and enzymes, manganese is present in all mammalian tissues and is active in maintaining normal immune function, regulation of blood sugar, and cellular energy, reproduction, digestion, bone growth, defense against free radicals and blood clotting in concert with vitamin K (Aschner et al 2005).



    Key brain functions of Manganese:



    Cofactor essential for production of ATP via gluconeogenesis

    Antioxidant functions through the action of Mn-SOD

    Regulates brain ammonia levels as a component of glutamine synthetase



    Manganese Metalloenzyme Function Consequence of Loss



    Glutamine synthetase Regulation of ammonia levels Severe brain modification

    Phosphoenolpyruvate carboxykinase (PEPCK)*



    Manganese-SOD Antioxidant defense Oxidative damage



    http://en.wikipedia.org/wiki/Phosphoenolpyruvate_carboxykinase

    Phosphoenolpyruvate carboxykinase (PEPCK)*


    As PEPCK acts at the junction between glycolysis and the Krebs energy cycle, it causes decarboxylation of a C4 molecule, creating a C3 molecule. As the first committed step in gluconeogenesis, PEPCK decarboxylates, and phosphorylates oxaloacetate (OAA) for its conversion to PEP, when GTP is present. As a phosphate is transferred, the reaction results in a GDP molecule.[11]

    Humans

    PEPCK is enhanced, both in terms of its production and activation, by many factors. Transcription of the PEPCK gene is stimulated by glucagon, glucocorticoids, retinoic acid, and adenosine 3,5-monophosphate (cAMP), while it is inhibited by insulin.[15] Of these factors, insulin, a hormone that is deficient in the case of diabetes, is considered dominant, as it inhibits the transcription of many of the stimulatory elements.[15] PEPCK activity is also inhibited by hydrazine sulfate, and the inhibition therefore decreases the rate of gluconeogenesis.[16]

    In prolonged acidosis, PEPCK is upregulated in renal proximal tubule brush border cells, in order to secrete more NH3 and thus to produce more HCO3-.[17]

    The GTP-specific activity of PEPCK is highest when Manganese (Mn2)+ and Magnesium (Mg2+) are available.[7] In addition, hyper-reactive cysteine (C307) is involved in the binding of Manganese (Mn2)+ to the active site.[11]

    Whereas most reactions of gluconeogenesis can use the glycolysis enzymes in the opposite direction, the pyruvate kinase enzyme is irreversible. The enzymes pyruvate carboxylase and phosphoenolpyruvate carboxykinase provide an alternate path to effectively reverse the actions of pyruvate kinase.
    Function in Gluconeogenesis

    It has been shown that PEPCK catalyzes the rate-controlling step of gluconeogenesis, the process whereby glucose is synthesized. The enzyme has therefore been thought to be essential in glucose homeostasis, as evidenced by laboratory mice that contracted diabetes mellitus type 2 as a result of the over expression of PEPCK.[8]

    A recent study suggests that the role that PEPCK plays in gluconeogenesis may be mediated by the citric acid cycle, the activity of which was found to be directly related to PEPCK abundance.[9]
    Animals

    In animals, this is a rate-controlling step of gluconeogenesis, the process by which cells synthesize glucose from metabolic precursors. The blood glucose level is maintained within well-defined limits in part due to precise regulation of PEPCK gene expression. To emphasize the importance of PEPCK in glucose homeostasis, over expression of this enzyme in mice results in symptoms of type II diabetes mellitus, by far the most common form of diabetes in humans. Due to the importance of blood glucose homeostasis, a number of hormones regulate a set of genes (including PEPCK) in the liver that modulate the rate of glucose synthesis.

    PEPCK is controlled by two different hormonal mechanisms. PEPCK activity is increased upon the secretion of both cortisol from the adrenal cortex and glucagon from the alpha cells of the pancreas. Glucagon indirectly elevates the expression of PEPCK by increasing the levels of cAMP (via activation of adenylyl cyclase) in the liver which consequently phosphorylates the S133 on a beta sheet in the CREB protein. CREB then binds upstream of the PEPCK gene at CRE (cAMP response element) and induces PEPCK transcription. Cortisol on the other hand, when released by the adrenal cortex, passes through the lipid membrane of liver cells (due to its hydrophobic nature it can pass directly through cell membranes) and then binds to a Glucocorticoid Receptor (GR). This receptor dimerizes and the cortisol/GR complex passes into the nucleus where it then binds to the Glucocorticoid Response Element (GRE) region in a similar manner to CREB and produces similar results (synthesis of more PEPCK).

    Together, Cortisol and Glucagon can have huge synergistic results. Activating the PEPCK gene to levels that neither cortisol or glucagon could reach on their own. It is most abundant in the liver, kidney, and adipose tissue.[2]

    Researchers at Case Western Reserve University have discovered that over expression of cytosolic PEPCK in skeletal muscle of mice causes them to be more active, more aggressive, and have longer lives than normal mice; see metabolic supermice.

    Metabolic supermice are mice which as a result of genetic modification have up to 100 times the concentration of the PEPCK-C enzyme in their muscles, compared to ordinary mice.

    They were created by a team of American scientists led by Richard Hanson, professor of biochemistry at Case Western Reserve University at Cleveland, Ohio,[1][2] to gain a greater understanding of the PEPCK-C enzyme, which is present mainly in the liver and kidneys.

    Professor Hanson noted that the supermice "are metabolically similar to Lance Armstrong biking up the Pyrenees. They utilize mainly fatty acids for energy and produce very little lactic acid. They are not eating or drinking and yet they can run for four or five hours. They are 10 times more active than ordinary mice in their home cage. They also live longer up to three years of age and are reproductively active for almost three years. In short, they are remarkable animals." However, "they eat twice as much as control mice, but they are half the weight, and are very aggressive. Why this is the case, we are not really sure."
     
    Gloria H and garcia like this.
  14. justy

    justy Senior Member

    Messages:
    2,679
    Likes:
    2,893
    U.K
    Hi Brenda - i think low manganese is often seen in PWME as per the mitochondrial function test done at Acumen labs. My Manganese was extremely low and ive been supplementing it for nearly two years - i also have a gene blockage on the Mn SODase gene, which is manganese dependant. I'm sure its doing me some good- but the only two supplements i can definately say have helped are MB12 injected daily and magnesium - orally and transdermally. I've tried the B2 a number of times - in fact Dr Myhill says nearly all her patients are B2 deficient as well as B12 and B6 which is why she gets them to take a multi B - but for me the B2 creates such awful nightmares that i cant tolerate it right now.
    All the best, Justy.
     
  15. dmholmes

    dmholmes Senior Member

    Messages:
    326
    Likes:
    78
    Houston
    Hi Justy, what kind of Mn are you supplementing with if I may ask?
     
  16. justy

    justy Senior Member

    Messages:
    2,679
    Likes:
    2,893
    U.K
    Hmm - i dont actually know - i use a transdermal multi mineral spray- made by Dr Myhill and manganese drops - also from DR Myhill in a clear plastic dropper bottle.
    Is there a difference?
     
  17. dmholmes

    dmholmes Senior Member

    Messages:
    326
    Likes:
    78
    Houston
    Hi justy,

    I'm not sure about those forms, but manganese from most sources doesn't get much absorption. 2 to 4%. Christine's approach uses ionic manganese from WaterOz. It's still too early for a definitive answer on my part, but it seems like the manganese tablets I was taking were very poor at repletion.
     
  18. brenda

    brenda Senior Member

    Messages:
    1,301
    Likes:
    656
    UK
    Justy

    My manganese was not bad according to my hair test and that is why Christine said that I was able to titrate b2 so quickly. Maybe you are using up more manganese than you are taking. The problem with taking multis is that we become imbalanced. This is what happened to me
     
  19. brenda

    brenda Senior Member

    Messages:
    1,301
    Likes:
    656
    UK
    Folic acid


    http://www.ajcn.org/content/87/3/517.short



    American Journal of Clinical Nutrition, Vol. 87, No. 3, 517-533, March 2008
    2008 American Society for Nutrition



    Is folic acid good for everyone?1,2



    A David Smith1, Young-In Kim1 and Helga Refsum1

    1 From the Oxford Project to Investigate Memory and Ageing (OPTIMA), Department of Physiology, Anatomy & Genetics, University of Oxford, Oxford, United Kingdom (ADS and HR); the Departments of Medicine and Nutritional Sciences, University of Toronto, Division of Gastroenterology, St Michael's Hospital, Toronto, Canada (Y-IK); and the Institute of Basic Medical Sciences, Department of Nutrition, University of Oslo, Oslo, Norway (HR)

    Fortification of food with folic acid to reduce the number of neural tube defects was introduced 10 years ago in North America. When fortification is introduced, several hundred thousand people are exposed to an increased intake of folic acid for each neural tube defect pregnancy that is prevented. Are the benefits to the few outweighed by possible harm to some of the many exposed? In animals, a folic acidrich diet can influence DNA and histone methylation, which leads to phenotypic changes in subsequent generations. In humans, increased folic acid intake leads to elevated blood concentrations of naturally occurring folates and of unmetabolized folic acid. High blood concentrations of folic acid may be related to decreased natural killer cell cytotoxicity, and high folate status may reduce the response to antifolate drugs used against malaria, rheumatoid arthritis, psoriasis, and cancer. In the elderly, a combination of high folate levels and low vitamin B-12 status may be associated with an increased risk of cognitive impairment and anemia and, in pregnant women, with an increased risk of insulin resistance and obesity in their children. Folate has a dual effect on cancer, protecting against cancer initiation but facilitating progression and growth of preneoplastic cells and subclinical cancers, which are common in the population. Thus, a high folic acid intake may be harmful for some people. Nations considering fortification should be cautious and stimulate further research to identify the effects, good and bad, caused by a high intake of folic acid from fortified food or dietary supplements. Only then can authorities develop the right strategies for the population as a whole.

    ++++++++++++++++++++++++++++++++++

    A Temporal Association between Folic Acid Fortification and an Increase in Colorectal Cancer Rates May Be Illuminating Important Biological Principles: A Hypothesis

    1. Joel B. Mason1,2,

    2. Aaron Dickstein2,

    3. Paul F. Jacques1,

    4. Paul Haggarty3,

    5. Jacob Selhub1,

    6. Gerard Dallal1 and

    7. Irwin H. Rosenberg1,2

    + Author Affiliations

    1. 1Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University; 2Tufts University School of Medicine, Boston, Massachusetts; and 3Rowett Research Institute, University of Aberdeen, Aberdeen, United Kingdom

    1. Requests for reprints:
    Joel B. Mason, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111. Phone: 617-556-3194; Fax: 617-556-3234. E-mail: joel.mason@tufts.edu

    Abstract

    Nationwide fortification of enriched uncooked cereal grains with folic acid began in the United States and Canada in 1996 and 1997, respectively, and became mandatory in 1998. The rationale was to reduce the number of births complicated by neural tube defects. Concurrently, the United States and Canada experienced abrupt reversals of the downward trend in colorectal cancer (CRC) incidence that the two countries had enjoyed in the preceding decade: absolute rates of CRC began to increase in 1996 (United States) and 1998 (Canada), peaked in 1998 (United States) and 2000 (Canada), and have continued to exceed the pre-1996/1997 trends by 4 to 6 additional cases per 100,000 individuals. In each country, the increase in CRC incidence from the prefortification trend falls significantly outside of the downward linear fit based on nonparametric 95% confidence intervals. The statistically significant increase in rates is also evident when the data for each country are analyzed separately for men and women. Changes in the rate of colorectal endoscopic procedures do not seem to account for this increase in CRC incidence. These observations alone do not prove causality but are consistent with the known effects of folate on existing neoplasms, as shown in both preclinical and clinical studies. We therefore hypothesize that the institution of folic acid fortification may have been wholly or partly responsible for the observed increase in CRC rates in the mid-1990s. Further work is needed to definitively establish the nature of this relationship. In the meantime, deliberations about the institution or enhancement of fortification programs should be undertaken with these considerations in mind. (Cancer Epidemiol Biomarkers Prev 2007;16(7):13259)

    ++++++++++++++++++++++++++++++++++++++++++++++++++

    Metal Ions in Biological Systems, volume 37, Manganese and its role in biological processes, edited by Astrid Sigel and Helmut Sigel, copyright 2000 by Marcel Dekker, Inc.

    "This author suggested that a reduction in Manganese Superoxide Dismutase (MnSOD) activity could increase the risk for colonic cancer. While the functional significance of a modest reduction in tissue manganese concentrations with iron supplementation is a matter of debate, this is an area that demands further study."

    ++++++++++++++++++++++++++++++++++++++++++++++++++++

    http://www.fao.org/DOCREP/004/Y2809E/y2809e0a.htm



    Differences in bio-availability of folic acid and food folate

    The RNIs suggested for groups in Table 13 used food folate as the source of dietary folate because most societies in developing countries consume folate from naturally occurring sources. As discussed in the introduction, natural folates are found in a conjugated form in food, which reduces its bio-availability by perhaps as much as 50 percent (4). In addition, natural folates are much less stable. If chemically pure folic acid (pteroyl monoglutamate) is used to provide part of the RNI, by way of fortification or supplementation, the total dietary folate, which contains conjugated forms (pteroyl polyglutamates), could be reduced by an appropriate amount. On average the conjugated folate in natural foods is considered to be only half as available as synthetic folic acid. For example, the recommendation of usual mixed forms of folate in the diet is 400 g/day, but 100 g of this given as pure folic acid would be considered to be equivalent to 200 g of dietary mixed folate. Hence, only an additional 200 g of dietary folate would be needed.

    The FAO/WHO expert group agreed with the findings of the Food and Nutrition Board of the US National Academy of Sciences (22):

    Since folic acid taken with food is 85 percent bio-available but food folate is only about 50 percent bio-available, folic acid taken with food is 85/50 (i.e., 1.7) times more available. Thus, if a mixture of synthetic folic acid plus food folate has been fed, dietary folate equivalents (DFEs) are calculated as follows to determine the EAR:

    mcg of DFE provided = [mcg of food folate + (1.7 x mcg of synthetic folic acid)]

    To be comparable to food folate, only half as much folic acid is needed if taken on an empty stomach, i.e., 1 mcg of DFE = 1 mcg of food folate = 0.5 mcg of folic acid taken on an empty stomach = 0.6 mcg of folic acid with meals (22).
     
  20. barbc56

    barbc56 Senior Member

    Messages:
    1,530
    Likes:
    938
    I had a look at the full study as well as others and yes indeed calcium concentration is related to heart disease.

    The same can be said about some of the other studies cited above.That being said, I don't know why hair mineral testing is used when there are more reliable tests? I think that is the issue and that issue is an important consideration.

    Barb C.:>)
     

See more popular forum discussions.

Share This Page