Mercury
Mercury’s recent presence in the body can be assessed with blood and urine samples because the initial half-life of blood mercury elimination is 3 days. The half-life of elimination for whole body mercury is between 60 and 90 days. Generally, the levels of mercury are below 10 mcg per liter in urine and below 40 mcg per liter in blood. Hair analysis can be useful as an estimate of long-term exposure to mercury.
To diagnose acute mercury toxicity, symptoms of respiratory distress are evaluated along with lab evaluation with a complete blood count and differential, serum electrolytes, glucose, liver and renal function tests, and urinalysis. Chest readiography and serial ABG measurements should be used for patients with severe inhalation exposure.
Reference: http://www.atsdr.cdc.gov/MHMI/mmg46.html
Lead
Blood lead levels can assess recent exposure to lead. It’s the primary screening method for lead exposure. It can also be measured with erythrocyte protoporphoryn, but this test is not sensitive enough to determine if children have levels below 25 mcg per deciliter. Because lead later travels to soft tissues and eventually to bones and teeth after several weeks, long-term exposure can be measured in bones and teeth with x-ray techniques.
Reference: http://www.atsdr.cdc.gov/toxprofiles/phs13.html
Cadmium
Cadmium in urine is best for determining level of recent and past exposure in the body. Analysis of hair and nails is not as useful because of factors of contamination from environment. Blood calcium can be useful to determine recent exposure in the body.
Reference: http://www.atsdr.cdc.gov/tfacts5.html
Eyeing the world of food, nutrition, and medicine through the lens of evidence and evolution.
29 January 2010
22 January 2010
What's wrong with hair zinc analysis?
Hair used for nutritional status of a mineral can be flawed because of exogenous contamination--from water, dust, cosmetics, shampoos, etc--and because of endogenous, nonnutritional factors such as hair growth rate, color, sex, pregnancy and age.
However, I do find it quite interesting that hair analysis could indicate a history of nutrition. Historical measurements would be otherwise difficult to get, but hair grows lsowly and so hair can reflect levels of zinc and other elements over time. Plus, it's an easy test since hair is easy to get.
Better non-invasive indicators of zinc deficiency are Bryce-Smith taste and sweat analysis. Loss of taste is one of the first symptoms of a deficiency because zinc is needed for an enzyme, gustin, present in saliva that modulates sense of taste. And sweat analysis may be even more sensitive as an index than blood biomarkers.
However, I do find it quite interesting that hair analysis could indicate a history of nutrition. Historical measurements would be otherwise difficult to get, but hair grows lsowly and so hair can reflect levels of zinc and other elements over time. Plus, it's an easy test since hair is easy to get.
Better non-invasive indicators of zinc deficiency are Bryce-Smith taste and sweat analysis. Loss of taste is one of the first symptoms of a deficiency because zinc is needed for an enzyme, gustin, present in saliva that modulates sense of taste. And sweat analysis may be even more sensitive as an index than blood biomarkers.
NSI Determine Checklists - Grandma and me
Grandma
My grandma, 79, scored a 6 on the NSI Determine Checklist, which puts her at “high nutritional risk.” Her eating habits are affected by GERD and she tries to avoid any processed foods high in sodium because of hypertension. She also eats alone most of the time and eats fewer than two meals per day. Although she dislikes eating fruits and vegetables, she does manage to obtain some of them in her diet. She drinks plenty of milk and uses dairy products liberally. She doesn’t drink alcohol, has enough money for food she needs (although she said she could use more), and only takes one prescription medication. She has not gained or lost 10 pounds without wanting to in the last six months. She shops and cooks for herself and reports that she also picks at food throughout the day.
Me
I, 31, scored a 0 on the NSI Determine Checklist. I have no conditions that affect my diet, I eat balanced meals along with vegetables, fruits and milk products, and don’t drink more than one glass of wine daily. I have no mouth problems, have money to buy food, eat with others most of the time, don’t take any prescriptions, have maintained the same weight for years, and often shop and cook for myself.
Thoughts
Although there is a stark contrast between my nutritional risk and that of my grandmother’s, it doesn’t escape me that in 48 years I could be in the same situation as she is now. I realize that when I eat too much I too am susceptible to GERD symptoms such as reflux and heartburn. This may affect my nutritional risk in the future unless I am conscientious enough to make change in my diet to reduce inflammation in my esophogaus. As for my grandma, her high nutritional risk concerns me greatly because at her age, she should be more focused on nutrition than I am. We will need to change that.
09 January 2010
Use of Organic Acids as Detoxification Markers
Environmental toxins, or xenobiotics, are foreign chemicals that enter our bodies and can potentially cause harm to our organs, tissues and cells. There are more than 60,000 known everyday chemicals that we are exposed to of which at least 200 are found in newborns at moment of birth. The most prevalent pollutants nowadays are phthalates and plasticizers, of which have been determined to be endocrine disruptors, and have been linked to thyroid diseases and various health conditions such as insulin resistance, metabolic syndrome, obesity, osteoporosis and arteriosclerosis. Other toxins are implicated in depleting folic acid leading to digestive disorders such as colitis or are known carcinogens.
Organic acids, of which are compounds used in metabolism, can be measured to assess how the body responds to toxins in the body or to evaluate nutrients related to processes of detoxification. For example, methylation is a vital step in the facilitation of converting homocysteine to methionine and in detoxifying chemicals. Without B12, methylation would be suppressed; thus, a resulting methylmalonic acid could be measured in urine at this point. If folic acid deficiency results, then the organic acid formiminoglutamate will accumulate and can be measured. A second example of an organic acid that can be used to evaluate nutrient deficiency resulting from toxins is xanthurenic acid. This acid appears in urine when chemicals deplete B6 (pyridoxine). A third example is measurement of fatty acids. When pthalates interfere with carnitine synthesis, then beta-oxidation in the mitochondria is impaired. THis, in turn, can result in elevated adipate, suberate, and ethylmalonate.
As markers of impaired detoxification or nutrient deficiency resulting from toxins, organic acids can help the clinical practitioner determine nutritional needs as well as possible nutrient or bioactive therapies. These therapies may include supplementation with B12, folic acid, n-acetyl cysteine, glutathione, CoQ10 and glycine. By correcting deficiency or otherwise, these nutrients potentially restore or boost detoxification in efforts to improve health of patients.
Summarized from
Rogers SA. Using Organic Acids to Diagnose and Manage Recalcitrant Patients. Alternative Therapies; July/Aug;12,4, 2006. Available at: http://blackboard.bridgeport.edu/@@437EB59FF6DF953742043192DBAC3894/courses/1/NUTR-560E-DLB-2009NF/content/_22128_1/OrganicsAcidCME.pdf
01 January 2010
How to differentiate between a B12 and a folate deficiency
Despite whether or not megaloblastic anemia is caused by a deficiency of folate or vitamin B12 (cobalamin), large doses of folate will correct the anemia (1). Because this is the case, the extra folate can potentially "mask" symptoms of vitamin B12 deficiency such as from pernicious anemia.
Unfortunately, an undiagnosed chronic vitamin B12 deficiency can lead to irreversible neuropathy. The cobalamin in methyl derivative form is necessary to methylate homocysteine to methionine (2). It's also necessary to convert methylmalonyl CoA to succinyl coA. In the absence of B12, then, leads to accumulation of both methylmalonic acid and homocysteine levels (2). As they accumulate, they lead to possible neuropathy via irreversible demyelination of nerves (3).
The mechanism by which this occurs is thought to be related to methylmalonyl CoA acting as an inhibitor of malonyl CoA's role in biosynthesis of fatty acids, which leads to myelin sheath degeneration (3). However, because this does not explain why both homocysteine and methylmalonic acid must be elevated for demyelination, more research is needed.
Correct treatment can depend on telling the difference between a deficiency of B12 from folate. It can be achieved through an assessment of both methylmalonic acid and homocysteine blood levels (2 & 4). A clinician can determine that an elevated level of both will indicate a B12 deficiency in tissues (4). Further, if both are normal, no B12 deficiency exists; and if only homocysteine levels are elevated, then a possible folate deficiency may exist (4).
References
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Devlin TM. Textbook of Biochemistry with Clinical Correlations. Philadelphia: Wiley-Liss, 2002
3. Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006
4. Lab tests online. Methylmalonic acid. Available at: http://www.labtestsonline.org/understanding/analytes/mma/test.html
Unfortunately, an undiagnosed chronic vitamin B12 deficiency can lead to irreversible neuropathy. The cobalamin in methyl derivative form is necessary to methylate homocysteine to methionine (2). It's also necessary to convert methylmalonyl CoA to succinyl coA. In the absence of B12, then, leads to accumulation of both methylmalonic acid and homocysteine levels (2). As they accumulate, they lead to possible neuropathy via irreversible demyelination of nerves (3).
The mechanism by which this occurs is thought to be related to methylmalonyl CoA acting as an inhibitor of malonyl CoA's role in biosynthesis of fatty acids, which leads to myelin sheath degeneration (3). However, because this does not explain why both homocysteine and methylmalonic acid must be elevated for demyelination, more research is needed.
Correct treatment can depend on telling the difference between a deficiency of B12 from folate. It can be achieved through an assessment of both methylmalonic acid and homocysteine blood levels (2 & 4). A clinician can determine that an elevated level of both will indicate a B12 deficiency in tissues (4). Further, if both are normal, no B12 deficiency exists; and if only homocysteine levels are elevated, then a possible folate deficiency may exist (4).
References
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Devlin TM. Textbook of Biochemistry with Clinical Correlations. Philadelphia: Wiley-Liss, 2002
3. Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006
4. Lab tests online. Methylmalonic acid. Available at: http://www.labtestsonline.org/understanding/analytes/mma/test.html
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