swimbikerun

http://www.sciencedirect.com/science/article/pii/S027153171200070X food intake in women two years or more after bariatric surgery meets adequate intake requirements. Does any one tell us this?

Sorry Fiddleman. That is not my intent at all. I apologize to any one who thinks that. What is, truly, is a wake up call to action. Action on the part of doctors for after care, to test *appropriately* and not just canned tests, for patients to look at their symptoms and have a body of work so they know what tests they may need if their doctors don't know them. It is much better for you to go to a doctor and show them, ask them, explain this, how might this affect me if I have X. They can get proper testing and be reassured or get the appropriate treatment sooner than later. This means for those with high B12 (truly I've seen about 2000 to be the limit where they want to test), rule out the leukemia's, liver issues, etc. That's pretty simple and doable. Letting things go is the issue. Because of what happened to me, is going to happen to me, this is why I preach what I do.

B12 here it is - Like liver disease, an elevated Vitamin B12 level cannot adequately provide a diagnosis of leukemia. But it may indicate the need for further testing. Leukemia is a type of cancer in which white blood cells are higher than normal in either your blood or bone marrow. It also causes a reduction in red blood cells and platelets, cells needed for clotting blood. This basically means that your body will not hold on to the vitamin unless it is used. The unnecessary vitamin remaining in your body will be excreted in your urine. As stated above, there are instances where a person's kidneys are not filtering properly & may cause an abundance of a multitude of substances. That being stated, the BUN & Creatine levels would have been out of the normal range indicating your kidneys are not functioning properly. Clinical Biochemistry Volume 36, Issue 8, November 2003, Pages 585–590 Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Hematologic disorders like chronic myelogeneous leukemia, promyelocytic leukemia, polycythemia vera and also the hypereosinophilic syndrome can result in elevated levels of cobalamin. Not surprisingly, a rise of the cobalamin concentration in serum is one of the diagnostic criteria for the latter two diseases. The increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases like acute hepatitis, cirrhosis, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. This phenomenon is predominantly caused by cobalamin release during hepatic cytolysis and/or decreased cobalamin clearance by the affected liver. Altogether it can be concluded that an observed elevation of cobalamin in blood merits the a full diagnostic work up to assess the presence of disease. It is customary to test for Tf (instead of TIBC) when evaluating a patient's nutritional status or liver function. Because Tf is made in the liver, levels will be low in patients with liver disease. Tf levels also drop when there is not enough Protein in the diet, so this test can be used to monitor nutrition status. Although serum ferritin measurement is the investigation of choice in Iron deficiency, many laboratories continue to offer iron and TIBC/ Tf measurements. In iron deficiency, serum Tf concentrations are elevated while iron concentrations are decreased, resulting in a decreased Tf saturation. However serum iron concentrations follow a diurnal variation and may be increased after meat ingestion. In some cases, iron and TIBC/ Tf are used instead of ferritin due to their lower cost while in other cases, ferritin is requested in addition to iron and TIBC/ Tf because of concerns regarding ferritin interpretation in inflammatory conditions. Tf can be measured either directly or indirectly by summing the results of serum iron and unsaturated iron binding capacity (UIBC) measurements to give total iron binding capacity (TIBC). A test called the siderocyte stain test checks the number of red blood cells that have particles of iron not bound to hemoglobin (siderocytes). Normally, very low numbers of siderocytes are present in blood. High levels of siderocytes in adults may mean a type of anemia, iron overload, lead poisoning, hemochromatosis, or a severe infection is present.

#1 - I couldn't answer that question. I doubt even No meat Athlete would know. He's got Fruitarian on tonight, and I doubt he would either. Let me see ... #2 - I would probably doubt it but have you tracked for a while to see what you are getting in? As in, here is what I get in terms of Vitamins A, B's, C, D, E, K and Iron, Calcium, zinc, copper ...

http://www.ncbi.nlm.nih.gov/pubmed/20202584 Postoperative metabolic and nutritional complications of bariatric surgery. Patients who have undergone bariatric surgery require indefinite, regular follow-up care by physicians who need to follow laboratory parameters of macronutrient as well as micronutrient malnutrition. Physicians who care for patients after bariatric surgery need to be familiar with common postoperative syndromes that result from specific nutrient deficiencies. http://www.ncbi.nlm.nih.gov/pubmed/20152742 Medical follow up after bariatric surgery: nutritional and drug issues. General recommendations for the prevention and treatment of nutritional deficiencies. The risk of nutritional deficiencies depends on the percentage of weight loss and the type of surgical procedure performed. Purely restrictive procedures (AGB, SG), for example, can induce digestive symptoms, food intolerance or maladaptative eating behaviours due to pre- or postsurgical eating disorders. Iron deficiency is common with the three types of bariatric surgery, especially in menstruating women. Rare deficiencies can lead to serious complications such as encephalopathy or protein-energy malnutrition. Long-term problems such as changes in bone metabolism or neurological complications need to be carefully monitored. In addition, routine nutritional screening, recommendations for appropriate supplements and monitoring compliance are imperative, whatever the bariatric procedure. Key points are: (1) virtually routine mineral and Multivitamin supplementation; and (3) regular, life-long, follow-up of all patients. The role of the general practitioner has also to be emphasized: clinical visits and follow-ups should be monitored and coordinated with the bariatric team, including the surgeon, the obesity specialist, the dietitian and mental health professionals. http://www.ncbi.nlm.nih.gov/pubmed/20363593 Micronutrient deficiencies after bariatric surgery. The literature suggests that bariatric surgery patients are at risk for deficiency of the following nutrients after surgery: Vitamins B(12), B(1), C, folate, A, D, and K, along with the trace minerals iron, selenium, zinc, and copper. Over-the-counter multivitamin and mineral supplements do not provide adequate amounts of certain nutrients such as Vitamin B(12), iron, or fat-soluble vitamins and patients will require additional doses of prophylactic supplementation life-long to maintain optimal micronutrient status. In addition, preconception care for adequate prenatal supplementation is critical for pregnant women who have undergone bariatric surgery, as iron, Vitamin A, vitamin B(12), vitamin K, and folate deficiencies are associated with maternal and fetal complications, including severe anemia, congenital abnormalities, low birth weight, and failure to thrive. All bariatric surgery patients would be best served by receiving regular monitoring of serum nutrient levels starting at 3 mo after surgery and periodically thereafter. http://www.ncbi.nlm.nih.gov/pubmed/22525731 Nutritional deficiencies after bariatric surgery. The major macronutrient deficiency after bariatric surgery is Protein malnutrition. Deficiencies in micronutrients, which include trace elements, essential minerals, and water-soluble and fat-soluble vitamins, are common before bariatric surgery and often persist postoperatively, despite universal recommendations on multivitamin and mineral supplements. Other disorders, including small intestinal bacterial overgrowth, can promote micronutrient deficiencies, especially in patients with diabetes mellitus. Recognition of the clinical presentations of micronutrient deficiencies is important, both to enable early intervention and to minimize long-term adverse effects. A major clinical concern is the relationship between Vitamin D deficiency and the development of metabolic bone diseases, such as osteoporosis or osteomalacia; metabolic bone diseases may explain the increased risk of hip fracture in patients after RYGB. Further studies are required to determine the optimal levels of nutrient supplementation and whether postoperative laboratory monitoring effectively detects nutrient deficiencies. In the absence of such data, clinicians should inquire about and treat symptoms that suggest nutrient deficiencies. http://onlinelibrary.wiley.com/doi/10.1002/oby.20461/pdf Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery*

Copper deficiencies, neuropathies after bariatric surgery (this was what I am suspected of having/figured out is the problem), and thiamine deficiencies. I don't know of ANY bariatric people who test for copper, zinc, deficiencies or do real screening for Iron deficiencies. http://www.ncbi.nlm....pubmed/17727313 Clin Chem Lab Med. 2007;45(10):1402-10. Clinical significance of the laboratory determination of low serum copper in adults. Kumar N, Butz JA, Burritt MF. Source Department of Neurology, Mayo Clinic, Rochester, MN55905, USA. kumar.neeraj@mayo.edu In six of the 57 patients with low serum copper, the low copper was due to Wilson disease. In the remaining 51 patients, copper deficiency due to an underlying cause was identified in 38 as a reason for the low serum copper. The most commonly identified neurological manifestation of copper deficiency was myeloneuropathy. Coexisting nutrient deficiencies and hematological manifestations of copper deficiency were often but not invariably present. CONCLUSIONS: Copper deficiency, Wilson disease (or a carrier state), and aceruloplasminemia are all associated with low serum copper. The presence of coexisting neurological or hematological manifestations that are recognized sequelae of copper deficiency should be considered prior to making a diagnosis of copper deficiency. Gastrointestinal disease or surgery is a common cause of acquired copper deficiency. Even in patients in whom low serum copper is indicative of copper deficiency, the cause of the copper-deficient state may not be evident. http://www.ncbi.nlm....pubmed/15249607 Neurology. 2004 Jul 13;63(1):33-9. Copper deficiency myelopathy produces a clinical picture like sub acute combined degeneration. Kumar N, Gross JB Jr, Ahlskog JE. Source Department of Neurology, Mayo Clinic, Rochester, MN, USA. kumar.neeraj@mayo.edu RESULTS: Thirteen such patients were found, 11 of them in a 15-month period. All patients presented with prominent gait difficulty, reflecting a sensory ataxia due to dorsal column dysfunction and lower limb spasticity. All patients had polyneuropathy. A high or high-normal serum zinc level was seen in 7 of the 11 patients for whom this information was available. Somatosensory evoked potential studies done in eight patients showed impaired conduction in central proprioceptive pathways. Dorsal column signal change on spine MRI was present in three patients. An initial clue to the diagnosis was a very low ceruloplasmin level; further tests of copper metabolism excluded Wilson disease. The cause remained unexplained in most patients. Oral copper supplementation restored normal or near-normal copper levels in 7 of the 12 patients in whom adequate follow-up data were available; parenteral supplementation restored normal level in 3 further patients. Copper supplementation prevented further neurologic deterioration, but the degree of actual improvement was variable. CONCLUSIONS: Unrecognized copper deficiency appears to be a common cause of idiopathic myelopathy in adults. The clinical picture bears striking similarities to the syndrome of sub acute combined degeneration associated with Vitamin B12 deficiency. Early recognition and copper supplementation may prevent neurologic deterioration. http://www.ncbi.nlm....les/PMC3432875/ J Obes. 2012; 2012: 608534. Published online 2012 June 13. doi: 10.1155/2012/608534PMCID: PMC3432875 The Neurological Complications of Nutritional Deficiency following Bariatric Surgery http://www.ncbi.nlm....pubmed/19365170 Am J Med Sci. 2009 Apr;337(4):256-8. doi: 10.1097/MAJ.0b013e31818ad0ff. Copper deficiency after gastric surgery: a reason for caution. Prodan CI, Bottomley SS, Vincent AS, Cowan LD, Greenwood-Van Meerveld B, Holland NR, Lind SE. Source From the Department of Neurology, Veterans Affairs Medical Center and the University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. calin-prodan@ouhsc.edu BACKGROUND: Acquired copper deficiency in adults leads to hematological and neurological manifestations that mimic vitamin B12 deficiency. A significant number of patients with copper deficiency syndrome have a history of gastric surgery, often remote. We sought to determine whether copper deficiency is present in a population of individuals with longstanding partial gastric resection. RESULTS: : Hypocupremia and symptoms of copper deficiency were detected in patients with partial gastric resection in contrast to controls (3/20 versus 0/50, P = 0.02). Serum copper and ceruloplasmin levels were significantly lower in individuals with partial gastric resection than in controls (P = 0.04 and P = 0.001, respectively). The mean interval between gastric surgery and testing was 20.7 years. CONCLUSIONS: : Our results indicate that a significant number of individuals with longstanding history of partial gastric resection have undiagnosed hypocupremia. Screening for copper deficiency after gastric surgery may prevent the development of hematological and neurological complications in these patients. http://www.jaoa.org/...1.full.pdf html Nutritional deficiencies after gastric bypass surgery http://ncp.sagepub.c...8.full.pdf html Nystagmus : An Uncommon Neurological Manifestation of Thiamine Deficiency as a Serious Complication of Sleeve Gastrectomy

http://www.medscape....warticle/490612 Omeprazole on oral iron replacement in patients with iron deficiency anemia.

Here is some of your Iron stuff. A low serum ferritin is the most sensitive lab test for iron deficiency anemia. However, serum ferritin can be elevated by any type of chronic inflammation and so is not always a reliable test of iron status if it is within normal limits (i.e., this test is meaningful if abnormally low, but less meaningful if normal). http://cjasn.asnjournals.org/content/1/Supplement_1/S4.full Transferrin may be low because of decreased transferrin synthesis in the setting of malnutrition and chronic disease http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2822907/ Evaluation and Treatment of Iron Deficiency Anemia: A Gastroenterological Perspective Patients with GI causes of IDA may occasionally complain of “alarm” symptoms such as a change in stool caliber, epigastric pain, and change in bowel habits, weight loss, early satiety, and poor appetite. Low transferrin can impair hemoglobin production (since to make hemoglobin, you have to have iron) and so lead to anemia. Low transferrin can be due to poor production of transferrin by the liver (where it's made) or excessive loss of transferrin through the kidneys into the urine. Many conditions including infection and malignancy can depress transferrin levels. The transferrin is abnormally high in iron deficiency anemia. It is customary to test for transferrin (instead of TIBC or UIBC) when evaluating a person's nutritional status or liver function. Because it is made in the liver, transferrin will be low in those with liver disease. Transferrin levels also drop when there is not enough Protein in the diet, so this test can be used to monitor nutrition. A transferrin test may be ordered along with other tests such as prealbumin when a doctor wants to evaluate or monitor a person's nutritional status. http://www.infed.com/iron-deficiency-assessment.asp Laboratory Assessment of Iron Deficiency Diagnosis of iron deficiency in most patients can be made based on the measurement of a low serum iron and low serum ferritin with an elevated total iron binding capacity (TIBC).3 Serum ferritin and stainable iron in tissue stores decrease even in the early stages of iron deficiency, as iron stores become depleted.7 Other parameters such as transferrin saturation (TSAT) and free erythrocyte protoporphyrin do not reach abnormal levels until tissue iron stores are completely depleted.7 Only when iron stores are insufficient for heme synthesis (i.e., iron deficiency anemia) do hemoglobin levels and red cell indices begin to decrease (Figure 1).7 Serum ferritin A low serum ferritin (<12 ng/mL) is virtually diagnostic of iron deficiency;9 however, an elevated serum ferritin level does not necessarily imply that iron stores are adequate. Serum ferritin can serve as a surrogate marker for iron stores, but it is also an acute-phase reactant and its levels may be elevated under conditions of chronic inflammation, liver disease, or malignancy, independent of iron status.28 Infection and systemic inflammation can induce secretion of hepcidin by the liver, which leads to sequestration of iron within storage sites and reduced intestinal absorption of iron.29 Thus, iron stores may be sufficient but may not be available for erythropoiesis. Under these conditions, serum iron is low, iron-binding capacity is low to normal, but serum ferritin may be normal to high.29 Therefore, in patients with inflammation, infection, or malignancy, serum ferritin may not be a reliable indicator of iron status. Iron is carried to the bone marrow by transferrin, which is an iron-transport protein that is found in plasma. Serum iron levels measure transferrin-bound iron. TIBC, or total iron binding capacity, measures the amount of circulating transferrin that is available to bind iron.28 iron deficient erythropoiesis http://www.merckmanuals.com/professional/hematology_and_oncology/anemias_caused_by_deficient_erythropoiesis/iron_deficiency_anemia.html Stages of iron deficiency: Laboratory test results help stage iron deficiency anemia. Stage 1 is characterized by decreased bone marrow iron stores; Hb and serum iron remain normal, but serum ferritin level falls to < 20 ng/mL. The compensatory increase in iron absorption causes an increase in iron-binding capacity (transferrin level). During stage 2, erythropoiesis is impaired. Although the transferrin level is increased, the serum iron level decreases; transferrin saturation decreases. Erythropoiesis is impaired when serum iron falls to < 50 µg/dL (< 9 µmol/L) and transferrin saturation to < 16%. The serum ferritin receptor level rises (> 8.5 mg/L). During stage 3, anemia with normal-appearing RBCs and indices develops. During stage 4, microcytosis and then hypochromia develop. During stage 5, iron deficiency affects tissues, resulting in symptoms and signs. http://www.medscape.org/viewarticle/721429_5 After Gastric Bypass Surgery: Managing Medical and Surgical Disorders: Macronutrient and Micronutrient Disorders

http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/ODonnellArticle.pdf Small but Mighty: Selected Micronutrient Issues in Gastric Bypass Patients http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/practicalgastrofeb04.pdf Bariatric Surgery: Nutritional Concerns on the Weigh Down http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/BanhArticle.pdf Serum Proteins as Markers of Nutrition: What Are We Treating? http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/ODonnell_November2011.pdf

http://www.ccmh.net/Services/Wellness/Need_Help_Understanding_Your_Results.aspx Low lipase levels in pancreas indicate that there might be a permanent damage to the lipase producing cells in the pancreas. Lipase deficiency causes problems in the digestion of fats which in turn can result in an increase in the levels of cholesterol and triglycerides in the body. This means there would be an increased risk of cardiovascular diseases. Deficiency of this enzyme also puts you at an increased risk of diabetes. Insufficient supply of lipase can lead to glycosuria, a condition characterized by the presence of excess sugar in the urine, in spite of normal blood sugar level. Since the enzyme is also required for metabolizing fat soluble Vitamins, low lipase levels may cause deficiency of fat soluble vitamins like, Vitamin A, D and E. People facing this problem can have decreased cell permeability (nutrients are not easily absorbed by the cell and waste materials are not easily thrown out). Individuals diagnosed with low levels of lipase encounter problems in losing weight and they may develop varicose veins. http://www.uwhealth.org/files/uwhealth/docs/pdf/bariatric_surgery_nutrition.pdf http://www.bariatricnews.net/?q=news%2F111242%2Ffemales-have-50-chance-iron-deficiency-after-bypass Females have a 50% chance or Iron deficiency after bypass http://www.bariatricnews.net/?q=news%2F111216%2Famerican-societies-publish-obesity-practice-guidelines American societies publish obesity practice guidelines.

Here is another one that I'd like to highlight: If you have problems with the fat soluble Vitamins, (would be nice if DS'ers knew about this), see the below. http://www.ncbi.nlm.nih.gov/pubmed/23642197 Annu Rev Nutr. 2013;33:183-203. doi: 10.1146/annurev-nutr-071812-161225. Epub 2013 Apr 29. Nutrient deficiencies after gastric bypass surgery. "Diet and Multivitamin use are unlikely to consistently prevent deficiency, thus supplementation with additional specific nutrients is often needed" However, despite supplementation practices already in place in the vast majority of bariatric programs, the prevalence of nutritional deficiencies among bariatric patients is still quite high as reviewed in the following sections, perhaps due to difficulties with adherence or because supplementation needs may vary among patients depending on adequacy of dietary intake and type of surgery.

Great! Over there on the long term supplementation area, I posted about PPI's and vitamin issues.

Good - keep us informed on your progress welcome back to your son and hopefully it is after a successful time at school

Same here, I did gain some weight back, up to another size but with the edema, we're not sure if it is true weight gain or edema that's making the problem. My legs and feet swell and my belly is starting to go like the kids you see on TV.

Yes they are relatively speaking. This is why I say and say and say, you have to know your stuff because doctors don't. Its why I'm having a hard time. All standard tests. The other item is that you need to understand how doctors think. They look at the test and think you are fine, its in your head. The problem is that ranges took "supposedly" healthy people and took the averages. Now if you are one of those where the bottom limit is too low for you, there is where you can get sick or ill and the doctors think all is well. What doctors CANT do in terms of B12 is the fact that it requires intrinsic factor for the body to use it. Without a stomach or just a bit of one, they can't measure how much intrinsic factor we make for the body to be able to use it. THAT is the problem with B12 ... and I can almost guarantee you even a GI won't pick that up. Yes that is possible. I have a hematologist who is just plain BRILLIANT and monitors me but yes, I will hit on Iron and NO just checking HGB is not what they should be doing. I have been zinc deficient before, including iron deficient at the same time. It took 5 rounds of IV iron, a B12 shot AND a B1 shot before my iron started coming up months later. "vit D - well I was always low no matter how much I supplemented previous to weight loss. I am puzzled by that except it seems that obesity interferes with either Vit D absorption OR the test." That and you have to remember, they may not have been testing the right thing. I have 2 Vitamin D tests that have been done on m Vitamin D 1,25 Dihydroxy & Vitamin D, 25 hydroxy. https://www.aruplab.com/Testing-Information/resources/TechnicalBulletins/Vitamin%20D,%201,25-Dihydroxy%20and%20Vitamin%20D.pdf will give you an idea about these 2 tests. They are Vitamin D but test for different things. http://www.oaml.com/PDF/2010/OAML%20Vit%20D%20Guideline%20Jn%20162010%20FINAL.pdf Vitamin D gets metabolized in the liver to produce 25-hydroxy vitamin D2 /D3. These compounds then undergo further hydroxylation, primarily in the kidneys, to produce 1,25-dihydroxy vitamin D. Serum 25-hydroxy vitamin D is the analyte of choice for assessment of a patient’s vitamin D level. It is preferred because it reflects precursor levels of vitamin D derived from cutaneous metabolism as well as from dietary intake. In addition, when compared to 1,25-dihydroxy vitamin D, its concentration is an order of magnitude higher, is less subject to physiological variation, has a longer half-life, and correlates well with bone mineral density.

http://www.medscape.com/viewarticle/803376?nlid=31820_464&src=wnl_edit_medp_gast&uac=202973SY&spon=20 Proton Pump Inhibitors and Risk of Vitamin and Mineral Deficiency PPIs have been associated with an increased risk of vitamin and mineral deficiencies impacting vitamin B12, Vitamin C, calcium, Iron and magnesium metabolism. While these risks are considered to be relatively low in the general population, they may be notable in elderly and malnourished patients.

I want to highlight this - wonder how I can do this? http://www.medpagetoday.com/Endocrinology/Obesity/40490?xid=nl_mpt_DHE_2013-07-17 Gastric Sleeve Works Long Term In terms of complications, one patient had a leak, two had incisional hernias -- which were deemed unrelated to treatment -- and 11 patients had new onset gastroesophageal reflux disease, which typically resolved with proton pump inhibitor therapy. Over 5 years of follow-up, 77.9% of patients developed Vitamin D deficiency, 41.2% had Iron deficiency, 39.7% had zinc deficiency, 39.7% had a vitamin B12 deficiency, 25% had a folic acid deficiency, and 10.3% developed anemia. ***These deficiencies occurred "despite routine supplementation, in a higher rate than we had expected," the researchers wrote.***

Random B12 information (includes some folate) Causes of non-megaloblastic macrocytosis (megaloblastic meaning large immature erythroblasts that come from the bone marrow, due to defective DNA synthesis, normally either B12, folate or both deficiencies. Macrocytosis refers to a blood condition in which red blood cells (RBC) are larger than normal) Liver disease can cause these items, as B12 can be stored for years in the liver. Unless released due to problems with the liver, it is normally good for 2-5 years. Serum folate levels are normally taken but red cell folate is more specific. Serum B12 is NOT not always an accurate reflection of deficiency at a cellular level. This is why some patients have symptoms when the injections or pills are reduced, even with normal B12 levels. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570488/ http://www.medscape.com/viewarticle/410469_4 "A low serum folate level may indicate only a decrease in folate intake over the preceding few days. [26] A better indicator of tissue folate status is RBC folate concentration, which remains relatively unchanged while a red cell is in the circulation and thus provides an assessment of folate turnover during the 2 or 3 months preceding measurement. Also, low RBC folate levels correlate better with the degree of megaloblastic changes in the bone marrow than do low serum folate levels. When there is coexistent Iron deficiency, liver disease, serum and RBC folate levels may be normal -- and serum B 12 levels may be normal or even elevated -- but tissue Vitamin deficiency can be present. This is only demonstrable via subtle hypersegmentation and/or deoxyuridine suppression test and is subsequently confirmed by response to vitamin therapy. Decreased serum total folate-binding capacity is another test that may indicate hidden folate deficiency." An elevated MCV can be associated with alcoholism (and if you look for signs & symptoms of alcoholism, malnutrition, vitamin deficiencies, you will see bariatric patients that mimic those symptoms when deficient! Vitamin B12 and/or folic acid deficiency has also been associated with macrocytic anemia (high MCV numbers).

http://www.medscape.com/viewarticle/412220 calcium citrate Shown to Have Superior Bioavailability and Protects Against Bone Loss

Calcium carbonate depends on stomach acid for absorption, and is absorbed better with food. Citrate doesn't have that problem. Carbonate is 40% calcium by weight: citrate is 21% calcium by weight. You need more citrate than carbonate. Don't go higher than 500 mg at one time, it won't be absorbed. Carbonate can cause more GI problems than citrate. For all the yak on Tums, it has carbonate not citrate.

Here is where there is a problem I see with bariatric patients, that I think is totally correct from Michigan chic. Some of us do NOT need the supplementation based on WHAT you eat. I eat healthier than pretty much most vegetarians I know as pasta's and rices figure heavily in their diet. I use Vega, which tends to work better for me vs. pills. I have had all my levels tested and they are good. Each body is different. The problem I found was that my former surgeon only wanted to test his list, not what might be a problem for me. Another reason to find someone who is willing to be flexible as you are an individual person and not some cookie cutter "this is what everyone checks for, standard pat list, cattle call" type of thing.

MichiganChic got it right. So that being said, I'll going to address a few things I learned with whatever medical resources I have. Please note that I have a local medical school with the best librarians in the world, and I use those resources a lot. I realized I don't have all of them on me, so I'll go this weekend and get specific references. Always pays to ask your doctor as the references I have come to 2 different conclusions (regarding Protein binding of calcium, whether or not its charged on the negative areas or truely is free of the protein molecule itself). I'll try to keep to the "lighter" end of things so you get useful info rather than a lot of scientific snooze material (or as my sister calls it, my reading & video material). Calcium: Several ways calcium can be measured: Serum blood Ionized Urine (24 hour collection) Differences between blood levels and ionized levels is serum blood calcium (what you find in a BMP (basic metabolic panel)) is your total calcium level, whereas the ionized calcium is the free in plasma type only. ** My sources differ on this** Serum blood calcium measures calcium that is attached to albumin/globulins or Proteins AND the free or ionized calcium in plasma OR it attaches to the negative charged sites on protein OR it is bound to proteins, bound to anions, and free/ionized. Parathyroid hormone & Vitamin D regulate your calcium. However, the kidneys assist in getting rid of the excess, so if they are not functioning right, you can find this out by doing urine studies. Many molecules attach to proteins or other blood particles and use them as a sort of "ferry" to get to where they need to be. If you have problems with abnormal levels of proteins like albumin or globulin, this may be one reason you need ionized levels checked. I'll list some items here that would be pertinent to us. Normal ionized calcium levels with high total calcium levels is called pseudohypercalcemia. It can happen due to hyperalbuminemia (basically an edema type condition where the Fluid leaks from your cells surrounding the tissue) or excess Vitamin D. Normal ionized calcium levels with low total calcium levels is called pseudohypocalcemia. It can happen due to hypoalbuminemia from liver/kidney disease. Low ionized calcium levels with low total calcium levels can happen due to parathyoid issues, Vitamin D/Magnesium deficiencies, and high phosphate levels. High ionized calcium levels with normal total calcium levels can happen due to hypoalbuminemia, parathyoid disorders, or acidosis. High ionized calcium levels with high total calcium levels can happen due to parathyroid issues. I'll stay away from high levels because lower levels would make more sense to us, excess Vitamins A & D would probably be the main causes for us. If you have lower levels, hypoparathyroidism, malabsorption, osteo types of problems, but mostly Vitamin D deficiency would be the big issues. Increases in pH levels in the blood, aka alkalosis, will cause more of the calcium to bind to the protein molecules and will decrease your ionized calcium levels. Decreased in Ph levels in the blood, aka acidosis, causes less of the calcium to bind to the protein molecules and will increase the free calcium levels. I add this due to authors' interest, as since the surgery, metabolic acidosis and alkalosis seem to be my buddies. Acidosis in the hospital after the surgery, alkalosis doing a number of endurance athletic competitions. When you get these tests done, make sure to review things such as your other electrolyte levels, PTH levels, Vitamin D, and phosphorus & magnesium. A change in this electrolyte can cause or be influenced by changes in other electrolytes. Calcium is excreted out of the body in urine and feces (a few other things but those are the most important). An increase in pH, alkalosis, promotes increased protein binding, which decreases free calcium levels. Acidosis, on the other hand, decreases protein binding, resulting in increased free calcium levels. Total calcium measurements, as you've seen, can be misleading. If you have hypoalbuminemia, you will have normal ionized calcium levels but total calcium levels decrease. There are ways to compensate for that, what I cheat and do is look online for the medical calculators. If you have kidney or low bicarbonate or serum albumin levels, you should measure the ionized free calcium to diagnose hypo/hypercalcemia. A few of the reasons to test the ionized calcium would be liver or kidney issues, abnormal total calcium issues, parathyroid issues, numbness or muscle spasms around the mouth, hands or feet. Drugs that can increase your ionized calcium levels would be things like thyroxine. Drugs that can decrease your ionized calcium levels would be things like heparin, epinephrine, alcohol. Urine tests measure how much calcium gets excreted out by the kidneys. It can look for problems with the parathyroid glands or the kidneys, or to check and see where the body is getting calcium from. Normal levels for urine calcium can be anywhere from 100-150 to 300. A calcium free diet goes from 5-40, low diets are 50-100 or 150. High levels can be caused by kidney issues, taking too much calcium, too much parathyroid hormone, and very high Vitamin D levels. Low levels can be caused by too little parathyroid hormone, low Vitamin D levels, and not enough calcium and/or malabsorption. If you show up with higher levels of serum calcium, lower levels of urine calcium, and possible bone loss changes, what is happening is that your body is leeching calcium from the bones (bone loss), causing the higher levels of blood calcium, the kidneys are holding on to the little bit you have and not urinating it out (low urine calcium).

As long as you getting out there and exercising, the fact that you now CAN, isn't that something to celebrate? While I'm all for pushing ones' self to become better, lets take a look at the same thing and think how far we've come and celebrate the positives in our new lives.

Can you stretch or just do boxing, the types of punches?

Cowgirl Jane - Sure 'nuf on starting a new thread but where would you all like to go? I could put some info I've learned together for you all. Just - put it in where? Do I need to ask Alex where is the best place? Btw, I do have sources, my doctors hate it when I quote to them.