swimbikerun

Wow. I'm sorry that all happened. Hope you keep watch on it and be careful. Best of luck.

Congratulations!!!!

Fiddleman that was very eloquent and every word I think is true. Excellent job.

The question that I have is why she is a year out and the surgeon didn't do something before now.

This is why you have to do your research and see what is best for you. I'm very glad that you are doing that. I really push people to look this over, as it is a lifetime commitment on their part.

Outstanding piece of work. Here's something you want to look out for: " "The limitation there is this was not a randomized, controlled study," Dr. Deas told Medscape Medical News. "It's hard, without randomizing patients, to differentiate what is truly a benefit from the intervention and what is perhaps a placebo effect. Study limitations included the lack of a control group and a study design that precludes direct comparisons with other therapies. The authors recommend follow-up prospective, randomized trials." The problem is that double blind type placebo like studies are the gold standard. If you look at the list of conflicts of interest, this study had it. I think the other problem we need to look at, is that there is a conflict of interest here for the surgeons. They're going to make more money and keep you longer if you go to bypass. This is more of a GI type of thing that goes to the surgeon. Most surgeons can be pretty conservative and they'd want to see more data before they'd risk it instead of a certain bypass. Does that make sense?

All our love to you guys.

It bothers me how little people check into this stuff. Its heart warming to see those who did. Yes, that is dead on - some of us need different types of supplementation. Having a dairy issue, and a few other things, I need something different than what some of the others I've seen get. The problem comes in the ability to get doctors to test per person and not just some standard lab panel, not just the regular stuff. I've had high copper levels before and borderline high. That would make 0 sense given my eating. Deficiencies are common but not high ones. That's why testing and supplementation should truly be unique and not blanket. As the above shows, I think people can get in their food but again, its WHAT they get in that makes a difference. I eat more fresh veggies, fruit, and lean Proteins than the vegetarians I know. However, the large combo of problems and the specific problems I have gives me a greater risk for some things. The other item that hasn't been thrown out here is our athletic endeavors. Now that I'm sidelined, I don't need to eat certain things, do certain things, because of that. Those who do, need extra help.

Only heard positives on Clark and Terracina ...

livvsmum, you go girlfriend!!!

What if people are getting what they need from Vitamins and supplements? I think it works two ways: what are people eating, how much of it are they eating, and do all of us need to supplement? Supplement with what? If I have someone 400 pounds who is now 200, maybe still obese, stretched the pouch some, but healthy and feeling good, do they need all the supplements or vitamins that someone 110 pounds who isn't healthy does? In the research above, calories were gotten in but not certain minerals/vitamins. If we supplemented with that, do you think that would suffice? Again, what I'm talking about is that the surgical community is doing a one size fits all with the vitamins, one size fits all with BMI, and there is nothing to suggest that that one size fits all answer works for everyone. What if people take Protein powders, things like Vega? Some people cant do the pills, some need more of it than others. That's where I think there needs to be better aftercare. Lets face it - if people gain back a fair amount of weight, they're getting in more calories and nutrients than they need. If not, they need to cut back on what they are getting too much of (calories) and concentrate on eating those nutrients they aren't. There are more people who gain back than struggle with malnutrition.

Yes it did. Explains me. LOL. There has been discussion of malnourishment being overweight. They've seen it with things like Vitamin D. I don't eat junk either, maybe now and then, but its salads (you can sprinkle Vega Protein berry or tropical, which is also good in applesauce) and chicken or turkey, eggs, etc. I have seen fellow WLS'ers eat donuts and/or Protein Bars and I grab a banana. Those protein bars are the ones that have sugar, etc. in them. Most but not all of my levels in terms of Vitamins and Minerals are in the normal range. That means only that it is in that range, not that it is the range I can be healthy in. They have never fleshed it out in the medical literature, there is question that because the stomach reservoir is not there, food does move differently down to the intestines and there are changes. I think that is an academic discussion at this point, not a proven or studied one.

food intake in women two years or more after bariatric surgery meets adequate intake requirements - supplements and what that data is based on? I mean some of these places do market to us, do we really need it?

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.

*** Reflux in Bariatric Patients http://www.ncbi.nlm.nih.gov/pubmed/21165778 Symptoms of gastroesophageal reflux following laparoscopic sleeve gastrectomy are related to the final shape of the sleeve as depicted by radiology. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505545/ Laparoscopic Sleeve Gastrectomy: Symptoms of Gastroesophageal Reflux can be Reduced by Changes in Surgical Technique http://www.ncbi.nlm.nih.gov/pubmed/21955743 Gastroesophageal reflux after sleeve gastrectomy in morbidly obese patients. http://www.ncbi.nlm.nih.gov/pubmed/21130052 Effect of sleeve gastrectomy on gastroesophageal reflux disease: a systematic review. http://www.bariatric-surgery-source.com/gerd-after-the-vertical-sleeve-gastrectomy-gastric-sleeve.html GERD after the Vertical Sleeve Gastrectomy (Gastric Sleeve) http://www.txtabs.org/pres/2013/16-Kennedy.pdf The Sleeve Gastrectomy: reasons for failure, indication for revision and options “Increase in gastroesophageal reflux disease symptoms and erosive esophagitis 1 year after laparoscopic sleeve gastrectomy in obese adults” Tao et al . Surg Endosc 2012 http://www.txtabs.org/pres/2013/03-Matin.pdf Reflux in Sleeve Gastrectomy. How Much Hiatal Hernia Repair? http://www.sages.org/meetings/annual-meeting/abstracts-archive/laparoscopic-sleeve-gastrectomy-does-not-worsen-gastroesophageal-reflux-disease-symptoms-in-morbidly-obese-patients/ Laparoscopic Sleeve Gastrectomy Does Not Worsen Gastroesophageal Reflux Disease Symptoms in Morbidly Obese Patients http://www.doctorweight.com/bariatricsurgery/narrowingstomach/antirefluxsleevegastroplasty/ At the same time, it is known that 30% of patients complain of heartburn after the procedure, necessitating administration of omeprazole (a drug reducing gastric acid production). This is because the original sleeve gastrectomy procedure destroys the valve mechanism of the junction between the esophagus and the stomach, converting it into a direct tube. If a sleeve gastrectomy is performed as the first stage of gastric bypass, then after the second stage (gastrojejunal bypass) the heartburn disappears. But if a sleeve gastrectomy is planned as a sole operation, then persistent heartburn might be a serious problem for the patient. http://www.soard.org/article/S1550-7289(11)00068-2/abstract Association between gastroesophageal reflux disease and laparoscopic sleeve gastrectomy http://www.sciencedirect.com/science/article/pii/S1550728910006842 Effect of sleeve gastrectomy on gastroesophageal reflux disease: a systematic review http://www.bmj.sk/2010/11104-11.pdf Complicated course after sleeve gastrectomy for obesity http://www.wlsdocs.com/weight-loss-surgery/sleeve-gastrectomy-dallas-texas.php Sleeve Gastrectomy Dallas, Texas http://www.bmi-india.com/acid-reflux-and-bariatric-surgery-part-two/ Acid reflux and bariatric surgery: Part 2

#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.