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Month: March 2016

Vitamin D2 Vs D3

March 24, 2016 9:17 am

Thank you to Contributor: Mariam Michelle Gyulnazaryan

Vitamins are organic, essential nutrients that are necessary to keep your body in good health. Most vitamins must be obtained through diet because they cannot be synthesized in the body. However, the human body is able to make its own vitamin D in the skin through sun exposure or it can be obtained by food and supplements of Vitamin D3.

Vitamin D is a fat-soluble vitamin that is responsible for regulating muscle contraction, immune function, bone health, and intestinal absorption of magnesium, calcium, phosphate, iron, and zinc. Good sources of Vitamin D include sun exposure, dairy products, fatty fish, fortified orange juice, cod liver oil, mushrooms, and supplements.

There are two types of Vitamin D: D2 (ergocalciferol) and D3 (cholecalciferol). Both types have the same mechanism of action, but different sources and kinetics.

vitd_sourcesCaption: Vitamin D sources

Ergocalciferol is easily obtained through Vitamin D-rich foods in normal anatomy. However, a post Duodenal Switch patient will have less absorption of Vitamin D via food due to fat malabsorption.  Ergocalciferol is hydroxylated to ercalcidiol [25(OH)D2] in the liver. Its second hydroxylation takes places in the kidney, where it is converted to the active form of Vitamin D2 known as ercalcitriol [1,25(OH)2D2]. Now in it’s active form, Vitamin D2 can bind to the Vitamin D receptor (VDR) and help the body where it’s needed.
In the epidermis of the skin, precursor 7-dehydrocholesterol (7-DHC) forms cholecalciferol as a result of UVB radiation. Several factors such as increased skin pigmentation, age, and sunscreen application reduce the skin’s production of choleciferol (6). Cholecalciferol is hydroxylated in the liver to become calcidiol [25(OH)D3]. It is then moved to the kidney for further hydroxylation to Vitamin D3’s active form known as calcitriol [1,25(OH)2D3], also called calcifediol. The active form allows binding to VDR for biological activity.

Caption: The mechanism and effects of Vitamin D.

Both forms of Vitamin D have been shown to effectively increase 25(OH)D levels. Research shows that after administering a single dose of 50,000 international units (IU) Vitamin D2 or D3, both experienced a similar increase in serum 25(OH)D concentration. However, Vitamin D2 levels rapidly declined while Vitamin D3 levels remained high (1). Further studies have confirmed that Vitamin D3 is more effective in elevating and maintaining 25(OH)D levels for a longer amount of time (5). Scientists believe the most reasonable explanation for Vitamin D3’s substantial efficacy is its higher affinity to metabolites, which results in a longer circulating half-life than Vitamin D2 making it more potent(4). For a post Duodenal Switch patient, due to fat malabsorption, it is important to use “Dry” Water Miscible form of Vitamin D3.

Example of a Dry Water Miscible form of Vitamin D3
Example of a Dry Water Miscible form of Vitamin D3

A 25-hydroxy Vitamin D blood test is the most accurate way to measure levels. A level between 20 ng/mL-50 ng/mL may be  considered sufficient, however in our bariatric practice we would like to keep the levels in 60-80 ng/mL.  It is worth nothing that recently the reference ranges was increase to 30-100 ng/mL.  Treatments of Vitamin D deficiency include frequent sun exposure, fortified foods, supplements, and injectables. in addition to 50000IU of vitamin D on daily basis in emulsified (water soluble) formulary or unto 600,000IU in injection form. The parallel guide for adequate vitamin D supplementation is normalization of PTH levels. Monitoring these levels is imperative in a post bariatric patient.

In conclusion, studies have shown that Vitamin D2 and D3 are not interchangeable. Although they have comparable absorption, Vitamin D2 has a shorter duration of action which makes it less potent than Vitamin D3. Researchers have shown that neither form is harmful to treat Vitamin D deficiency, but they should not be considered bio-equivalent.

1. Armas LAG, Hollis BW, Heaney RP. Vitamin D2 is much less effective than Vitamin D3 in humans. Journal of Clinical Endocrinology & Metabolism. 2004; 89(11) 5387-5391.
2. Creighton D, Ignaszewski A, Francis G. Vitamin D: new d-fence against cardiovascular disease. BCMJ. 2012; 54(3) 136-140.
3. Holick MF, Schnoes HK, DeLuca HF. Identification of 1,25-Dihydroxycholecalciferol, a form of Vitamin D3 metabolically active in the intestine. PNAS. 1971; 68(4) 803-804.
4. Hollis BW. Comparison of equilibrium and disequilibrium assay conditions for ergocalciferol, cholecalciferol and their major metabolites. J Steroid Biochem. 1984; 21(1) 81-86.
5. Houghton LA, Vieth R. The case against ergocalciferol (Vitamin D2) as a vitamin supplement. Am J Clin Nutr. 2006; 84 (4): 694-697.
6. Howick Mf, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad MH, Weaver CM. Evaluation, treatment and prevention of Vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011; 96(7) 1911-1930.
7. Johal M, Levin A. Vitamin D and Parathyroid Hormone in general populations: understandings in 2009 and applications to chronic kidney disease. CJASN. 2009; 4(9) 1508-1514.
8. Tetley EA, Brule D, Cheney MC, Davis Cd, Esslingen KA, Fischer PWF, Friedl KE, Green-Finestone LA, Guenther PM, Klurfeld DM, L’Abbe MR, McMurry KY, Starke-Reed PE, Trumbo PR. Dietary reference intakes for Vitamin D: justification for a review of the 1997 values. Am J Clin Nutr. 2009; 89(3) 719-727.
9. Tripkovic L, Lambert H, Hard K, Smith CP, Bucca G, Penson S, Chope G, Hypponen E, Berry J, Vieth R, Lanham-New S. Comparison of Vitamin D2 and Vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. Am J Clin Nutr. 2012; 95(6) 1357-1364.

Enhanced Cognitive Function after Bariatric Surgery

March 18, 2016 6:51 am

The adverse effects of obesity reduce the body’s natural potential of optimal physical, mental health and cognitive function. Obesity is associated with a greater risk of health problems such as hypertension, stroke, diabetes, and sleep apnea. These issues attribute to an increased risk of dementia and cognitive dysfunction.

Glucose homeostasis plays a key role in the neural mechanisms of the brain. Insulin signals nutrients by circulating within the body in proportion to body fat mass. In addition to other regulatory mechanisms, this allows the brain to control feeding behavior by stimulating energy storage and metabolic homeostasis. Metabolic imbalances modify insulin sensitivity and lead to impaired glucose output inhibition [Qatanani and Lazar et al., 2007 (1)].

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System effects of free radicals

Free radicals are formed when weak molecular bonds are split. Their instability causes them to attack neighboring stable molecules and lead to a chain reaction of disturbing living cells. Antioxidants, such as vitamins C and E, defend the body from the damaging effects of free radicals by acting like scavengers. They protect cells from tissue damage that can potentially lead to disease.

Moreover, insulin resistance links oxidative stress, which is the continuous imbalance between free radical production and the body’s antioxidant defenses to detoxify its harmful effects. Enhanced oxidative stress is a result of accumulated fat, which impairs the secretion of insulin and damages glucose uptake in muscle and fat. Increased oxidative stress is the underlying cause of pathogenesis in vascular cell walls that lead to the development of cardiovascular problems, plaque formation. Data suggests, in a study conducted by Dr. Convit (2) in 2002, that management of blood sugar levels may enhance memory and possibly decrease the risk of Alzheimer’s disease.

In congruence with these findings, added stress due to excess weight can negatively affect the anatomy and physiology of the body. A study in 2010, led by Dr. Thompson (3), concluded that obesity is associated with “atrophy in brain areas targeted by neurodegeneration: hippocampus, frontal lobes, and thalamus” [Raji et al., 2010 (3)]. These brain regions play a critical role in the maintenance of memory, executive function, and sensory interpretation, respectively.

Central respiratory function is also disrupted by the mechanical effects of obesity. Reduced lung expansion is especially destructive during sleep. Obstructive sleep apnea is a disorder where breathing stops for brief periods because of an obstructed upper airway. Excess weight and increasing body mass index (BMI) restricts expansion of the chest wall and increases airway resistance, which decreases lung volume [Zammit et al. 2010 (4)]. This boosts respiratory muscle workload for consistent breathing. Complications of sleep apnea include fatigue, heart problems, metabolic syndrome, and more.

Cognitive impairments lead to deficits in executive function, response, reflex time, planning, and memory [Spitznagel et al. 2013 (5)]. Blood sugar levels, oxidative state, respiration and other mechanisms influence our cognitive abilities. Weight loss from bariatric surgery may reduce the comorbidities of an obese patient. The primary outcomes are improvements with diabetes, blood pressure, glucose levels, sleep apnea, BMI, and excess weight resolutions.

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Schematic of how cognition is effected by obesity. Source (1)

Weight loss surgery reverses the stressors of the body to permit the development and preservation of cognitive function. By improving anatomical aspects of physical health, the overall mental well-being of patients is remarkably enhanced.

A number of studies have looked at the short [Gunstad 2011(6)] and intermediate  [Alosco 2013, (7)] term improvement in memory function after weight loss surgery

Thank you to Contributor: Mariam Michelle Gyulnazaryan

References for Cognitive Function

  1. Qatanani M, Lazar MA. Mechanisms of obesity-associated insulin resistance. Genes & Dev. 2007; 21: 1443-1455.
  2. Convit A, Wolf OT, Tarshish C, de Leon MJ. Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly. PNAS. 2013; 100 (4): 2019-2022.
  3. Raji CA, Ho AJ, Parikshak N, Becker JT, Lopez OL, Kuller LH, Hua X, Leow AD, Toga AW, Thompson PM. Brain structure and obesity. Hum Brain Mapp. 2010; 31(3): 353-364.
  4. Zammit C, Liddicoat H, Moonsie I, Makker H. Obesity and respiratory diseases. Int J Gen Med. 2010; 3:335-343.
  5. Spitznagel MG, Alosco M, Strain G, Devlin M, Cohen R, Paul R, Crosby RD, Mitchell JE, Gunstad J., Cognitive function predicts 24-month weight loss success following bariatric surgery. Surg Obes Relat Dis. 2013; 9(5): 765-770.
  6. John Gunstad, Gladys Strain, Michael J. Devlin, Rena Wing, Ronald A. Cohen, Robert H. Paul, Ross D. Crosby, James E. Mitchell, 2011, ‘Improved memory function 12 weeks after bariatric surgery’, Surgery for Obesity and Related Diseases, vol. 7, no. 4, pp. 465-472
  7. Michael L. Alosco, Mary Beth Spitznagel, Gladys Strain, Michael Devlin, Ronald Cohen, Robert Paul, Ross D. Crosby, James E. Mitchell, John Gunstad, 2013, ‘Improved memory function two years after bariatric surgery’, Obesity, vol. 22, no. 1, pp. 32-38
  8. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, Nakayama O, Makishima M, Matsuda M, Shimomura I. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest. 2004; 114(12): 1752-1761.
  9. Mitchell JE, de Zwaan M. Psychosocial assessment and treatment of bariatric surgery patients. 2011;6: 103-109.
  10. Nguyen JCD, Killcross AS, Jenkins TA. Obesity and cognitive decline: role of inflammation and vascular changes. Front Neurosci. 2014; 8: 375.
  11. Chan JSY, Yan JH, Payne VG. The impact of obesity and exercise on cognitive aging. Front Aging Neurosci. 2013; 5: 97.

Shared Success Story – Albert L.

March 07, 2016 10:46 am

Lose weight, eat smaller portions, eat healthy, go to the gym, don’t eat bread, don’t eat starches, try this diet try that diet….. on and on.
It is so easy for dietitians, nutritionists, cardiologists, family members to speak these words. Being the one with the weight issue, it would drive me crazy hearing all the smart advice everyone had for me. I tried it all without success! Some for one day, some for longer, the results were always the same. I would lose a few pounds and in the end I would gain more. I imagine that the advice givers really didn’t understand the fatigue and appetite that comes with the extra pounds. At 39 years old, 245lbs, on blood pressure and cholesterol meds, all I could see was a life of diabetes and heart disease. Oh, the days I spent in department stores looking at designer clothes I couldn’t wear, talking to women who wouldn’t see past my belly, being the guy at the pool with his shirt on and most of all facing a very rocky future.

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Before surgery
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8 months after surgery

The day I walked into Dr Keshishian’s office was the day my life changed. He looked me in the eyes and told me it’s all going to be better. I had my surgery in June and my recovery was unusually fast. The pounds were dropping daily and within 6 weeks my cardiologist took me off my blood pressure and cholesterol medications. At eight months after surgery,  I am so close to my goal of 180lbs. I have to admit that I would have reached my goal months ago. But a trip to Australia, wining and dining my new fiancé put me off track. But I’m happy to say I’m well on my way to success. Because I am feeling so much healthier, I have joined a gym. Since surgery, I don’t have a huge appetite so I am eating smaller and healthier portions. The future is looking very very bright. Thank you Doc.”

-Albert L.

Billroth I or II and Diabetes

March 01, 2016 8:37 am

I have previously discussed the two variations  of anastomosis that can be created between the stomach and the first segment of the small bowel. Historically, Billroth I and II procedures were named after Dr. Theodor Billroth who did the first of this type of operation in the 1881 (BI) and then in 1885 (BII).

The following article  published in Bariatric Times 2016;13(2);8-10.  discusses the resolution of diabetes and its outcomes based on these two types of the anastomosis  between the stomach and the small bowel.

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Billroth I VS Billroth II

This study concludes that  “In summary, we concluded that based on our analysis of the literature, BII reconstruction is more effective than BI reconstruction for achieving postoperative diabetes control.”

Lets remind ourselves that Duodenal switch is a BII reconstruction where as the SIPS, SADI and other lookalikes are BI.

This study only reiterates that these unproven operations need to be studies further and that the patients need to be aware of the consequences of their decisions when choosing a particular operation. Be aware and informed to know the differences between Duodenal Switch and the procedures that are promoted as similar one – which they are not.

Visual comparison of Duodenal Switch and SADI/SIPS/Loop here.

Further description of Duodenal Switch here.