Category Archives: Nutrition

Bone health in pediatrics

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Due to the survival of chronically ill children, exposure to skeletal toxic treatments, and wider availability of bone health measurement technology, osteoporosis in pediatrics has become a widespread problem.  A useful concise review is available (J Pediatr 2012; 161: 983-88).

One of the biggest problems is the limited pediatric evidence on which to base treatment decisions.

Specific points regarding osteoporosis and bone health:

  1. Bone accretion: most of one’s bone mass is reached by late adolescence or early adulthood
  2. Frequency of bone fractures: in the general population, 1/2 of boys and 1/3rd of girls have sustained a fracture by 16 years of age.  Thus, bone pathology should be suspected in those with unusual fractures.
  3. Pathological fractures: “meaningful” history of fracture history includes a lower extremity long bone fracture, 2 or more upper extremity long bone fractures and/or vertebral compression fracture.
  4. Testing: due to cost and precision, dual-energy x-ray absorptiometry (DXA) remains most widely used measurement tool. However, quantitative computed tomography (QCT) has some advantages.  It is less biased by bone size and directing generates a measurement of volumetric bone mineral density.
  5. Primary osteoporosis: osteogenesis imperfecta (OI), idiopathic juvenile osteoporosis (IJO), and osteoporosis-pseudoglioma syndrome (related to loss of function in low-density lipoprotein receptor-related protein 5 [LRP5]).
  6. Secondary osteoporosis: neuromuscular diseases, malabsorption syndromes, medication-induced (glucocorticoids, diuretics), chemotherapy, and radiation treatments.
  7. 1st line treatment: adequate nutrition –especially adequate calcium and vitamin D and exercise (especially weight-bearing exercise).  It is noted that with cystic fibrosis patients there has been a better response to vitamin D3 (cholecalciferol) than D2 (ergocalciferol); as a consequence, the CF Foundation recommends all CF patients receive vitamin D3.  With regard to weight-bearing exercise, the data are conflicting regarding its efficacy.
  8. 2nd line treatment: treat underlying disorder.  For example, with inflammatory bowel disease (IBD), treatment of chronic inflammation with infliximab has been shown to improve markers of bone formation.  Inflammation in IBD has been shown to play a more important role than glucocorticoid dosing in terms of predicting bone health.
  9. 3rd line treatment ??? a) “Currently, teriparatide is the only available treatment with anabolic actions on bone.” But, a black box warning has cautioned against its use in pediatric patients   b) bisphosphonates: pamidronate, aleondronate, and zoledronic acid. A review of the small pediatric studies, primarily in OI patients, have shown some improvement in fractures, skeletal pain, and mobility.  Optimal dose, frequency, and duration remain unknown.
  10. Safety of bisphosphonates: potential problems include ‘acute phase reaction,’ hypocalcemia, musculoskeletal pain, gastrointestinal side effects, and many other adverse reactions. Atypical fractures and jaw osteonecrosis have been reported in adults.

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Ethanol locks -jump on the bandwagon

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http://ncp.sagepub.com/content/early/2012/12/10/0884533612468009.abstract

From Nutrition in Clinical Practice, published online before print, December 11, 2012, doi:10.1177/0884533612468009 (Thanks to Kipp Ellsworth for this link from his twitter feed):

“Our group of patients (n=14) showed a 73% reduction in CABSIs and a 77% reduction in catheter removal due to infection after ethanol lock therapy. In our patient population, weekly ethanol lock therapy for 2 hours is an effective technique to reduce CABSIs and catheter removal in long-term home PN patients.”

CABSIs =catheter-associated bloodstream infections

Another option for line locks

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A pediatric study from London with 19 patients demonstrates the utility of taurolidine line locks (JPGN 2012; 55: 403-7).

Taurolidine has broad antimicrobial activity against Gram-positive and Gram-negative bacteria in addition to antifungal properties.  Also, taurolidine prevents biofilm formation which can help minimize colonization of catheters.  It acts by binding to the cell walls of organisms; this results in the prevention of bacterial adhesion to biological surfaces. TauroLock™ | TauroLock™

15 of the 19 patients had a history of recurrent central catheter infections and 4 were started on the line locks empirically.  At the completion of the parenteral nutrition, 0.7 to 1 mL of the taurolidine solution was instilled and left for at least 12 hours.

Taurolidine-treated patients had 1.1 episodes per 100 catheter days of CVL infections; this compared with a rate of 8.6 episodes per 1000 catheter days for heparin control.  Furthermore, 74% (14) had no infections for up to 33 months after changing to taurolidine.  No reports of mulitresistant organisms or adverse effects were reported.  Taurolidine is nontoxic for humans and rapidly metabolized to taurine, carbon dioxide, and water.

To my knowledge, taurolidine is not available in the U.S.  Nevertheless, the data on line locks indicate that antimicrobial line locks are associated with reductions in catheter infections.

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Additional reference:

Improvement in obesity rate?

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In case you didn’t see it, this article link, OBESITY IN YOUNG IS SEEN AS FALLING IN – THE NEW YORK TIMES, appeared in multiple news outlets (December 10, 2012) and suggests that in some cities there has been a modest reduction in obesity rates of 3-5%.

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Does bone density improve with IBD therapy?

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Long term followup is needed to determine the significance of low bone mineral density (BMD) in children and adolescence with IBD; data with 2 year followup is available (JPGN 2012; 55: 511-18).

In this study from Sweden, 144 patients with IBD were enrolled and 126 were available at 2-year followup (2003-2005).  Among the 144 patients, there were 93 males and 83 with UC. Low BMD was noted in children with both UC and CD for the lumbar spine at baseline and no improvement was noted at 2 years.  Only boys had lower BMD z scores for the lumbar spine (LS) (-1.1); girls had normal LS z scores (0).

While the investigators could not demonstrate catch up in bone mineral density, they note that gains in BMD may accrue beyond late adolescence into early adulthood; this takes place after completion of linear growth.  In the subgroup of subjects in early adulthood, there was improvement in BMD:

  • For boys: from -1.7 at baseline (age 17.9) to -0.5 at followup (age 20.0)
  • For girls: from -0.4 at baseline (age 17.1) to 0.4 at followup (age 19.2)

With greater use of biologic therapy, these data are likely to change.  Among medical treatments, only biologic therapies have been shown to improve bone formation and improve catchup growth.

Related blog entry:

Additional references:

  • -JPGN 2011;53: 361. Similar prevalence of low Vitamin D as general population –58% with less than 32.
  • -JPGN 2011; 53: 11. Guidelines for low bone mineral density in IBD.
  • -JPGN 2009; 48: 538. Need to adjust bone density for bone age.
  • -Gastroenterol 2009; 136: 123. Longitudinal bone health study. Steroids did NOT adversely affect bones. n=78.
  • -Clin Gastro & Hep 2008; 6: 1378. IFX improves biomarkers of bone formation.
  • -J Pediatr 2008; 153: 454, 484. Use of biomarkers of bone turnover in Crohn dz; even when controlling for other factors like delayed bone age, delayed puberty, etc, still evidence of decrease bone formation and increased resorption.
  • -JPGN 2007; 45: 538. Ca/Vit D supplements -no change in BMD in IBD patients over 12 months.
  • -Clin Gastro & Hep 2007; 5: 721. DXA may not predict risk well.
  • -IBD 2007; 4: 416. Inflammation, not steroids, is key factor in bone mineral density.
  • -IBD 2006; 13: 42. Natural hx of bone mineral density in IBD; steroid dose did not correlate with BMD. Children did not have “catch up” bone density.
  • -JPGN 2006; 43: 597. Crohn’s patients had similar rate of fractures as siblings w/o IBD.
  • -Clin Gastro & Hep 2006; 4: 152. Osteoporosis in IBD.
  • -IBD 2006; 12: 797. Review of bone mineral density with IBD
  • -Clin Gastro & Hepatol 2005; 3: 113-121, 122-132 & editorial 110. In 1st article, budesonide better for bones than other steroids. In 2nd article, unable to show benefit of addition of etidronate to Ca++/Vit D.
  • -NEJM 2002; 351: 868. Intermittent steroids in nephrotic syndrome did NOT change bone mineral density.
  • -Gastro 2001; 121: 1485-88. Tanning bed Rx of vitamin D deficiency.
  • -Gastro 2000; 119: 639-46. Alendronate increases BMD in pts c Crohn’s
  • -NEJM 1998; 339: 292-9/ J Bone Miner Res 2000; 15: 1006-13. Bisphosphonates effective in steroid-induced bone disease

Congenital Sucrase Isomaltase Deficiency

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Congenital Sucrase Isomaltase Deficiency (CSID) has an extensive review in a recent JPGN supplement (JPGN 2012; supplement 2: S1-47).

A concise update of the clinical aspects is provided by William Treem (S7-S13).   Specific points that he makes includes the following:

  • CSID was first described in 1960 by Weijers and colleagues
  • Sucrase-isomaltase gene (3q25-26) identified in 1992; now more than 55 mutations have been described.  At least one of the four most common mutations are identified in about 80% of affected individuals.
  • Prevalence: estimates range from 1 in 500 to 1 in 2000 in caucasians; the prevalence is lower in other populations.  Some patients suspected of having CSID may be heterozygotes with low enzyme activity (but not truly deficient).
  • Clinical features determined by degree of enzyme deficiency and amount of sugar and starch consumed.  In the U.S. typically 60% of calories consumed are derived from carbohydrates and 30% from sucrose.  A typical U.S. adult consumes 150 lb of sugar per year.
  • Classical presentation: severe watery diarrhea and poor weight gain in a 9- to 18-month old after exposure to juices, baby foods/fruits, and other starches.
  • Other symptoms: gas/bloating, abdominal pain, irritable bowel syndrome
  • Diagnosis: intestinal biopsy analysis.  A potential pitfall includes mishandling of biopsy specimens. An alternative means of diagnosis is the 13-C sucrose breath test.
  • Treatment: 1. dietary avoidance results in improvement in many, though only 10% respond fully to diet. 2. enzymatic treatment. Baker’s yeast (Saccharomyces cerevisiae) contains a sucrase.  Development of sacrosidase (Sucraid) from Baker’s yeast has allowed 81% of patients to consume an unrestricted diet.  Dosing: 1 mL with meals/snacks if <15 kg and 2 mL if >15 kg.
  • Despite sacrosidase treatment, 27% of patients required strict sucrose restriction with either mild or strict starch restriction to maintain acceptable suppression of symptoms.
  • What is not noted in this summary–cost information: sucraid may cost as much as $3700 per month.  A similar product in Europe costs about $400 per month

Multiple other articles in this supplement address related subjects.

On page S31, information is given from parent support group.  This parent support group (CSIDinfo.com) offers dietary advice specific for each phenotype (A,B,C,D and F) which is based on their disaccharidase levels, ability to outgrow symptoms, and tolerance of starch and maltodextrins.

On page S34, the major genetic mutations are discussed.  Use of genetic testing will detect the majority with CSID which could become an alternative means of diagnosing CSID in this population.

Additional Information

Less stress after gastrostomy tube placement

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It has been said that it is easier to feed a child with a gastrostomy tube (GT) than by mouth.  Now a study reports improved maternal stress after GT placement (JPGN 2012; 55: 562-66), perhaps because it is easier to provide nutrition.

34 mothers from Norway took part in questionnaires (before, 6 months after, and 18 months after) as part of a study (2003-2005) to see how gastrostomy placement in a child affects maternal stress levels.  Median maternal age was 32 years.  The study was limited by a suboptimal response rate of 59% (34 of 59) and only 19 mothers answered questionnaires at all 3 timepoints.

While all of the children had some peristomal complications, 85% of the mothers reported that their preoperative expectations were met and that their child had improved quality of life.  Mothers had reduced psychological  distress at 6 and 18 months following placement, including less anxiety.

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Six year outcomes with bariatric surgery

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Recently I read that suicides were increased in a group of individuals who underwent bariatric surgery.  This piqued my interest in finding the reference (JAMA 2012; 308: 1122-31 -21 authors).

This Utah study was a prospective trial between 2000-2011 involving 1156 severely obese participants between 18-72 years of age.  There were 3 groups.  The treatment group of 418 underwent Roux-en-Y gastric bypass (RYGB).  The second group (control group 1 =CG1) sought bariatric surgery but did not have surgery, and the third group (control group 2 =CG2) were a randomly selected population-based sample.

All participants had BMI ≥35.  RYGB group had average BMI of 47.3, CG1 was 46.3 and CG2 43.8.  The respective average age was 42.5, 43, and 49.4 years.  In CG1, 84 had undergone bariatric surgery by six years; in CG2 17 had undergone bariatric surgery by six years.

Results at six years:

  • Weight loss: RYGB (92.6% retained at followup): 27.7% loss of initial body weight; CG1 (92.6% followup) 0.2% weight gain, and 0% in CG2 (98% followup)
  • Diabetes remission rate: RYGB 62%, CG1 8%  and CG2 6%.  In addition, there was a 5- to 9-fold reduction in the risk of new diabetes in surgical patients compared to nonsurgical controls.
  • Mortality: No improvement in mortality was evident at six years.  RYGB 12 deaths, CG1 14 deaths  and CG2 3 deaths. None of the RYGB deaths occurred within 30 days of surgery.
  • Suicide:  all 4 patients who took their own life were in the RYGB group and 2 of 3 poisonings (undetermined intention) were in the RYGB group as well.
  • Mental health: The authors note an absence of improvement in the SF-36 mental component score in the surgical group which is in contrast to the SF-36 physical component score.
  • Glucose/insulin, Lipids & Blood pressure: Marked improvements in all of these parameters were noted at six years (Table 2).

It appears that much longer followup will be needed to show mortality benefits from bariatric surgery* and that preoperative/postoperative psychological assessment is needed.

* Mortality benefit has been evident in some studies (see references below)

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References:

  • -JAMA 2011 [doi: 10.1001/jama.2011.817]). Large study failed to show that roux-en-Y gastric bypass prolonged life. n=850 VA pts to 41,244 controls. Same group showed no cost savings during initial 3 yrs: Med Care 2010; 48: 989-98.
  • -NEJM 2011; 365: 1365. Increased frequency of bariatric surgery in adolescents.

Complications from surgery:
Early: bowel obstruction, DVT, GI bleed, leaks, pul embolism, wound infection
After 30 days: anastomotic stricture, bowel obstruction, gallstones, dehiscence, fistula, Bleeding, Incisional hernia, nutrient deficiencies (iron, B12; calcium, Vit D (w RYGB), folate, B6/riboflavin)
Suggested Nutrient Monitoring–every 3 months x 3, then yearly: Vitamin A, B12, Folate, Ceruloplasmin, Vit D-25OH, Iron studies, Zinc, thiamine, Selenium, Intact PTH, Mg, PT/PTT
Suggested supplements per references: Calcium c vitamin D 1200mg, Iron, MVI with zinc/selenium
Also if duodenal switch, add Vitamin A and Vitamin D3 1200units daily or 50,000 units weeekly

Supplements:
Roux-en-Y: MVI 200%, Calcium 1500-2000mg, Fe at least 18-27mg/day, B complex (optional)
Gastric Band: MVI, Calcium, B complex (optional)
Biliopancreatic/duodenal switch: MVI, ADEK: A 10,000 IU, D 2000 IU, K 300 mcg, Calcium, Fe, B complex

  • –NASPGHAN 2011:

Bariatric surgery:
Complications from gastric band: food impaction, erosion (now banned in Finland!), band slippage, gastric volvulus, band too tight, port infection

Roux-y gastric bypass:
anastomotic leak 1.2%, anastomotic ulcers/stricture

If post-op pain: epigastric –>do EGD & if neg do ‘RUQ w/u’, RUQ –> check U/S, LFTs possibly CT
If post-op vomiting –>do EGD
If post-op nausea –>Rx PPI and EGD if not improving
Anastomotic stricture in stomach –>dilate to 10-12mm in 1 session

  • -NEJM 2009; 361: 445/520. perioperative safety.
  • -NEJM 2007; 357: 741, 753, 818. Bariatric surgery improves mortality rate.
  • -NEJM 2007; 356: 2176. Review
  • -Gastro 2006; 130: 1848, 1564, 1617. Bariatric surgery frequently improves steatosis/NAFLD. Less improvement if ongoing insulin resistance.
  • -J Pediatr 2005; 147: 10-19. Review of bariatric surgery. suggests gastric bypass/gastric banding for adolescents.
  • -Pediatrics 2004; 114: 217-23, & 252, 253, 255. Consensus panel recommendations and commentary.

Note: Medication dosages should be checked in standard references for individual patients.  The blog may have transcription errors with regard to dosages listed with references.

Skipping breakfast –boomerang effect for obesity

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A recent article shows unfavorable biochemical variables associated with skipping breakfast in obese children and adolescents (J Pediatr 2012; 161: 871-4).

After recruiting 174 Brazilian subjects (6-16 years) through advertising, the investigators assessed their body composition with dual-energy-dray adsorptiometry and assessed fasting blood glucose and lipid profiles.  Face-to-face interviews with parents determined the frequency of skipped meals.  The median BMI in the cohort was 27.

Results:

  • Skipping breakfast was commonplace.  Only 46% of subjects consumed breakfast daily.  Skipping lunch or dinner was infrequent, approximately 10% and 22% at times skipped lunch and dinner respectively.
  • Consumption of breakfast was inversely correlated with the odds of obesity (OR 0.73).
  • Skipping breakfast was correlated with increased glucose, triglycerides, and very low density lipoprotein cholesterol.

The authors speculate that a prolonged period of fasting in the morning could affect ghrelin secretion which promotes increased food intake.  In addition, ghrelin could affect pancreatic insulin secretion.

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Dietary supplements — safe and effective?

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Most people consider dietary supplements as likely to be beneficial but at the very least ‘there not going to make you worse.’  That sentiment is wrong.  A review recently published has shown that some dietary supplements may increase the risk of cancer (Journal of the National Cancer Institute 2012; 104: 732-39).

Nearly half of the US adult population uses one or more dietary supplements but there is very little evidence that these supplements reduce cancer risk; in fact, the contrary is true.  Based on numerous studies, the authors make extensive comments regarding the studies of antioxidants, folic acid, and vitamin D/calcium which are summarized below.

Antioxidants

While observational data has suggested benefits from fruit and vegetable consumption, data on antioxidant supplement consumption has not shown a beneficial effect.  The review highlights a number of studies with regard to β-carotene, vitamin A, vitamin C, and vitamin E/α-tocopherol.  Specifically, vitamin C and E do not protect against total cancer incidence. α-tocopherol and β-carotene do not protect against cancer or cancer mortality.

  • The Selenium and Vitamin E Cancer Prevention Trial (SELECT) followed 35,533 men at average risk for prostate cancer for approximately 5.5 years.  This study was halted due to lack of benefit.  In addition, the extended followup reported that α-tocopherol significantly increased the risk of prostate cancer by 17%.
  • The β-carotene and Retinol Efficacy Trial (CARET) had a 39% increase in lung cancer incidence compared to the placebo arm.
  • In two of three large studies of β-carotene, the intervention increased the risk of all-cause mortality.
  • The Nutritional Prevention of Cancer (NPC) extended followup found that selenium supplementation statistically increased the risk of squamous cell skin cancer by 25% and non-melanoma skin cancer by 17%.

Folic Acid

Folic acid which is a synthetic oxidized form of folate is commonly used in fortification and supplements.  Recent meta-analysis of randomized controlled trials (RCTs) has found no effect of folic acid supplementation on the risk of colorectal adenomas over a 3-year treatment period.  In addition, one study demonstrated an increased risk of advanced colorectal adenomas (relative risk = 1.67).  Also, in observational studies, higher intake of folic acid has been linked with increased prostate cancer risk.

Vitamin D and Calcium

The Institute of Medicine published recommendations with regard to Vitamin D and calcium intake in 2011 and found that “there is not enough evidence to state that there is a causal association between low vitamin D intake and increased cancer risk.”  The authors summarize several conflicting results with regard to breast, colorectal, and prostate cancers. In addition, a recent meta-analysis of RCTs indicated that calcium supplementation was associated with a statistically-increased myocardial infarction risk.

Why are supplements so widespread if they are not beneficial and potentially dangerous?

  • The authors also summarize regulatory efforts.  In 1990, due to unsubstantiated health claims by food manufacturers, Congress passed the Nutrition Labeling Education Act (NLEA).
  • To limit FDA authority over supplements, at the behest of nutritional supplement manufacturers, in 1994 Congress passed the Dietary Supplement Health and Education Act.  This classified supplements as food and limited the role for the FDA.
  • In 2006, in reaction to deaths from ephedra, Congress passed the Dietary Supplement and Non-prescription Drug Consumer Protection Act.  This allows the FDA to collect adverse reports on supplements but did not give additional regulatory powers.

Conclusions from this review

  1. In populations with a high background of normal nutrient status, risk is accentuated if there can be harm at higher doses.  For selenium (in the NPC study), apparent benefits have been confined to individuals with the lowest baseline blood selenium levels.
  2. It is not reasonable to assume that consumption of a single nutrient would exert a chemopreventive effect equally in all tissues.  In addition, there are substantial variations in formulations and doses of supplements available.
  3. Efficacy and harm are typically tested over several years.  Given the natural history of cancer, it may take decades to assess supplement impact.
  4. Multiple consensus recommendations have indicated that supplements do not prevent cancer and do not prevent chronic disease (Table 1 in reference).  The most recent was from the American Cancer Society in 2012. “Present knowledge indicates that dietary supplements do not lower cancer risk.”
  5. Despite the evidence, the authors note that believers in supplements are unlikely to accept ‘mainstream’ science.  Some may think that unconventional treatments are ignored by science for monetary reasons. Some may think that these products are regulated and would not be offered if they were not beneficial.

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