Author Archives: endodoc

About endodoc

I am a pediatric endocrinologist at the University of Missouri Health Sciences Center in Columbia, Missouri.

Attention All “Foodies” and Dieters

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FYI: There is a very important (and interesting) article in the NYT today.  The piece is entitled “Food for thought” and was written by Jeff Gordinier.  Basically, the article reviews the idea of “mindful eating” a concept that most likely comes from a book written by Brian Wansink, entitled “Mindless eating: why we eat more than we think,” published a while back by Bantam books.  Dr. Wansink is a professor of marketing at Cornell University in Ithica , NY.  As an aside, I am excited that he will be coming to the University of Missouri to lecture at our annual Bond Life Sciences & Society Symposium March 16-18, 2012 (the conference is called “Food Sense”).  Anyway, the NYT article  discusses in considerable detail the concept of thoughtful eating as a way to both enjoy eating more and perhaps, to eat healthier.  Don’t be put off by the rather Buddhist bent to the discussion.  Trust me, it’s good stuff and we would all benefit from reading the article and putting the advice to work for ourselves.

If you find the NYT article interesting, I strongly recommend that you consider tracking down a copy of Professor Wansink’s book (it’s only about $3.00 new on Amazon) and learn something about the psychology of how we eat, particularly why we all eat so much (mostly too much!).  Professor Wansink is the one who did all those fascinating studies about the effects of the size of the container (e.g., glass or plate) and how much we consume.

Does It Really Matter That The U.S. Leads (By A Lot) The World In Health Care Costs?

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In deciding what to write about, I try my best to steer clear of the political side of medicine.  But, today’s NYT has 3 articles that I just couldn’t ignore.  Basically, all three are opinion pieces that address from different directions, one of the most important problems facing U.S. health care, the question of cost.  The first piece was entitled, “What we give up for health care,” and written by Ezekiel J. Emanuel, the brother of Chicago, Illinois major, Raum Emanuel.  The second piece was entitled, ” The dangerous notion that debt doesn’t matter,” and written by Steven Rattner, a Wall Street executive.  The third piece was entitled, “The money traps in U.S. health care,” and written by Philip M. Boffey.

Basically, the Raum and Boffey articles opine on the fact that U.S. health care costs are extraordinary and that if we do not find a way to bring costs down quite a bit, we will have very difficult decisions about what other things we hold near and dear (e.g., education, infrastructure, national defense) that we will need to cut back on.  The Rattner article focuses on the long-term dangers of high U.S. debt.  I found the data in the Bossey piece on comparative costs for various medial services in Britain, Canada, France, Germany, and the U.S., particularly interesting.  For example, the average cost for cataract surgery in the U.S. (public and private sector) at $14,764 beats the closest competitor by $11,412.  It is truly breathtaking how much we in the U.S. (physicians, hospitals, and clinics) charge for routine medical services relative to the rest of the world, particularly since our outcomes are not generally superior to outcomes elsewhere.

In my opinion, based on my reading of the 3 articles in the NYT, at some point, the U.S. will have to go on a health care cost diet.  I predict the diet will be very difficult for us (the general public and the health care providers) to start and to follow.  How in the world will we be able to keep all the stakeholders reasonably happy with the process and the result?  This is scary stuff.

 

The ABCs of Diabetes: A Lecture Outline

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I will be giving a lecture to the Family and Community Medicine Department resident physicians at the University of Missouri Health Sciences Center in a few days.  I thought I would post the lecture outline which includes what I think are important references about diabetes care.  It is interesting that in preparing the talk, I looked over some of my notes from previous talks to the same group.  The oldest talk was in 1979 and the most recent, in 2009.  I was surprised how little things have changed over the past decade in terms of new and important information on diabetes patient care.  Maybe that’s because we made so much progress in the 1980s and 90s?  Anyway, I was a bit surprised.  I do have one minor correction to make to the outline- in the table on medications for patients with type 2 diabetes, just the other day, the FDA rejected the drug dapagliflozin, a sodium-coupled glucose co-transporter inhibitor (see reference 22).  I don’t know why the drug did not get FDA approval but I suspect it was because of so little long-term data on side-effects.

The ABCs of Diabetes Mellitus

1. What is Diabetes Mellitus: Insulin deficiency; Hyperglycemia; Chronic Complications

2. Classification: Type 1 diabetes (B-cell destruction, usually leading to absolute insulin deficiency); Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance); Other specific types (genetic defects of B-cell function, genetic defects in insulin action, diseases of the exocrine pancreas, endocrinopathies, drug or chemical induced, infections, uncommon forms of immune-mediated diabetes, other genetic syndromes sometimes associated with diabetes); Gestational diabetes mellitus

3. Diagnosis

  1. HbA1c = or >6.5%.  The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*
  2. FPG= or >126 mg/dl (7.0 mmol/l).  Fasting is defined as no caloric intake for at least 8 h.*
  3. 2-h plasma glucose = or >200 mg/dl (11.1 mmol/l) during an OGTT.  The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.*
  4. In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose = or > 200 mg/dl (11.1 mmol/l).

*In the absence of unequivocal hyperglycemia, criteria A-C should be confirmed by repeat testing.

4. Initial Presentation

  1. Type 1 diabetes
  2. Type 2 diabetes

5. Initial Management

  1. Type 1 diabetes
  2. Type 2 diabetes

6. Ongoing Management

  1. General Principles/Care goals: Best outcomes with comprehensive, well-organized, patient-centered approach; General care goals: HbA1c <7%; LDL-cholesterol <100 mg/dl; blood pressure <130/80

7. Monitoring for Complications/Associated Disorders

Retinopathy

Nephropathy

Neuropathy

Cardiovascular diseases

Autoimmune disorders (in patients with type 1 diabetes): thyroiditis, pernicious                            anemia, celiac disease

8. Screening for Diabetes?

9. The Future?

References:

  1. American Diabetes Association (ADA) Clinical Practice Recommendations.  On an annual basis, the ADA publishes diabetes care recommendations in the journal Diabetes Care (www.diabetes.org/diabetescare).  This very useful resource is updated every January.
  2. www.endodoc.org.  This is my medical blog and it contains quite a number of entries on various aspects of diabetes care as well as other endocrine and health care topics.
  3. Gwande A: The bell curve.  What happens when patients find out how good their doctors really are?  The New Yorker, December 6, 2004, p 82-91 (www.newyorker.com/archive/2004/12/06/04).
  4. Ishani A et al: Effect of nurse case management compared with usual care in controlling cardiovascular risk factors in patients with diabetes: a randomized controlled trial.  Diabetes Care 2011;34:1689-94
  5. Hu Y et al: Short-term intensive therapy in newly diagnosed type 2 diabetes patients partially restores both insulin sensitivity and B-cell function in subjects with long-term remission. Diabetes Care 2011;34:1848-53
  6. Fajans SS, Bell GI: MODY: history, genetics, pathophysiology, and clinical decision making. Diabetes Care 2011;34:1878-84.
  7. Nathan DM et. al.: Medical Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy.  Diabetes Care 2008;31:1-11.
  8. The Action to Control Cardiovascular Risk in Diabetes Study Group (ACCORD): Effects of Intensive Glucose Lowering in Type 2 Diabetes.  N Engl J Med 2008;358:2545-59.
  9. The ADVANCE Collaborative Group:  Intensive Blood Glucose Control and Vascular Outcomes in Patients with Type 2 Diabetes.  N Engl J Med 2008;358:2560-72.
  10. Nathan DM, et. al.: Impaired fasting Glucose and Impaired Glucose Tolerance: Implications for Care.  Diabetes Care 2007;30: 753-9.
  11. Diabetes Prevention Program Research Group.:  Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or Metformin.  N Engl J Med 2002;346:393-403.
  12. DCCT Research Group:  The Effect of Intensive Treatment of Diabetes on the Development and Progression of Long-term Complications in Insulin-Dependent Diabetes Mellitus.  New Engl J Med 1993;329:977-86.
  13. DCCT-EDIC: Retinopathy and nephropathy in patients with type 1 diabetes four years after a trial of intensive therapy. The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. N Engl J Med 2000;342:381-89.
  14.  DCCT/EDIC Public Website: slides can be obtained 6 months after publication of data.  http://www.gwu.edu/Edic/.  In addition, Susan Hitt the DCCT/EDIC Study Coordinator (Hitts@health.missouri.edu) can furnish you with a full list of DCCT/EDIC publications, abstracts, and presentations.
  15. UKPDS: Intensive blood-glucose control with sulfonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Diabetes Study (UKPDS) Group.  Lancet 1998;352:837-53.
  16. UKPDS: Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group.  Lancet 1998;352:854-65.
  17.  National Glycohemoglobin Standardization Program (NGSP) website: http://www.ngsp.org.
  18. Goldstein DE et. al.: Tests of Glycemia in Diabetes.  Diabetes Care 2004;27:1761-73.
  19. Sacks DNB et. al.: Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus.  Clin Chem 2002;48:436-72.
  20. Nathan DM et. al.: Translating the A1c assay into estimated average glucose values. Diabetes Care 2008;31:1473-8.
  21. Gilbert RE, Marsden PA.: Activated Protein C and Diabetic Nephropathy.  N Engl J Med 2008;358:1628-30.
  22. Nauck MA et al: Dapagliflozin versus glypizide as add-on therapy in patients with type 2 diabetes who have inadequate glycemic control with metformin.  Diabetes Care 2011; 34:2015-22.
  23. Bunck MC et al: Effects of exenatide on measures of B-cell function after 3 years in metformin-treated patients with type 2 diabetes.  Diabetes Care 2011;34:2041-47.
  24. DeFronzo RA et al: Pioglitazone for diabetes prevention in impaired glucose tolerance.  N Engl J Med 2011;364:1104-15.

 

 

TABLE 1. Medications for Patients with Type 2 Diabetes

Insulin

Medications that stimulate insulin release

  1. Sulfonylureas (SURs): Advantages- long-term experience, inexpensive, oral administration; Disadvantages- weight gain, ?increased risks for cardiovascular diseases, hypoglycemia
  2. Glinides (e.g., repaglinide, nateglinide): Advantages- shorter-acting than SURs, only occasional hypoglycemia; Disadvantages- expensive, GI side-effects, weight gain

Medications that enhance insulin action

  1.  Incretin mimetics (glucagon-like peptide agonists, or GLP-1 agonists such as exenatide): Advantages- weight loss, infrequent hypoglycemia, can be given weekly; Disadvantages- expensive, requires injections, frequent GI side-effects
  2. Incretin sustainers (dipeptidyl peptidase-4 inhibitors or DPP4 inhibitors such as sitagliptin): Advantages- oral administration, rare hypoglycemia; Disadvantages- costs, GI side-effects
  3. Amylin-like agents (e.g., pramlintide): Advantages- ?weight loss; Disadvantages- hypoglycemia, injections tid, costs
  4. Thiazolidinediones or TZDs (e.g., pioglitazone):Advantages- improved lipid profiles, no hypoglycemia, ?prevent/slow loss of insulin secretory capacity; Disadvantages- costs, weight gain, fluid retention and heart failure

Medications that inhibit glucose absorption from the gut or reabsorption from the kidney

  1. Alpha-glucosidase inhibitors (e.g., acarbose): Advantages- ?weight loss; Disadvantages- costs, GI side-effects (frequent), tid dosing
  2. Sodium-coupled glucose co-transporter (SGLT2) inhibitors (e.g., dapagliflozin): Advantages- rare hypoglycemia, weight loss; Disadvantages- UTIs, polyuria, costs, uncertain risk/benefit ratio

Medications that decrease hepatic glucose production (e.g., metformin): Advantages- no hypoglycemia as monotherapy, inexpensive, oral administration, ?weight loss; Disadvanages- rare lactic acidosis, GI side-effects (generally mild)

The Affordable Health Care Act vs Childhood Obesity: Good Intentions Running Amok

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This morning I read an article in the NYT that actually made me feel sorry for health insurance companies and wonder just how affordable the Affordable Heath Care Act will be.  The article was entitled “Learning to be lean.  With few proven models, health sector takes on childhood obesity,” and was written by Reed Abelson.  Apparently, the new federal health care law, among its many provisions, requires both health insurers and employers to pay the cost of screening children for obesity and providing them with appropriate counseling.  This has health insurers scrambling to find what just what appropriate counseling might be.

I don’t need to remind any of my readers that childhood obesity is a big (no pun intended) problem; about 30% of children are considered overweight (the politically correct terms are “at risk for overweight” and “overweight.”  Please don’t ever call a child obese.  Anyway, there are considerable data in the scientific literature to show that childhood obesity is a risk factor for adult obesity and its many health problems.  So, screening for overweight or whatever we want to call it is appropriate as is conveying the information to parents.  This task is not terribly complicated or costly- just a quick height and weight measurement, calculation of a BMI, and information about what the data mean.  This information should be part of any well child medical care visit and the information can also be provided to parents through the schools, something already done in many places.  So far so good.  But what about “appropriate counseling” for those children found to be overweight?  As the NYT article notes, there are few if any proven models (how about no proven models with good long-term success?) to chart a way forward for insurers and employers.  So, is the U.S. health care system (to the extent we have a system) now taking the tack of requiring health insurers and employers to do the research and determine what constitutes appropriate counseling? It’s sort of like requiring insurers to screen for cancer and when a diagnosis is made, to do the research to find the most effective therapy.   In my opinion this is not health care reform at its best.  We should not identify health care problems such as childhood obesity and then require action that is very likely to be time and money poorly spent.  Good intentions do not justify unproven interventions.

I do not want to seem like a total grinch about this subject.  I like many provisions in the Affordable Health Care Act and I  would recommend that we screen children for weight status along with other health measures and require that health care providers offer nutritional counseling  (covered by the health insurer) on an annual basis, much like Medicare already does for people with diabetes mellitus.  That would be a reasonable start and one that might make the Affordable Health Care Act more affordable than the road we seem to be going down.  We must not outpace the science with our desire to do all that is possible in an effort to make our children healthy.

Can We Prevent Weight Gain Over the “Holidays”?

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Like clockwork, every year, starting in early November and running well into the new year, newspapers and magazines are packed full of articles to warn us about the well-known holiday season weight gain and what to do about it.  This year was no exception.  In this entry, I want to highlight what I think were some of the most interesting articles.  I don’t need to remind you that we in the U.S. are, as a group, on the heavy side.  How did we get that way?  Many studies have documented our  slow but steady weight gain beginning in early adulthood, averaging about 2-2.5 lbs each year.  That doesn’t seem like a big deal, but you can do the math- 2 lbs/yr X 30 yr = overweight. Studies have also shown that most of the annual weight gain actually does take place in November and December.  So, can we do anything about holiday-induced “weight creep?”

The first article I recommend to you is entitled “the Fat Trap,” and was written by Tara Parker-Pope (NYT Magazine, Sunday January 1, 2012).  Ms. Parker-Pope bemoaned the fact that it is difficult to lose weight and summarized a study carried out by a group of European investigators (Sumithran P et. al.: Long-term persistence of hormonal adaptations to weight loss.  N Engl J Med 2011;365:1597-1604).  Fifty overweight people were put on a 10 week weight loss program.  The investigators measured a large number of hormones related to appetite at baseline, 10 weeks, and after 62 weeks.  They found that weight loss was associated with both increased appetite and increased levels of the appetite-stimulating hormones.  Unfortunately, most of the patients regained the weight they lost and still had increased appetite and increased levels of the appetite-stimulating hormones at 62 weeks.  The investigators concluded that mediators of appetite encourage weight gain.  Ms. Parker-Pope put it more bluntly: once we become fat, most of us despite our best efforts will probably stay fat.

The second article I recommend to you is entitled “New way calories can add up to weight gain,” written by Ron Winslow (Wall Street Journal Wednesday January 4, 2012).  Mr. Winslow summarized a study published that day in the Journal of the American Medical Association or JAMA (lead author George Bray from the Pennington Biomedical Research Center, Baton Rouge, LA).  The investigators fed 25 men and women about 1000 excess calories every day for 56 days but with diets that varied in the percentages of protein and fat  they contained (carbohydrates were about 40% of total calories for both diets.  The investigators found that although the subjects ingesting the low protein diet gained the least weight (about 7 lbs), they had as much gain in fat mass as the subjects on the normal and high-protein diets, whose excess weight gain was largely related to a gain in lean body mass.  The investigators concluded that “fad” diets with widely varying proportions of fats, carbohydrates, and fats, may not be the way to go in dieting, but rather, should focus on decreasing total calories and fat content.  In addition, the data showed that the BMI, a traditional way of assessing a patient for weight status, may not be very good at picking out those who have high body fat mass as opposed to high lean body mass.  As an aside, on the same page as the Bray study report, is a report by the same journalist, Ron Winslow,  on a Swedish study touting the health benefits of bariatric surgery for weight reduction (“Procedure’s benefits go beyond weight loss”).

The third article challenges Parker-Pope’s pessimistic view of weight reduction efforts.  It is entitled “Be it resolved,” and was written by John Tierney (NYT Sunday, January 8, 2012).  The article is all about the power of New Year’s resolutions to help people lose weight.  Tierney recently co-authored a book with Roy F. Baumeister entitled “Willpower: rediscovering the greatest human resource”.  I confess that I have not read the book, only the newpaper article.  Dr. Baumeister is a social psychologist at Florida State University.  The lengthy article presumably summarizes the book’s message: setting goals is most useful if the goals are accompanied by firm (written down) resolutions,  and that it is possible to reinforce one’s willpower; studies have shown that setting goals without concomitant resolutions, is far less likely to result in long-term successl.  I cannot say that I was much impressed with the recommendations other than that they are logical but  rather complicated,  and it is my guess that anyone willing to do all the things that are recommended to make the resolution work, doesn’t dare fail.  I can’t think of any good reasons not to try the resolution advice.

The last article also appeared in the Sunday January 8. 2012 issue of the NYT.  It was entitiled “Young, obese and in surgery: youth procedures rise, despite doubts,” written by Anemona Hartocollis.  I found the article well written but very disturbing.  I will offer no other comments.  Read the article and let me know what you think.

Conclusions

So, it’s another year, another few more pounds, and no new sure-fire ways to trim down and stay trimmed-down.  As I have tried to emphasize in a number of earlier entries on weight loss therapies, almost every diet out there works in the short run but fails in the long run.  I am convinced that for most people, the best way to lose weight and keep it off is to REALLY, REALLY want to lose weight (?maybe goals and resolutions?) is to aim for weight loss of no more than 1 pound per month (my wife’s mantra), to eat only moderate amounts of healthy foods (a la Michael Pollen) with only small amounts of meats/fatty foods, few if any highly processed foods (particularly potato chips and french fries-a painful task), no sugared sodas and sport drinks, AND to exercise regularly- at least 30 minutes 3 days/week.  Good luck.

High Fructose Corn Syrup: Dietary Friend, Foe or Fall Guy?

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For quite some time, I have been thinking of  writing a piece about high-fructose corn syrup (HFCS).  HFCS consumption, mostly in soda drinks and highly processed foods, has grown steadily over the past 30-40 years and now represents a sizable percentage of both total carbohydrate and total calorie intake in the U.S.  HFCS has been both praised as a low cost nutrient and vilified as one of the primary causes of our obesity and diabetes epidemics.  A few weeks ago, I saw an ad on TV that was promoting HFCS as healthful “corn sugar,” implying that somehow that HFCS was a natural (and healthful) nutrient derived from corn.  Not surprisingly, the ad was produced by the Corn Refiner’s Association (CRA) and was clearly part of a PR campaign.  The ad was criticized by several food industry watch dogs, including the U.S. Food and Drug Administration (FDA) and  representatives from the sugar maker’s industry; accusing the CRA  of false advertising.

Here Comes The Judge

What got me to actually sit down at the computer and start writing was a recent news report in my local newspaper (the Columbia Daily Tribune, Friday, October 21, 2011, page 5B; columbiatribune.com) that U.S. District Judge Consuelo Marshall issued a ruling that a false advertising lawsuit filed by the sugar industry against the CRA could go forward.  The CRA had argued that the lawsuit should be dismissed because HFCS is equivalent to sugar in the way it is metabolized and that the lawsuit was “an attempt to stifle a national conversation about the merits of HFCS versus sugar.”  In addition, the CRA lawyers argued that educational campaigns form the CRA shouldn’t be considered advertising.  The judge dismissed those claims stating that the CRA’s educational campaigns constitute commercial speech and that the industry group is not insulated from federal false advertising regulations just because its “educational” statements relate to a public health issue.  I almost forgot to mention that the CRA had asked the FDA’s permission to use the term “corn sugar” rather than HFCS in both advertising and product labeling.  As far as I know, the FDA has not ruled on the request.  So, what is this all about?

What is HFCS anyway?

To understand what HFCS is and isn’t, we need to discuss a little basic chemistry.  Don’t be afraid, it’s not complicated.  To most people, the word “sugar” means good old table sugar, a sweet-tasting white crystalline substance called sucrose and which is composed of a molecule of glucose and a molecule of fructose.  Another word for sugar is saccharide.  So,  sucrose is a disaccharide; glucose and fructose are six-carbon monosacharides.  Another important disaccharide is lactose (milk sugar), which is composed of a molecule of glucose and a molecule of galactose.  Saccharides are a class of carbohydrates, molecules that are composed of carbon, hydrogen, and oxygen.  Carbohydrates, along with proteins and fats are the basic body building blocks.  Sugars can be composed of many monosaccharide molecules linked together, called polysaccharides, which are important storage forms of sugars in both animals and plants.  Although all sugars (by definition) are sweet, there is a large difference in the sweetness of individual sugars: fructose is the sweetest sugar, almost twice as sweet as glucose.

Sucrose comes mainly from sugar cane (60%) and from sugar beets (40%).  Sugar cane was first found in Papua New Guinea and was domesticated about 10,000 years ago.  The discovery of beet sugar was not until about 250 years ago.  The history of sugar is a fascinating one which has been chronicled by N Deerr in The History of Sugar (volumes 1 and 2, London, Chapman and Hill Ltd., 1949 v-258/1950 v-259-636).  An excellent summary of the subject was written by M. Gracey, N Kretchmer, and E. Rossi (A glimpse into the history of sugar, in: Sugars in Nutrition, Ed. M. Gracey, N. Kretchmer, and E. Rossi.  Nestle Nutrition Workshop Series, Vol 25; Nestec Ltd., Vevey/Raven Press, Ltd., N.Y., 1991).  I can assure you that HFCS is no more controversial than sugar itself, which has been considered by many historians to be most responsible for slavery (both in the U.S. and globally).

Anyway, for a variety of reasons, beginning in the 1970′s, HFCS was introduced as an ingredient in many processed foods.  HFCS is made from corn syrup, a liquid composed mostly of glucose molecules.  It is commercially available from a number of manufacturers, but perhaps, the best known form of corn syrup is Karo Syrup (ACH Food Companies, Inc.).  Corn syrup is made first by milling corn into corn starch, and then adding an enzyme, alpha-amylase, which breaks the starch into oligosaccharides (small chains of glucose molecules).  The next step is adding another enzyme, glucoamylase (also know as gamma-amylase) which results in a syrup consisting of only glucose molecules.  To make HFCS, the corn syrup is converted into fructose by another enzyme, D-xylose.  The manufacturing process results in HFCS with 90% fructose (HFCS 90) or 42% fructose (HFCS 42).  HFCS 90 is used to make HCFS 55, which is used to sweeten sodas and various sport drinks.  HFCS 42 is used in many processed foods including some yogurts, frozen desserts, breakfast cereals, and baked goods, and has about the same composition as sucrose.

How much sucrose and HFCS do Americans actually consume?

You may find it hard to believe, but since 1970, U.S. consumption of HFCS has risen from zero to about 40 lbs/yr/person.  At the same time, consumption of sucrose has decreased from about 70 lbs per person to about 40 lbs per person.  Net (total) sugar consumption has risen from about 80 lbs/yr to about 100-120 lbs/yr.  Thus, virtually all of the increase in total sugar consumption is the result of increased consumption of HFCS in its various forms.  But, the ratio of fructose to glucose intake has remained about the same over time

Why is HFCS so widely-used?

The development of HFCS was to a great extent the result of political and economic circumstrances.  Cane sugar quotas in the U.S. have kept the price of can sugar high while corn subsidies have made growing corn relatively inexpensive.  The bottom line is that it is cheaper to make HFCS than to process cane sugar.  It is also important to note that HFCS has some desirable qualities; It mixes well with foods and keeps foods moist.

How is HFCS metabolized?

Remember that HFCS and sucrose are composed of glucose and fructose molecules.  It is the fructose that most experts have focused on as a possible health culprit, beyond the fact that sugar in the form of glucose, sucrose or fructose add calories to the diet- about 4 calories/gram consumed.  Metabolism of glucose is relatively simple.  Glucose can be used by all cells in the body for energy, it can be stored in the form of glycogen (long chains of glucose molecules, much like starch, and used as a building block for polysaccharides.  Fructose, on the other hand, is taken up mainly by the liver and can be converted into glucose, glycogen, triglycerides  and some fatty acids.  It is the role of fructose in fat metabolism that has generated the most controversy.  There are considerable data in both animal and humans that consumption of large amounts of fructose raise triglyceride levels and increase insulin levels, promoting insulin resistance.  Does fructose promote cardiovascular disease?  Does fructose promote the development of diabetes mellitus? Does high fructose intake stress the liver?  These are just some of the questions that have been raised about dietary consumption of fructose, and by extension, consumption of HFCS.

Is HFCS metabolized differently than sucrose derived from cane and beet sugars?

There is considerable controversy whether HFCS has unique properties such that it is metabolized differently than sucrose derived from cane or beet sugar.  In my opinion, there are no credible data to show that HFCS and sucrose are metabolized differently or that the fructose in HFCS is any different than frucose in sucrose or fructose in fruits, honey, maple sugar, agave syrup or brown rice.

So, what’s the problem?

In my opinion, the problem is that we in the U.S., consume far more calories than we need and many of those calories come from foods containing various sugars, including HFCS.  The latest data show that Americans currently consume, on average,  about 130 lbs of sugar a year which works out to be almost 40 teaspoons of sugar every day.  It’s extraordinary.  We have twin epidemics of obesity and diabetes mellitus and plenty of cardiovascular disease to go around.  We don’t need to single out a single food or food additive (i.e., HFCS) as the reason for our many ills; there is plenty of blame to go around, including our fondness for inactivity.  But, it is clear that if we curb our sugar intake, we will benefit.  I am neither defending or condemning the use of HFCS in foods.  I seriously doubt that if tomorrow, the use of HFCS in foods and drinks were banned, it would have any impact on the prevalence of obesity, diabetes or heart disease.  We  will still eat too much (including an extraordinary amount of the various sugars) and exercise too little.

If you find this subject interesting, I urge you to read an article by Mary Franz (“High-fructose corn syrup: what’s the fuss about?,” published in Diabetes Self-Management, May/June 2011, pages 33-37) and an article by Gary Taubes (“Is sugar toxic?,” published in the New York times Magazine, April 17, 2011).  The Taubes article discusses the highly controversial views of Robet Lustig, a physician from the University of California San Francisco.  Don’t miss the Lustig video on You-Tube which is a lecture he gave in 2009 entitled “Sugar: the bitter truth.”  I’m not saying whether I agree or disagree with Lustig’s views, but………..

Finally, what about calling HFCS corn sugar?  In my opinion, it’s clearly false advertising.  Why don’t the corn growers just call HFCS something like “sugar derived from corn?”  Or, maybe, just continue to call it HFCS?

Risks vs. Benefits of Medical Care Decisions: Lessons From DES

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In several previous entries I have discussed the issue of risks vs. benefits regarding this or that medical therapy, generally use of some medication where sufficient data have not been obtained to determine long-term risks. The other day,  I was going through my pile of New England Journal of Medicine (NEJM) issues from January-June 2011,  working on a continuing education program offered by the journal (it “forces” me to actually read each of the issues which come weekly), I spied a short article that I had not noticed previously, entitled ,”Long-term effects of in utero exposures- the DES story,” written by Annekathryn Goodman, John Schorge, and Michael Greene, all professors at Harvard Medical School in Boston and serves as an important reminder about the importance of assessing “risk vs. benefit” for medical therapies.

The Diethylstilbesterol (DES) story

DES is a synthetic nonsteroidal estrogen that was developed in the late 1930s.  It was widely used as a supplement to cattle feed (to fatten them up) and in humans as estrogen replacement therapy and for treatment of prostate and breast cancers.  In the late 1940s, one study showed that DES could prevent miscarriage if given early in pregnancy.  Other studies had shown no benefit, yet DES was widely used for quite a long time despite very convincing data that accumulated showing no benefit with respect to miscarriages.  Eventually, doctors got the message and use of DES faded away.  Then, in 1971, the NEJM published results from a very scary study performed by Herbst et al., showing an association between DES use during pregnancy and development of a rare vaginal cancer (clear-cell adenocarcinoma) many years later in female offspring of these mothers.  I still remember when the news hit.  I was a pediatric resident physician and doing my pediatric endocrinology rotation.  Even back then I was reading the NEJM regularly (I have been a regular subscriber since 1965).  I remember the many discussions we all had about the data.  As it turned out, by the early 1990s, 431 cases of the rare cancer had been identified in young women exposed to DES in utero.  The median age of cancer diagnosis was 19 years.  We now know that the mechanism for the development of the cancer was probably drug-induced abnormal development of the Mullerian ducts (these ducts develop into the uterus, fallopian tubes,  and a bit of the vagina).  It was all a nightmare for the mothers, the young women, and the physicians involved in their care.

What did we learn from the DES catastrophe?

I am not certain what the collective “we” learned from the DES story.  I do know what I learned- that all medical treatments, be they procedures or medications, have risks and benefits.  Many times we know what the potential benefits are for a given treatment, but do not know what the risks might be.  Thus, it is always important to consider and to weight unknown risks vs. the potential benefits.  This is no easy task but it needs to be done and physicians who do not do this, do a disservice to their patients.  The potential benefit of a given treatment must be compelling enough to counter the unknown risks of the therapy, whatever the therapy might be.  We (here I mean the collective “we”), keep learning this lesson over and over.  Just this week, I read an article (and two accompanying editorials) in the NEJM entitled ” Stenting versus aggressive medical therapy  for intracranial arterial stenosis.”  In summary, the study showed that stenting was associated with many more deaths than the medical therapy.  As it turned out, the stenting procedure was approved by the FDA in 2005 after a small non-randomized study showed benefit from the stenting vs. medical therapy.  Now the “experts” are moaning and groaning about the fact that FDA approval for the stenting procedure was probably inappropriate given the very limited data and that a large randomized trial should have been performed, which as it turns out was the substance of the current NEJM article.  Then there is the story about the “metal-on-metal” hip replacement devices that is turning out to be another medical therapy catastrophe (see “Medical Devices-balancing regulation and innovation, ” written by Curfman GD and Redberg RF in this week’s NEJM).  I could go on and on.  We as caregivers all need to go back and review the DES story and understand why we need to learn as much as possible about risks and benefits of any given therapy/device before we “jump in.”  Obviously, if a patient faces certain death and a new therapy comes along, it would not be appropriate to “sit on one’s hands.”  But, few new medical treatments meet that urgency standard.  Pressures from device manufacturers and pharmaceutical companies and the researchers who either developed or tested the treatments, should not trump the need for careful unbiased assessment of the risks and benefits of the proposed treatment.

Effects of Parenting Style on Glycemic Control in Adolescents with Type 1 Diabetes

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For patients, parents, and health care providers, managing type 1 diabetes can be quite a challenge, particularly during adolescence.  A very interesting article in the August 2011 issue of Diabetes Care offers some insights into how parenting style might play an important role in efforts to achieve optimal diabetes control in adolescents.  The study was entitled “Role of Parenting Style in Achieving Metabolic Control in Adolescents with Type 1 Diabetes ,” and written by Maayan Shorer and colleagues (Diabetes Care 2011;34:1735-37).  Parents of 100 adolescents with type 1 diabetes completed questionnaires designed to assess parenting style.  Both parents and patients rated patient adherence to the treatment plan.  Glycemic control was assessed by hemoglobin A1c (HbA1c) determinations.

The Findings

The investigators found that an authoritative parenting style was associated with better adherence to the treatment plan and lower HBA1c levels than was an authoritarian parenting style.  I had actually never heard the term “authoritative parenting style” before.  This parenting style is characterized by a parent who sets clear limits for the child in a noncoercive way.  This parenting style is to be distinguished from a permissive parenting style and an authoritarian parenting style.  The latter style is characterized by harsh, coercive, and punitive parenting.  The investigators found that only in fathers did the authoritative parenting style reap benefits for the child.  Among the mothers, a permissive parenting style was associated with less well controlled diabetes as was an authoritarian style.  For both mothers and fathers, a sense of helplessness was associated with less well controlled diabetes (for fathers) and poorer adherence to treatment (for mothers).  The investigators concluded that their study results were consistent with previous studies on parenting style in adolescents with diabetes and that more involvement by fathers who exhibit an authoritative style of parenting would be beneficial.

Translation of these research results to patient care?

These data may explain differences in glycemic control among adolescents with diabetes, but can the information be used to actually improve glycemic control in adolescent patients?  That study has yet to be carried out.  For now, it makes good sense to work with mothers and fathers of children with diabetes and strive to promote authoritative parenting styles (as opposed to permissive or authoritarian styles) and in particular, to promote more involvement by fathers in the care of their children and adolescents with diabetes. In closing, I must confess that I have no idea how to teach parents to be authoritative rather than authoritarian or permissive in dealing with their teenagers, nor do I know if it can actually be taught. effectively.  But, it seems to be worthwhile to try.  I wonder what kind of a parent I was to my children when they were teens?  Maybe I don’t want to know?

Failure To Thrive: Endocrine Causes

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Yesterday I wrote about the clinical entity failure to thrive (FTT).  This morning I realized that I had not really addressed the question of endocrine gland disorders that can be associated with FTT.  Probably, the reason I did not mention endocrine disorders was that they do not often cause FTT and if they do, the signs and symptoms usually make it easy to make a diagnosis.

As I discussed in the previous entry, the key feature in all patients with FTT is poor weight gain, with or without short stature.  With only a few exceptions, endocrine disorders that cause short stature are rarely associated with poor weight gain.  For example, patients with either growth hormone deficiency, hypothyroidism or Cushing’s disease (glucocorticoid excess) typically present with short stature, but are generally overweight for height.  The endocrine conditions that typically present with poor weight gain (with or without short stature include type 1 diabetes mellitus, adrenal insufficiency (i.e., Addison’s disease), and conditions associated with hypercalcemia such as hyperparathyroidism.  Usually, the signs and symptoms for these disorders are such that very little detective work is needed to figure out what the problem is.  The one exception might be adrenal insufficiency; I have been amazed at how often that diagnosis is delayed for a long time if the patient is being followed by a primary care doctor, despite many clues from the medical history and physical examination.  I suspect the main difficulty in diagnosing adrenal insufficiency, is that the various disorders that cause adrenal insufficiency are rare and many physicians (not pediatric endocrinologists) have little or no experience in dealing with the problem.  Be warned.

A Medical Whodunnit: 16 Month Old Female with Failure to Thrive

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A couple of weeks ago I received a telephone call from SS, one of my daughter’s close friends from college.  SS, who lives in New York City, called my daughter, who lives in California, because she was concerned about her younger sister’s (RS) daughter, KS .  RS had been worried about her daughter’s growth.  RS told her sister SS about the problem and SS promptly called my daughter; I suspect SS called my daughter because the daughter of a pediatrician would be expected to know almost as much as a pediatrician.  Right?  Anyway, my daughter called me and I was warned to be expecting a phone call from SS, which I got the next day.  SS wanted to know if I would be willing to talk with her sister.  Of course I agreed and talked with RS the next day.  I learned that KS was 16 months old and had  been  diagnosed with failure to thrive (FTT).  RS wanted to know what FTT was and what I thought should be done.  The situation was a bit complicated because RS lives in the Netherlands and was just visiting the U.S.  The family (RS, her husband, and 2 daughters, MS, age 4 years, and KS) has health insurance in the Netherlands but no coverage in the U.S.  The diagnosis of FTT had been made by a pediatrician in New York who recommended that a large number of laboratory studies be carried out as soon as possible.  One question RS had for me was whether the tests needed to be done immediately or could wait until the family returned to the Netherlands in about 2 weeks; the pediatrician estimated that the tests would cost about $5000-$10,000 (blood work, x-rays, and MRI, etc).

The Medical History

I first told RS that I would be happy to discuss things with her but that she needed to understand that it is always risky to get “curbside” consultations and that without actually seeing a patient, it is difficult for a physician to give a well-reasoned opinion,  and that my advice should be considered in that light.  KS was born full-term after an uneventful pregnancy.  There were no problems at birth and initially the infant seemed to do very well, following the 50% for height and weight until about age 6 months.  RS and her husband were of average height and their older daughter, MS was at about 60% for height and weight.  The infant was being exclusively breast-fed. After age 6 months, the infant slowed her growth rate, falling to about 40% for height and 5% for weight by age 1 year; at age 15 months, the height was still at about 40% but the weight percentile fell further, to about 2%.  At no time did the infant show actual weight loss.  KS seemed to be feeding well and was a happy baby although her development seemed to be a bit slower that that of her older sister; KS was babbling but still not walking.

The New York pediatrician who  saw KS  made the diagnosis of FTT based on the infant’s weight and the history of slow weight gain.  The pediatrician felt the physical examination was normal except for the weight and perhaps, slightly delayed motor development, and slightly decreased muscle tone.  As discussed above, the pediatrician recommended a series of studies but felt they could be delayed a few weeks (until the family returned to the Netherlands.  The pediatrician did order a complete blood count and basic blood chemistry tests (electrolytes, serum CO2, BUN, etc.) all of which showed normal results.  Hence, no anemia, and no evidence of kidney disease or metabolic disease associated with acidosis.

What is FTT, how is it diagnosed, and how is it treated?

The best definition I have yet seen of FTT was written by Cindy Christian and Nathan Blum in the textbook, Nelson Essentials of Pediatrics, 5th Edition (2006), Chapter 21, (Failure to thrive).  The authors wrote the following: “Failure to thrive (FTT) is a term given to malnourished infants and young children who fail to meet expected standards of growth.”  The authors went on to say that that the term FTT most often describes malnutrition related to environmental or psychosocial causes but that most children with FTT also have organic contributors.  The list of possible organic contributors is a long one and includes most every body system (e.g., genetic/congenital/anatomic, gastrointestinal, metabolic,  neurologic, renal, and hematologic disorders, as well as infections.  Thus, FTT is not really a specific diagnosis of anything but rather, a descriptor of certain signs and symptoms with poor weight gain always the “centerpiece.”  It’s sort of like a diagnosis of “limp,” which could be caused by anything from a rock in one’s shoe, to a serious bone or joint disease.  Regardless, once a paient is diagnosed with FTT,  every effort must be made to determine a specific etiologic diagnosis so that proper treatment, if any can be given in timely fashion.

How to sort through the myriad of diagnostic possibilities?

Once a diagnosis of FTT is made, the next step is for some knowledgeable health professional (e.g., nurse practitioner, pediatrician, pediatric endocrinologist) to get a detailed medical history.  The history should include as much information as possible about previous height and weight measurements and  laboratory test results.  In addition, the history should include detailed information about the infant’s feeding history and details about the family social history in an effort to uncover any potential environmental/psychosocial factors.  Next, a comprehensive physical examination should be performed that includes a developmental assessment. Well done medical histories and physical examinations are always “just what the doctor ordered” in any patient encounter, and in patients with FTT,  they are critically important.

The next step: developing a differential diagnosis

Armed with information from the medical history and physical examination, one can begin to develop a plan of action.  I usually start by asking myself 3 questions.  The first is whether, based on all the information available, I am reasonably confident the patient is normal and that the “poor” weight gain is/was a variant of normal and that no studies or treatment is needed.  Being reasonably confident is not the same thing as being 100% confident, and generally, such a patient should be seen for a follow-up clinic visit in the next 1-2 months.  The second question is whether I am reasonably confident the patient has a specific medical disorder that can explain the poor weight gain.  For example, if the history and physical examination strongly suggest a gastrointestinal basis for the poor weight gain, such as celiac disease, the next steps in the evaluation process are straightforward.  The third question is the most difficult one to deal with and is whether I am unable to decide whether the patient likely  is either normal or has some (as yet unknown) environmental/psychosocial and/or organic process to explain the poor weight gain.  Unfortunately, in my experience, even after a detailed medical history and physical examination, the answer to this question is often “yes,” necessitating considerable detective work.

Is the FTT merely a variant of normal growth?

It should be obvious that to determine if the FTT is not really FTT but only a normal growth variant, requires an understanding of normal growth.  I have discussed this subject in some detail in earlier entries but I will review things a bit for those of you who do not wish to hunt down the appropriate entries (I can’t even remember which ones, but they can be found by checking out entries in the growth disorders category.   Principle #1: children generally follow both weight and height growth channels very closely; if a child is at 50% for height at age 2 years, he or she is very likely to still be at that percentile at age 8 or 9 years of age.  Many normal children do not have height and height at the same percentile; it can be perfectly normal to be at 50% for height and 10% for weight and vice versa (but less desirable for a number of reasons that we will not discuss here).    There are 2 important exceptions to this principle; first, during infancy, children often do not stay in their height and weight channels.  Infants who are genetically programmed to be bigger than their height percentile at birth would suggest (to be precise, in children we pediatricians and pediatric endocrinologists, generally carry out length rather than height measurements up until age 2-3 years of age), show acceleration in both height and weight from the beginning, reaching the growth channel they will follow by about 1 year of age; premies often take somewhat longer.  For infants who are programmed to follow lower height and or weight channels than their height and or weight at birth, first follow the birth channels for about 6 months and then, gradually slow their growth rates- we call it “lag-down,” until about 18-20 months of age, at which point they track “like glue.”  The second exception to principle 1 is puberty.  All bets are off as to the growth rate (both height and weight) at puberty.  Children who are “destined” to end up at lower or higher height and or weight percentiles as adults than they followed during childhood, will generally fulfill their destinies.  Remember the following: Scottie dogs generally have Scottie dogs and Great Danes generally have Great Danes.  That saying is actually principle #2.

Back to KS

Remember KS, the 16 month old we were discussing?  Her growth pattern could be merely normal lag-down but I doubt it, since lag-down usually affects both height and weight.  Earlier, I didn’t mention that at the time of the visit to the pediatrician, RS was concerned that perhaps, KS was not getting adequate calories from the breast feeding alone.  KS decided to taper off the breast feeds and add table foods.  I got a follow-up from KS just the other day.  The family returned to the Netherlands, went to the clinic where the diagnosis of FTT was confirmed by a nurse practitioner, and an appointment was set up with a pediatrician; in the Netherlands, the primary care providers are often nurse practitioners.  But, RS told me that since decreasing the breast feeding and adding table foods ad lib, KS had been gaining weight like crazy and had progressed substantially with her development. So, in this instance it looks like the problem was inadequate calories and maybe a bit of vitamin D deficiency?  I am just speculating about the vitamin D deficiency but given that KS had not received any vitamin D supplementation and had been exclusively breast-fed, that’s a good possibility- vitamin D deficiency could explain the poor muscle tone and slow development.  The primary health care provider felt the problem was likely a nutritional one because of the much lower weight than height percentile and was betting on celiac disease or something like that (a reasonable hypothesis).  Anyway, we will need to wait until RS gives me another follow-up to find out if the problem in this case was more or less an environmental/psychosocial one rather than a systemic disorder.  I promise to let you know.  Finally, please do not infer from my entry that I am not a fan of breast feeding.  I think breast feeding is the way to go but that occasionally, problems do arise.  That’s why infants and children need regular check-ups by health care professionals who know all about monitoring growth (and breast feeding).  I suspect that for KS, part of the problem was related to the discontinuity in medical care because of the family travels between the U.S. and the Netherlands.  I am hoping things will turn out well.