February 28, 2010 · 2:00 AM

Which Pedometer Should I Get?

Setting a goal of walking 10,000 steps a day could motivate you to become active enough to gain the health benefits of exercise.  You count steps automatically with a pedometer.  Regular exercise also helps keep lost weight from returning.

Thanks to the Internet, you can waste spend hours reviewing features of pedometers before you make a purchase. 

Consumer Reports magazine in February, 2009, reviewed pedometers and their #1 Best Buy recommendation was the Omron HJ 112, which you can clip to your belt or waistband, or carry in your purse.  Available for around $15-30 (U.S. dollars). 

No. 2 was the Accusplit AE 170 XLG ($30-35).  The Accusplit AE 170 is probably just as good.  The only differences I see are that you can enter specific goals into the XLG and it tracks your progress and the time you’re moving. 

The Omron HIP (HJ 150, $20) is also very popular and probably the simplest one to use on this page.

The guys at Obesity Panacea blog recommend the Omron HJ-303 ($35), which you can carry in your pocket instead of clipped to your waistband.

You don’t have to be a marathoner or gym rat to gain most of the health benefits of exercise.  Why not start a walking program today?

Steve Parker, M.D.

Disclosure:  I was not paid to mention these products.  I haven’t owned or used any of them.  If you are a device manufacturer or sales representative and would like me to try your pedometer, please contact me by e-mail.

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February 27, 2010 · 4:05 AM

Alcohol Habit (Especially Wine) Started in Middle-Age Reduces Heart Attack and Stroke

Jesus turned water into wine at a wedding.  His mother asked him to do it.  Of all the miracles he performed and could have performed, I wonder why this is the first one recorded in the Holy Bible.

We have known for years that low or moderate alcohol consumption tends to lower the risk of cardiovascular disease such as heart attack and stroke, and prolongs life span.  Physicians have been hesitant to suggest that nondrinkers take up the habit.  We don’t want to be responsible for, or even accused of, turning someone into an alcoholic.  We don’t want to be held accountable for someone else’s drunken acts.  Every well-trained physician is quite aware of the ravages of alcohol use and abuse.  We see them up close and personal in our patients.

A scientific study published in 2008, however, lends support to a middle-aged individual’s decision to start consuming moderate amounts of alcohol on a regular basis.  It even provides a positive defense if a doctor recommends it to carefully selected patients.

This research, by the way, was supported by a grant from the National Heart, Lung, and Blood Institute, not the wine/alcohol industry.

Methodology

Researchers at the Medical University of South Carolina examined data on 15,637 participants in the Atherosclerosis Risk in Communities (ARIC) study over a 10-year period.  These men and women were 45 to 64 years old at the time of enrollment, living in four communities across the U.S.  Of the participants, 27% were black, 73% nonblack, 28% were smokers, and 80% of them had high blood pressure, high cholesterol, or diabetes.

Out of 15,637 participants at the time of enrollment, 7,359 indicated that they didn’t drink alcohol.  At baseline, these 7,359 had no cardiovascular disease except for some with high blood pressure.    Subsequent interviews with them found that six percent of the nondrinkers – 442 people – decided independently to become moderate alcohol drinkers.  Or at least they identified themselves as such.

“Moderate” intake was defined as 1-14 drinks per week for men, and 1-7 drinks a week for women.  Incidentally, 0.4% of the initial non-drinking cohort – 21 people – became self-identified heavy drinkers.

93.6% of the 7,359 non-drinkers said that they continued to be non-drinkers.  These 6,917 people are the “persistent nondrinkers.”

Type of alcohol consumed was also surveyed and broken down into 1) wine-only drinkers, or 2) mixed drinkers: beer, liquor, wine.

Researchers then monitored health outcomes for an average of 4 years, comparing the “new moderate drinkers” with the “persistent nondrinkers.”

Results

  •  Over 4 years, 6.9% of the new moderate drinkers suffered a cardiovascular event, defined as a heart attack, stroke, a coronary heart disease procedure (e.g, angioplasty), or death from cardiovascular disease.
  • Over 4 years, 10% of the persistent nondrinkers suffered a cardiovascular event.
  • The new moderate drinkers were 38% less likely than persistent nondrinkers to suffer a new cardiovascular event (P = 0.008, which is a very strong association).  The difference persisted even after adjustment for demographic and cardiovascular risk factors.
  • There was no difference in all-cause mortality (death rate) between the new moderate drinkers and the persistent nondrinkers.
  • New  drinkers had modest but statistically significant improvements in HDL and LDL cholesterol and mean blood pressure compared with persistent nondrinkers.
  • 133 new moderate drinkers consumed only wine
  • 234 new moderate drinkers consumed mixed types of alcohol
  • Wine-only drinkers were 68% less likely than nondrinkers to suffer a cardiovascular event.
  • “Consumers of moderate amounts of beer/liquor/mixed (which includes some wine) tended to also be less likely to have had a subsequent cardiovascular event than nondrinkers…but the difference was not significant.”

A Few Study Limitations

  • Four years is a relatively brief follow-up, especially for cancer outcomes.  Alcohol consumption is associated with certain types of cancer.
  • If moderate alcohol consumption indeed lowers death rates as suggested by several other studies, this study may not have lasted long enough to see it.
  • The alcohol data depended on self-reports.

Take-Home Points

The study authors cite four other studies that support a slight advantage to wine over other alcohol types.  It’s a mystery to me why they fail to stress the apparent superiority of wine in the current study.  Several other studies that found improved longevity or cardiovascular outcomes in low-to-moderate drinkers suggest that the type of alcohol does not matter.  Perhaps “the jury is still out.”  In the study at hand, however, it is clear that the reduced cardiovascular disease rate in new moderate drinkers is associated with wine.

In all fairness, other studies show no beneficial health or longevity benefit to alcohol consumption.  But at this point, the majority of published studies support a beneficial effect.

Wine is a component of the traditional healthy Mediterranean diet.  The Mediterranean diet is associated with prolonged life span and reduced cardiovascular disease.  This study strongly suggests that wine is one of the health-promoting components of the Mediterranean diet.

Starting a judicious wine habit in middle age is relatively safe for selected people and may, in fact, improve cardiovascular health, if not longevity.

Now the question is, red or white.  Or grape juice?

Steve Parker, M.D.

Reference:  King, Dana E., et al.  Adopting Moderate Alchohol Consumption in Middle Age: Subsequent Cardiovascular Events.  American Journal of Medicine, 121 (2008): 201-206.

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February 24, 2010 · 5:41 AM

Recipe: Arizona’s Baked Cheesecake (low-carb)

My daughter, Arizona, enjoys baking.  I’m nudging her into low-carb baking since I miss my sweets.  I’m still low-carbing, so I can’t eat a lot of what she bakes.  

Arizona is used to the commercial cheesecakes based on a pre-mixed box: you mix then refrigerate.  The one below is more work, but I think well worth the effort.  We had fun making this together. 

Arizona’s Low-Carb Baked Cheesecake    

Ingredients for crust:

Ground nuts (pecan, walnut, or almond), 1.5 cups (226 g)

Butter, melted, 4 tbsp (10 g)

Cinnamon, ground, 1/2 tsp (2g)

Egg white, one (33 g)

Splenda No Calorie Sweetener, Granulated, 1 tbsp (optional)

Ingredients for filling:

Cream cheese, 24 oz (675 g)

Sour cream, 1 cup (230 g)

Eggs, 4 large (50 g each)

Splenda No Calorie Sweetener, Granulated, 1 cup (28 g  I think)

Lemon juice from 1 lemon (47 g)

Vanilla extract, 2 tsp (4 g)

Preparation

Have the following ingedients at room temperature before you start: eggs, cream cheese, sour cream.

Preheat oven to 350.

Crust first: Put ground pecans, 4 tbsp melted butter (fine to microwave briefly), cinnamon, 1 tbsp Splenda (granulated), and egg white in bowl, then blend all.  Spread onto bottom of greased (with melted butter 1.5 tbsp) 9″ springform pan. Cover with plastic wrap to aid spreading evenly.  Bake in 350 degree oven for 10-15 minutes then remove.  Then reduce heat to 325.

Filling: Use a mixer on low to medium setting to beat the cream cheese until fluffy.  Blend in the Splenda incrementally, a little at a time, beating until creamy.  Then mix in the lemon juice and vanilla extract.  Gently mix in one egg at a time and beat on low speed after each egg.  Mix in the sour cream last.  Pour cream cheese mixture into the crusted springorm pan.  Place on the top rack in the 325 degree preheated oven for 50-60 minutes. On the rack below that, place a pie pan full of water.  [The water pan and gentle handling of the eggs help prevent cracking of the finalproduct.]  When time is up, turn off the oven and open the oven door but leave the cake in the oven to cool slowly.  After an hour, remove from oven.  After it cools to room temperature, put it in the refrigerator to age for 24 hours.

NOTES:

  • The filling has one cup of Splenda, which I estimate is one ounce (28 g). This has 96 calories, which I assume is mostly from maltodextrin rather than sucralose.
  • Many cooks just use a glass pie pan instead of the springform pan. The volume of this recipe is likely too much for a 9″ pie pan, so you could reduce the amounts; or make a larger pie or two smaller ones.
  • Some cooks don’t bother to bake the crust first.
  • Reduce the carb count even further by omitting the crust. 
  • For higher fiber, substitute flaxmeal for about  a third or 1/2 of the ground nuts. 
  • The Splenda in this recipe is not the same as in the individual serving packets.

Nutritional Analysis (thanks to NutritionData.com):

Recipe makes 12 servings.  Each serving has 444 calories (382 calories from fat), 8 g of carbohydrate, 2 g of fiber, 6 g of digestible carbohydrate.

Steve Parker, M.D.

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February 19, 2010 · 2:00 AM

Drug Review: Insulin

I was going to do a brief review of insulin therapy here, but I found a good one at About.com.  So why re-invent the wheel?

If interested, click through to the article by Michael Bihari, M.D.: Insulin for type 2 diabetes: What you need to know.

Steve Parker, M.D.

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February 17, 2010 · 2:00 AM

Brief Drug Review: Pramlintide

Pramlintide is sold in the U.S. as Symlin.  It’s only used in patients already taking meal-time rapid-acting insulin.  Pramlintide may have a role in treatment of overweight type 2 diabetics inadequately controlled on insulin, or who experience weight gain refractory to diet and exercise.

Remember that drug names vary by country and manufacturer.  This is a brief review; consult your physician or pharmacist for details.

Class:  amylin analogue

How does it work?

Amylin is a hormone stored in pancreas beta cells and is secreted along with insulin.  It affects glucose levels by several mechanisms, including slowed stomach emptying, regulation of glucagon secretion after meals, and by reducing food intake.  Amylin and insulin levels rise and fall together,working jointly to control blood sugar levels.   Amylin is relatively deficient in many cases of type 2 diabetes.

Pramlintide is a chemical similar in structure to amylin, and causes similar effects.  It allows insulin therapy to more easily match the body’s needs in the after-meal period.  It also promotes modest weight loss in obese patients. 

Pramlintide therapy reduces hemoglobin A1c by 0.5 to 1% (absolute decrease, not relative).

We have no data on long-term outcomes with this drug.

Uses

Pramlintide is FDA-approved for use in both type 1 diabetes and insulin-requiring type 2 diabetes.  It can be used with metformin and/or sulfonylureas as long as insulin is also part of the regimen.  It’s probably best not to use it with exenatide and other GLP-1-based therapies.

Dosing

It’s injected subcutaneously just before meals, starting with 60 mcg in type 2 diabetics.  To avoid hypoglycemia at the start of treatment, the pre-meal rapid-acting injected insulin dose is usually reduced by half.  Pramlintide should only be administered before meals that contain at least 30 grams of carbohydrate or 250 calories.  The maximum dose is 120 mcg with each meal. 

Side effects

Nausea is the most common side effect but clears up in a few weeks.  Pramlintide by itself does not cause hypoglycemia, but since it is always used with injectable insulin, hypoglycemia may occur—usually within three hours.

Don’t use if you have . . .

. . . gastroparesis or hypoglycemia unawareness.

Steve Parker, M.D.

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February 15, 2010 · 2:00 AM

Drug Review: Colesevelam

Colesevelam is used primarily to reduce elevated levels of LDL cholesterol.  It’s sold in the U.S. as WelChol.  Remember that drug names vary by country and manufacturer.  This is a brief review; consult your physician or pharmacist for details.

Class:  Bile acid sequestrant

How does it work?  Unclear

Uses

Colesevelam is FDA-approved for treatment of type 2 diabetes in conjunction with insulin or diabetic pills.

Dosing

Three tablets twice daily with meals, or six tablets once daily with a meal.

Side effects

Constipation in one of every 10 users.

Do not use if you have . . .

. . . serum triglycerides over 500 mg/dl, or have gastroparesis, other gastrointestinal motility disorders, risk factors for bowel obstruction, or recent major gastrointestinal procedures.

Steve Parker, M.D.

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February 13, 2010 · 2:00 AM

Drug Review: Dipeptidyl-Peptidase-4 Inhibitors (sitagliptin, saxagliptin, linagliptin, alogliptin)

The four dipeptidyl-peptidase-4 inhibitors available in the U.S. are sitagliptin (sold as Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), and alogliptin (Nesina). Vildagliptin is available in other countries.

Remember that drug names vary by country and manufacturer.  This is a brief drug review; consult your physician or pharmacist for details.

How do they work?

DPP-4 inhibitors decrease both fasting and after-meal blood sugar levels primarily by increasing insulin release from pancreas beta cells.  How they do it is complicated.

First off, you need to know that two gastrointestinal hormones levels—glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide—increase in response to a meal.  These hormones increase insulin secretion by pancreas beta cells, suppress glucagon secretion from pancreas alpha cells after meals, help suppress glucose production by the liver, and improve glucose uptake by tissues outside the liver.  GLP-1 also slows emptying by the stomach and reduces food intake.  All this tends to lower glucose levels after meals.

Did I mention it was complicated?

If we could make these gut hormones hang around longer, their glucose-lowering action would be enhanced.  How can we make them hang around and work longer?  Easy: suppress the enzyme that degrades them: dipeptidyl-peptidase-4.  That’s what DPP-4 inhibitors do.

The small intestine hormone GLP-1 is a major player in normal carbohydrate metabolism.  GLP-1 levels, by the way, are decreased in type 2 diabetes.

For the DPP-4 inhibitors, we have no data on long-term safety, mortality, or diabetic complications.

Uses

Sitagliptin is FDA-approved as initial drug therapy for the treatment of type 2 diabetes, and as a second agent in those who do not respond to a single agent, such as metformin, a sulfonylurea, or a thiazolidinedione.  It can also be used as a third agent when dual therapy with a sulfonylurea and metformin doesn’t provide adequate blood sugar control.

Saxagliptin, linagliptin, and alogliptin are FDA-approved as initial drug therapy for the treatment of type 2 diabetes (in adults) or as add-on drugs for those who do not respond to a single drug, such as metformin, a sulfonylurea, or a thiazolidinedione.  In case you’re wondering, you wouldn’t use several of the DPP-4 inhibitors at the same time.  In the summer of 2012, the FDA approved linagliptin as an add-on drug for type 2 diabetics already taking insulin.  Linagliptin and alogliptin haven’t been studied in nursing or pregnant women; I’m not sure about sitagliptin and saxagliptin in those settings.  Alogliptin is approved for combined use with metformin, pioglitazone, insulin, and perhaps sulfonylureas.

Dosing

The DPP-4 inhibitors are given by mouth.   The usual dose of sitagliptin is 100 mg once daily, with reduction to 50 mg for moderate to severe kidney impairment and 25 mg for severe kidney impairment.  The usual dose of saxagliptin is 2.5 or 5 mg once daily, with the 2.5 mg dose recommended for patients with moderate to severe kidney impairment.  Linagliptin’s dose is 5 mg daily, regardless of liver or kidney funtion.  The alogliptin dose is 25 mg daily, with lower doses for those with kidney impairment.

Side Effects

Generally well-tolerated.  No risk of hypoglycemia when used as the sole diabetes drug.  They do not cause weight gain.  Sitagliptin, linagliptin, and alogliptin might cause pancreatitis.  Alogliptin may cause liver disease or abnormal liver function blood tests. Saxagliptin and alogliptin may increase the risk of heart failure, particularly in those with pre-existing heart or kidney disease.

Don’t use if you have . . .

. . . moderate or severe kidney impairment (sitagliptin) or severe kidney impairment (saxagliptin).
Use sitagliptin or alogliptin with caution and careful monitoring if you have a history of pancreatitis.

Steve Parker, M.D.

Updated April 7, 2016

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February 10, 2010 · 2:00 AM

Another Sacred Cow Slaughtered: Fruits and Vegetables DON’T Prevent Cancer

We’ve been told by the authorities repetitively that eating plenty of fruits and vegetables will lower our risk of cancer.  However, a recent study in the American Journal of Clinical Nutrition says that ain’t so.

Fire up the grill—we’re havin’ steak tonight!

Researchers looked at data from over 450,000 participants (men and women over 50) in the National Institutes of Health—AARP Diet and Health Study.  Diet data was collected by self-administered questionnaire.  State-level cancer registries identified the cancers that developed during the average follow-up of seven years.

Their conclusions and selected comments:

Intake of fruit and vegetables was generally unrelated to total cancer incidence in this cohort.

However, on the basis of animal studies, human case control and cohort studies, and randomized controlled trials, there is likely no harm associated with the consumption of fruit and vegetables and their consumption may prevent cardiovascular disease.

Indeed, analyses in this cohort and in others that have investigated dietary patterns rich in fruit and vegetables have found reduced risks of colorectal cancer [three references cited] and mortality, including death from cardiovascular disease and all cancers [one reference was cited supporting reduced deaths from CVD and all cancers—a Mediterranean diet study].

As in all good science reports, the researchers compare and contrast their findings with similar published research.  They note that theirs is one of only four large cohort studies that have examined this issue.  Two of the other three (see references below) also found no association between total cancers and fruit and vegetable consumption.  The one that did find a beneficial linkage was the smallest of the four, so not as compelling.

Before this research was published, some experts suggested that adequate fruit and vegetable intake could prevent between 5 and 12% of cancers.

Eat your fruits and vegetables because they taste good, provide myriad nutrients, and may have some other healthful properties.  But not to lower overall cancer risk.  

Steve Parker, M.D.

References:

George, Stephanie, et al.   Fruit and vegetable intake and risk of cancer: a prospective cohort study.  American Journal of Clinical Nutrition, 89 (2009): 347-353. 

Hung, H.C., et al.  Fruit and vegetable intake and risk of major chronic disease.  Journal of the National Cancer Institute, 96 (2004): 1,577-1,584.

Takachi, R., et al.  Fruit and vegetable intake and risk of total cancer and cardiovascular disease [in Japan].  American Journal of Epidemiology, 167 (2008): 59-70.

Benetou, V., et al.  Vegetables and fruit in relation to cancer risk: evidence from the Greek EPIC Cohort Study.  Cancer Epidemiology, Biomarkers, and Prevention, 17 (2008): 387-392.

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February 9, 2010 · 2:00 AM

Drug Review: Sulfonylureas

sulfonylureas, meglitinide, and repaglinide for type 2 diabetesSulfonylureas (SUs) in 2010 are still the most widely used drugs for treatment of type 2 diabetes.  At least six different SUs are in common usage in the U.S., including glipizide, glimiperide, and glyburide.  They are often prescribed for patients who do not respond adequately to lifestyle modification and are intolerant of metformin, the usual first-choice drug. 

Sulfonlylureas make the pancreas beta cells secrete more insulin into the bloodstream.  The other drugs that do this are the meglitinides; these two classes are sometimes lumped together as insulin secretagogues.  The sulfonylureas are less expensive. 

This is a brief review pertinent to type 2 diabetes only—consult your physician or pharmacist for details.  Remember that drug names vary by country and manufacturer.  

How do they work?

Sulfonylureas increase the pancreas’ production of insulin after a meal (second phase insulin secretion).  If the pancreas beta cells are no longer producing any insulin, SUs won’t work.  SUs decrease fasting blood sugar by about 20% and hemoglobin A1c by 1 or 2% (absolute, not relative).

[Metiglinides have about the same effectiveness as SUs.  Repaglinide and nateglinide  increase the pancreas’ output of insulin, working faster than sulfonylureas.  They don’t last as long as sulfonylureas, which may help avoid hypoglycemia.  These two “glinides” work mostly to reduce sugar levels after meals.]  

We don’t know if these SUs affect death rates. 

Uses

May be used alone or in combination with certain other diabetic drugs.  Since they have the same mechanism of action, sulfonylureas and meglitinides would not normally be used together.  In combination therapy, you want to use drug classes that work by different mechanisms. 

Dosing

SU dose depends on the particular one used.  Some are taken by mouth once daily, others twice.

Side effects

Hypoglycemia is the most severe adverse effect of the sulfonylureas.  The duration of hypoglycemia seen with SUs is often much longer than you would predict by how much drug is in the bloodstream.  Hypoglycemia is more common with the longer-acting drugs, such as glyburide and chlorpropamide.  There is some concern that sulfonylureas are linked to poorer outcomes after a heart attack.  SUs occasionally cause nausea, skin reactions, and elevations of liver function tests. 

Weight gain is common. 

When used with insulin or thiazolidinediones, these sulfonylurea adverse effects are more likely to appear: weight gain, fluid retention, congestive heart failure.

Precautions . . .

Consult your personal physician or pharmacist.

Steve Parker

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February 8, 2010 · 2:00 AM

You Know About Insulin. And Now, the REST of the Story . . .

When we digest carbohydrates, blood sugar rises.  If it goes too high it causes problems.  Everybody knows that insulin lowers blood sugar levels, right?  Less well-known is that regulation of blood sugar is the result of complex interactions of multiple hormones, not just insulin.

[As is my habit, I will use “sugar” and “glucose” interchangeably in this post.] 

Allow me to review the main hormones involved in blood glucose regulation:

1. Insulin is made and stored in pancreas beta cells.  As a meal is digested, blood sugar rises; the pancreas releases insulin to bring blood sugar back down by driving it into cells.

2. Amylin is also made and stored in pancreas beta cells and works to reduce blood sugar levels.  Blood levels of amylin rise and fall in concert with insulin levels.  Amylin slows emptying of the stomach, reduces food consumption, and regulates another hormone—glucagon—after meals.

3. Glucagon is from pancreas alpha cells.  It works to raise blood sugar by promoting the liver’s breakdown of glycogen into glucose, and by promoting the liver’s manufacture of new glucose molecules.

4. Glucagon-like peptide -1 (GLP-1) is produced in small intestine cells and it’s main action is to promote insulin secretion by the pancreas beta cells after absorption of food, which lowers blood sugar levels.  GLP-1 (like amylin) also inhibits emptying of the stomach, inhibits glucagon release, and inhibits appetite, all of which would tend to keep a lid on blood sugar levels. 

5. Gastric inhibitory polypeptide (GIP) promotes secretion of insulin following absorption of food.  GIP is also known as glucose-dependent insulinotropic polypeptide.

You can see that some hormonal mechanisms raise glucose levels; others lower glucose levels.  Homeostasis is all about reaching a happy medium between the two, without wild swings one way or the other.  In healthy people, eating food leads to release of gastrointestinal peptides (GLP-1 and GIP), insulin, and amylin.  The interaction among them keeps blood sugar levels in a fairly level low range.  In diabetes, one or more malfunctions in the system leads to abnormally high blood sugars.

The good news is that scientists have used this knowledge to devise new, effective treatments for diabetes.  Examples are GLP-1 analogues and DPP-4 inhibitors.

Steve Parker, M.D.

PS:   In lab animals, GLP-1 stimulates formation of new pancreas beta cells, so it hold promise in halting the progressive beta cell failure characteristic of type 2 diabetes.

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