Reactive Hypoglycemia--An Experiment?

Reactive hypoglycemia is a condition which is characterized by unusually low blood sugar that occurs one to four hours following a meal. The symptoms are the typical ones for low blood sugar--shakiness, light-headedness, weakness, confusion, anxiety, depression, hunger, pounding heartbeat and sweating.

Progressive development of insulin resistance is often the cause of reactive hypoglycemia. When the pancreas becomes insulin resistant, it is unable to release the proper amount of insulin in response to the stimulus of carbohydrates and proteins. Sometimes the pancreas will overshoot its estimate of the amount of insulin needed to store ingested carbs and proteins. The excess insulin produces hypoglycemia and its associated symptoms. A more detailed explanation of the process can be found in my original post called Reactive Hypoglycemia. (Be sure to read the comments section.)

Reactive hypoglycemia can be diagnosed with a glucose tolerance test. If the test is positive, the patient will typically be advised to eat every 2-3 hours to relieve the symptoms. Although freqent ingestion of food does keep blood sugar from falling too low, it will not provide a long-term resolution of the underlying problem.

One of my readers, Alex, who blogs at Low Carb New England, entered the discussion on the original post with the story of how he has been dealing with reactive hypoglycemia since he was a teenager. Over the years he has systematically tried many different approaches and has taken careful note of what result each personal experiment has produced. To summarize briefly, Alex initially tried eating less sugar and eating frequent meals, but eventually he gained nearly 100 pounds. Next he investigated low-carb eating. By using the Atkins diet, he lost weight and many of his symptoms improved considerably. In an effort to reduce the remaining symptoms, Alex tried eliminating artificial sweeteners and caffeine, and this helped somewhat. He also tried extremely low-carb and even no-carb eating, which didn't help.

Eventually Alex realized that he needed to limit his protein intake to the amount recommended by Drs. Mike and Mary Dan Eades in The Protein Power Lifeplan. (Remember, eating protein also causes insulin release, and thus can contribute to insulin resistance.) Again, his symptoms improved, but were not entirely gone. The final piece of the puzzle seemed to arrive when he read my first comment under the Reactive Hypoglycemia post and decided to try waiting 5-6 hours between meals to allow his insulin levels to come back to baseline and give his body a chance to re-establish a normal level of insulin sensitivity.

After a month of using this three-legged stool approach (low-carb/moderate-protein/5-6 hours between meals) to dealing with reactive hypoglycemia, Alex has finally experienced relief from the symptoms of reactive hypoglycemia. He gives a much more complete version of the story on his blog in a post called "I'm back!" (For those who don't have access to The Protein Power Lifeplan, another method of calculating one's daily protein need can be found here.)

And now I've reached the main point of this post. If the three-legged stool approach (illustrated in the picture above) has worked for Alex, would it work for anybody else out there who has reactive hypoglycemia? Each leg of the stool is designed to reduce insulin resistance and, one hopes, to restore some degree of insulin sensitivity in muscle, liver, brain and pancreas. If any of my readers is interested in trying to follow this plan for a few weeks or a month, I would be very interested in getting your feedback. If this method actually works, it's possible that a series of anecdotal experiences could convince a low-carb researcher to design a study to see if using the three legs of the stool is an improvement over frequent feeding as a way to treat reactive hypoglycemia. If these informal personal experiments don't work, that's also important information. It's possible that there are other pieces of the puzzle that aren't obvious, or perhaps that the mechanisms of reactive hypoglycemia are different from one individual to the next. If you decide to try this, please be very careful, and please don't do anything that would put your health in danger. That said, if you try it and you have observations you would like to share, please put them into the comments and we shall see where this might lead.

Does Exercise Produce Weight Loss?

Common wisdom suggests that exercising will cause a person to lose weight. Superficially this makes sense. A 150 pound person at rest will use about 60 calories an hour. If this person jogs at 5 mph for an hour, he or she will use an additional 540 calories per hour. Because a pound of fat represents 3500 calories, a faithful jogger should lose a pound every 6.5 days. However, as exercisers can attest, this does not seem to work out in the real world. Why would that be?

1. Vigorous exercise can produce physical stress. Stress in turn causes the release of cortisol, which stimulates carbohydrate synthesis (gluconeogenesis) for quick energy. Gluconeogenesis produces an elevation in blood glucose which then stimulates insulin release. If this sequence happens repeatedly during days and months of an ongoing exercise program, it becomes more and more likely that the chronically physically-stressed person will start gaining weight.

2. Vigorous exercise can cause fatigue. The person who exercises may be expending more calories during his workout, but if he becomes exhausted by his efforts, he may compensate by conserving energy (being more sedentary or even napping) during his other daily activities.

3. Exercise in the form of resistance training may cause the exerciser to overestimate how much energy his body consumes post-exercise. A 2006 article by Ralph La Forge states that, for the non-athlete, the excess post-workout oxygen consumption is less than 100 calories per day.

4. Vigorous exercise may cause the body's homeostatis mechanisms for fat storage to overcompensate. Exercise activates the enzyme lipoprotein lipase (LPL) in muscle tissue, allowing muscles to take up fatty acids as fuel. Once the exercise stops, the activity of LPL in muscle decreases and the activity of LPL in fat tissue increases. Calories will be pulled into fat cells and stored there to prepare for the next round of exercise. Although an individual's appetite might be depressed immediately after a workout session, later in the day there may be a more-than-compensatory drive to eat to replace lost fat stores.

5. Exercise plus frequent meals can cause weight gain. Eating frequently prevents both leptin levels and insulin levels from returning to baseline. As earlier posts have discussed, persistently elevated leptin levels can hinder satiety signals and cause excess consumption of calories. Elevated insulin levels will produce storage of those excess calories as muscle and as fat. Underweight bodybuilders use exercise plus frequent meals as a method to gain weight. However, without careful monitoring, overweight body builders can also gain weight on this regimen.


Exercise is a good thing. It can strengthen the heart and lungs, elevate mood, create a better physique and improve stamina. But for a number of very good reasons, exercise by itself does not necessarily produce weight loss, and if the circumstances are right, it may even result in weight gain.

Transgenerational Obesity

Americans are getting fatter. According to a recent article in Obesity, by 2030, 86.3% of American adults will be overweight. The average adult BMI (Body Mass Index) is now 28, which is in the overweight range. By 2030 the average adult BMI is predicted to be 31.4, which is well into the obese range.

One factor that contributes to this phenomenon is the fact that fat mothers produce fatter offspring. In some senses this is not surprising. If there are genes that predispose to obesity, those will be passed down from parents to children. If there are lifestyle choices that contribute to an increased BMI, children will learn those by example from their parents.

What is not expected is the presence of a multiplier effect in generational obesity. In both rats and mice that are susceptible to obesity, a fat rodent mother gives birth to offspring which will become fatter than she was, and they, in turn, give birth to pups which grow up to be fatter than they were. The same phenomenon happens in humans. It is harder to observe in humans because it takes decades to progress from mother to daughter to granddaughter, while rodents can easily produce several generations in a few months or years. In rodents it is also much easier to control for genetic and environmental factors.

In both rodents and humans, the cause of the multiplier effect has not been established. It could result from a relatively high blood sugar in the mother causing the fetus to produce extra insulin-secreting cells in the developing pancreas. This could lead to increased insulin resistance and subsequent obesity as the child matures into an adult. It is possible that the high levels of leptin in an obese mother could cause her fetus to become leptin resistant. Methylation studies described in the rat reference above, suggest that maternal obesity may produce long-term modifications in the regulatory regions of obesity-related genes in her offspring. These modifications would be epigenetic, not mutational modifications. In other words, the actual DNA coding sequence is not changed, but while the fetus is in the womb, the 3-dimensional conformation of its DNA is modified, causing obesity-related genes to be more or less easily expressed even after the baby is born.

There is also evidence that the cycle of increasing transgenerational obesity can be broken. In 2006 an article in Pediatrics described a group of 113 obese mothers who had undergone biliopanceatic diversion (BPD) surgery for weight loss. This group of mothers had 45 childen before the surgery and 172 after the surgery. All were followed for 2-18 years. Comparing the 172 children born after BPD surgery with the 45 born before it, the prevalence of obesity decreased by 52% and severe obesity decreased by 45%. The effect was gender-specific, with the prevalence of overweight in the daughters decreasing from 56% to 42% and in the sons decreasing from 50% to 25%.

Apparently obesity does not have consequences just for the obese mother, but its effects extend into the lives of her children as well.

I'm Back!

Thanks to all the people who left excellent comments on my archived posts. Each one of your observations has been very much appreciated. As I've realized during this month of real-life challenges, the most important information about the science of low-carbing can already be found on the previous posts in this blog.

Woodswalker tactfully pointed out that the subject of low-carbing may not be inexhaustible. She's right. There are lots of interesting aspects of low-carb that we will address in the future, but the basics involve a few well-known principles of biochemistry and physiology. Medical students have learned about these for years, but once they graduate into the world of practicing medicine, they seem to absorb the dogma about low-fat/low-cholesterol/low-calories and forget about their original training.

So, a word to the wise. Go back often. Review frequently. Remind yourself of the many scientific reasons we have for low-carbing. Most of the mainstream medical and nutritional community hasn't caught up to us yet. Someday it will. In the meantime, let's do all we can to keep ourselves on the path to good health that low-carbing provides.