The first low-carbohydrate diet dates all the way back to the mid- nineteenth century.
In 1863, William Banting (1796, 1878), an English undertaker, published the pamphlet Letter on Corpulence, Addressed to the Public,1 which is often considered the world’s first diet book.
Weighing 202 pounds (91.6 kilograms), Banting had tried unsuccessfully to lose weight by eating less and exercising more.
But, just like today’s dieters, he was unsuccessful.
On the advice of his surgeon, Banting tried a new approach.
When he strenuously avoided the bread, milk, beer, sweets, and potatoes that had previously made up a large portion of his diet, he lost weight and
successfully kept it off.
For most of the next century, diets low in refined carbohydrates were accepted as the standard treatment for obesity.
For all the success of low-carb diets, the carbohydrate-insulin hypothesis remains incomplete.
While refined carbohydrates are certainly an important contributor to hyperinsulinemia, they are not the only contributor.
There are many other significant influences.
One of the most important is insulin resistance.
As we’ve seen, insulin acts like a key to open a gate for glucose to enter the cell.
But sometimes, in a state of insulin resistance, the usual levels of insulin are not sufficient and glucose piles up in the bloodstream because it cannot get into the cells.
To compensate, the body produces more insulin to overcome this resistance and force the blood glucose inside.
The effect is to restore normal blood glucose levels but at a cost of persistent hyperinsulinemia.
We care about insulin resistance so much because this compensatory hyperinsulinemia drives overall weight gain.
But here’s the million-dollar question: How does this insulin resistance develop in the first place?
Figure 5.4.
Hormonal obesity II: Insulin resistance causes hyperinsulinemia
INSULIN RESISTANCE: THE OVERFLOW PHENOMENON
OBESITY TYPICALLY PRECEDES the diagnosis of type 2 diabetes by a decade or more.
Obese but otherwise normal (nondiabetic) patients have substantially increased insulin resistance compared to lean patients.
Fasting insulin, a measure of the amount of insulin in the blood that reflects underlying insulin resistance, increases through the spectrum of obesity, prediabetes, and then type 2 diabetes (see Figure 6.1).1 This suggests that obesity could be the root cause of increased insulin resistance.
But despite spending millions of dollars and doing decades of intensive research on possible hormonal mediators between obesity and insulin resistance, no causal link could be made.
After all, if obesity causes insulin resistance, how could type 2 diabetes develop in normal-weight patients?
And why do so many obese people not develop type 2 diabetes?
Figure 6.1. Changes in insulin as obesity progresses toward type 2 diabetes2
The converse, the idea that insulin resistance causes obesity, is implausible since obesity typically predates insulin resistance. The only remaining possibility is that some X factor is the underlying cause of both obesity and insulin resistance. The connection, as we shall see, is too much insulin. The X factor is hyperinsulinemia. Figure 6.2. Hyperinsulinemia: The X factor causing both obesity and insulin resistance
RESISTANCE AS A PROTECTIVE MECHANISM
THE HUMAN BODY follows the fundamental biological principle of homeostasis. If things change too far in one direction, the body reacts by changing in the opposite direction to try to return to its original state. For instance, if we become very cold, the body adapts by shivering to generate more body heat. If we become very hot, the body sweats to cool
itself.
Adaptability is a prerequisite for survival and generally holds true for all biological systems.
Resistance is simply another word for this adaptability.
The body resists change out of its comfort range by adapting to it.
Exposure creates resistance.
Excessively high and prolonged levels of anything provoke resistance by the body.
This is a normal phenomenon.
Consider the following.
Laura was only 25 when she was diagnosed with an insulinoma,3 a rare tumor that secretes abnormally large amounts of insulin in the absence of any other significant disease.
This condition forces glucose into the cells, causing recurrent episodes of hypoglycemia, or low blood glucose.
As a result, Laura was constantly hungry and, as insulin is a major driver of obesity, she soon began to gain weight.4 Her glucose levels were too low to maintain adequate brain function, which led to problems with concentration and coordination.
One night, as she was driving, she lost control of her feet and narrowly avoided an accident.
She had experienced a seizure related to hypoglycemia.
Laura’s symptoms may appear severe, but they would have been much worse if her body had not taken protective steps.
As her insulin levels increased, insulin resistance increased in lock step.
Without insulin resistance, her high insulin levels would rapidly have led to very, very low blood glucose and death.
Since the body doesn’t want to die (and neither do we), it protects itself by developing insulin resistance, demonstrating homeostasis.
The resistance develops naturally to shield against the unusually high insulin levels.
Insulin causes insulin resistance.
Fortunately, the correct diagnosis was soon made and she had corrective surgery.
With the tumor removed, insulin resistance dramatically reverses, as do associated conditions.5 Reversing the high insulin levels also reverses insulin resistance.
Exposure creates resistance.
Removing the stimulus also removes the resistance.
This rare disease gives us a vital clue in understanding the cause of insulin resistance.
HOW RESISTANCE WORKS
HOMEOSTASIS IS SO fundamental to survival that the body will find many different ways to develop resistance. Survival depends on it. Let’s take a
look at a few different resistance mechanisms.
Noise resistance THE VERY FIRST time you yell at somebody, they jump back and pay attention.
Incessant yelling, though, soon negates its effect.
In essence, they have developed resistance.
The boy who cried wolf soon learned that the villagers became resistant to its effect.
Exposure creates resistance.
Removing the stimulus removes the resistance.
What happens when the yelling stops?
If the boy stopped crying wolf for a month, the villagers would start listening again.
This prolonged silence reverses the resistance.
The next time he cries wolf, it will have an immediate effect.
Have you ever watched a baby sleep in a crowded, noisy airport?
The ambient noise is very loud, but constant, and the baby sleeps soundly, as it has become resistant to the noise.
That same baby sleeping in a quiet house might awaken at the slightest creak of the floorboards.
This is every parent’s worst nightmare.
Even though it is not loud, the noise is very noticeable, as the baby has no resistance.
The baby immediately wakes up crying, to the parents’ dismay.
Antibiotic resistance WHEN NEW ANTIBIOTICS are introduced, they eradicate virtually all the bacteria they’re designed to kill.
Over time, most bacteria develop the ability to survive high doses of these antibiotics, which turns them into drug-resistant “superbugs.” As the superbugs multiply and become more prevalent, the antibiotic loses its effectiveness.
This is a large and growing problem in many urban hospitals worldwide.
Every single antibiotic has lost effectiveness due to resistance.
Antibiotic resistance is not a new phenomenon.
Scottish biologist Alexander Fleming discovered penicillin in 1928 and mass production began in 1942, with funds from the U.S. and British governments, for use during World War II.
In his 1945 Nobel lecture, “Penicillin,” Dr.
Fleming correctly predicted the emergence of resistance two years before the first cases were reported.
How did Dr.
Fleming so confidently predict this development?
He understood the fundamental biological principle of homeostasis.
biological system that becomes disturbed tries to go back to its original state.
As we use an antibiotic more and more, organisms resistant to it are naturally selected to survive and reproduce.
Eventually, these resistant organisms dominate, and the antibiotic becomes useless.
Persistent, high-level use of antibiotics causes antibiotic resistance.
Exposure creates resistance.
Removing the stimulus removes the resistance.
Unfortunately, the knee-jerk reaction of many doctors is just the opposite: to prescribe more antibiotics to overcome the resistance, which backfires and creates even more resistance.
Preventing antibiotic resistance means severely restricting their use.
This has led many hospitals to develop stewardship programs to preserve the effect of the most powerful antibiotics by using them only in life-threatening situations.
Lowering the exposure of bacteria to the antibiotic creates less resistance, which can save lives.
Viral resistance RESISTANCE TO VIRUSES such as diphtheria, measles, chicken pox, or polio develops from the viral infection itself. Before the development of vaccines, it was popular to hold “measles parties” or “pox parties,” where unaffected children would play with a child who was actively infected with the virus in order to deliberately expose them. Not the funnest of parties, but having measles once protects a child for life.
Exposure creates resistance.
Vaccines work on this exact principle.
Edward Jenner, a young doctor working in rural England, heard the common tale of milkmaids developing resistance to the fatal smallpox virus because they had contracted the milder cowpox virus.
In 1796, he deliberately infected a young boy with cowpox and observed how he was subsequently protected from smallpox, a similar virus.
By being inoculated with a dead or weakened virus, we build up immunity without actually causing the full disease.
In other words, viruses cause viral resistance.
Drug resistance WHEN A DRUG such as cocaine is taken for the first time, there is an intense reaction, the “high.” With each subsequent use of the drug, this high
becomes progressively less intense.
Drug abusers may start to take larger doses to achieve the same high.
Through repeated and prolonged exposure, the body develops resistance to the drug’s effects, a condition called tolerance.
People can build up resistance to many different types of drugs, including narcotics, marijuana, nicotine, caffeine, alcohol, benzodiazepines (tranquilizers), and nitroglycerin.
Again, exposure creates resistance.
Removing the stimulus removes the resistance.
In order to restore sensitivity to the medication, it is necessary to have a period of low drug use.
If you stop drinking alcohol for a year, the first drink afterwards will have its full effect again.
What do all of these examples have in common?
In the case of noise, stimulus fatigue is the mechanism of resistance.
The human ear responds to changes rather than the absolute noise levels.
In the case of antibiotics, the natural selection of resistant organisms is the mechanism.
The bacteria that adapt to the drugs are the ones that survive and multiply.
In the case of viruses, the development of antibodies is the mechanism of resistance.
In the case of drug resistance, or desensitization, a decrease in the number of cell receptors is the mechanism.
While the mechanism in each of these cases may differ, the end result is always the same.
That’s the point.
Homeostasis is so fundamental to survival that biological systems always find a way to compensate.
Exposure creates resistance.
And what does this tell us about insulin resistance?
Insulin causes insulin resistance.