CONCEPTUALLY, EXERCISE SEEMS like an ideal way to burn off the excess ingested calories of glucose.
Standard recommendations are to exercise thirty minutes per day, five days per week, for a total of 150 minutes per week.
At a modest pace, the result is an extra energy expenditure of 150 to 200 kcal per day, or 700 to 1000 kcal per week.
These amounts pale in comparison to a total energy intake of 14,000 calories per week.
In studies, all exercise programs produce substantially fewer benefits than expected.
There are two main reasons: First, exercise is known to stimulate appetite.
This tendency to eat more after exercise reduces expected weight loss.
Second, a formal exercise program tends to decrease non-exercise activity.
For example, if you have been doing hard physical labor all day, you are unlikely to come home and run 10 kilometers for fun.
On the other hand, if you’ve been sitting in front of the computer all day, that 10-kilometer run might sound pretty good.
These compensation effects are a well-described phenomenon in exercise studies.
As you increase exercise intensity or duration, you may find that you eat more or do fewer other non-exercise activities.
These compensations directly reduce the beneficial effects of the exercise program.
In the end, the main problem is that type 2 diabetes is not caused by lack of exercise.
The underlying problem is excessive dietary glucose and fructose causing hyperinsulinemia.
Exercise can only improve insulin resistance of the muscles.
It does not improve insulin resistance in the liver at all.
The fatty liver is the key to developing type 2 diabetes, and you cannot exercise your liver to health.
Reversing type 2 diabetes depends upon treating the root cause of the disease, which is dietary.
Imagine that you turn on your bathroom faucet full blast.
The sink starts to fill quickly, as the drain is small.
Widening the drain slightly is not the solution because it does not address the underlying problem.
The
obvious solution is to turn off the faucet. In type 2 diabetes, a diet full of refined carbohydrates and sugars is filling our bodies quickly with glucose and fructose. Widening the drain by exercising is minimally effective. The obvious solution is to turn off the faucet. And that leads us to the next section, how to effectively treat type 2 diabetes.
ELENA Elena, 63, was diagnosed with type 2 diabetes three years before I met her.
She also had a history of high blood pressure, high cholesterol, and obesity, the classic manifestations of metabolic syndrome, and evidence of fatty liver damage.
She was taking metformin for diabetes as well as medications to lower her blood pressure and cholesterol.
Her A1C was 6.2%.
When Elena joined the IDM program, we discussed low- carbohydrate, healthy-fat diets and she began a fasting regimen of 36 hours, three times per week.
Having long been told to eat frequent small meals throughout the day, fasting required a new mindset.
Within two weeks of starting the program, however, she was able to stop taking metformin.
A year after she began, she also stopped taking hypertension medication, as her blood pressure had normalized.
At our last meeting, her A1C was 5.2%, which is well within the normal range.
Today, Elena is considered nondiabetic.
The blood markers that indicate liver damage have completely normalized, meaning she no longer suffers from the fatty liver that causes chronic liver damage.
Furthermore, she has dropped 60 pounds, lost 24 cm off her waist, and completely reversed her metabolic syndrome.
RICHARD Richard, 76, was diagnosed with type 2 diabetes about a decade ago.
In addition, he had high blood pressure, stroke, peripheral vascular disease, an irregular heartbeat (atrial fibrillation), and chronic kidney disease.
Six years later he started on insulin (36 units daily), in addition to two oral hypoglycemics, yet his A1C remained elevated at 8.4%.
I met Richard just after he started taking insulin.
Following the IDM program, he began a low-carbohydrate, healthy-fat diet and a 24-hour fast three days per week.
Within a month he was off insulin, and after six months he was completely off all his oral medications, as well.
His urine albumin-to-creatinine ratio, a measure of diabetic kidney damage, dropped by two- thirds; he lost 13 pounds; and his waist size shrank by 12 cm.
Today, Richard’s A1C is 5.4% without medications, which classifies him as nondiabetic.
LESSONS FROM BARIATRIC SURGERY
AT 203 KILOGRAMS (448 pounds), Adrian was morbidly obese and suffered from type 2 diabetes.
Medically unfit to work due to all his associated illnesses, he lost his job in 2014.
He eventually chose to undertake weight-loss surgery, also called bariatric surgery, and within five weeks his diabetes had completely disappeared.1 Interestingly, this story of type 2 diabetes reversal is not the exception but a general rule after surgery.
How often have we heard type 2 diabetes called a chronic and progressive disease?
This idea has only become accepted as if it were fact because we have spent decades treating the symptom (hyperglycemia) rather than the cause.
Bariatric surgery proves that this notion is simply mistaken: type 2 diabetes is a reversible and preventable disease.
When we treat the cause (hyperinsulinemia), we can reverse diabetes.
Remember Dr.
Hallberg’s advice in chapter 12: ignore the guidelines.
What does bariatrics teach us about type 2 diabetes?
Quite a lot, it turns out.
EARLY ATTEMPTS AT WEIGHT-LOSS SURGERY
THE EARLIEST ATTEMPT to surgically cure obesity was to simply wire the jaws shut. The logic is obvious, if not very imaginative. This restrictive treatment, though, was ultimately unsuccessful. Patients could still drink
fluids, and enough high-calorie sugary drinks derailed weight loss.
The severe side effects were the limiting factor.
Dental infections and vomiting were insurmountable problems that often progressed over time.
More often than not, these intolerable problems led to reversing the surgery.2 In 1925, the Lancet noted that partial removal of the stomach for peptic ulcer disease often caused weight loss and complete resolution of sugar in the urine, now called diabetes.3 The smaller stomach volume effectively reduced the amount a person could eat.
Similar reports followed sporadically in the 1950s and 1960s.
This was an interesting finding, but the results often did not endure.
Over time, the smaller stomach could expand and patients could eat normally.
Weight would rebound, and with it, type 2 diabetes.
Jejunocolic bypass surgery THE MODERN AGE of bariatric surgery began in 1963 with the observation that removal of the small bowel, which absorbs most of the ingested nutrients, caused significant weight loss.
This led to the development of the jejunocolic bypass operation, in which bypassing the small bowel reroutes food from the stomach directly to the colon.
Success!
Patients lost significant amounts of weight using this malabsorptive approach.
But the side effects became immediately obvious.
Bypassing the small bowel did not allow the food to undergo the normal digestive process.
This was the point: if the food passed right through, it could not hang around long enough to be absorbed and eventually stored as body fat.
Instead, this food energy was immediately excreted in the stool.
However, this rapid passage also meant essential food nutrients were not absorbed properly or at all.
Patients developed night blindness from vitamin A deficiency, and osteoporosis from vitamin D deficiency.
Other common problems included severe diarrhea and bacterial overgrowth, liver failure, and kidney stones.
The continual diarrhea from the malabsorbed fat led to anal excoriations and hemorrhoids.
No fun.
This procedure, too, was soon abandoned.
Jejunoileal bypass THESE COMPLICATIONS FORCED the switch to the less-intensive jejunoileal bypass, in which most, but not all, of the small bowel is bypassed by
rerouting food from the stomach directly to a very short section of the small bowel.
Although absorption improved slightly, the complications were still unacceptable, rendering this surgery a historical footnote.
However, this incremental improvement allowed others to build upon these initial experiences.
In 1967, the seed of modern bariatric surgical procedures was planted with the use of restrictive and malabsorptive components combined.
This approach physically limited the intake of food by removing most of the stomach, and also reduced the absorption of whatever food made it through.
In addition to the partial bypass of the small bowel, part of the stomach was removed.
With the basic idea in place, further refinements were added over time.
WEIGHT-LOSS SURGERY TODAY
COMPARED TO THE number of obese people in the United States, the number of bariatric surgeries remains very small. In 2015, approximately 200,000 weight-loss surgeries were performed in the United States.4 Outside the U.S., this procedure is performed even less often, though there are few reliable statistics.
Roux-En-Y gastric bypass THE STANDARD FORM of bariatric surgery today is Roux-En-Y gastric bypass, which takes its name from the creation of a blind loop of the small bowel that makes a Y shape of the small intestines.
Most of the healthy stomach is removed until the only portion remaining is approximately the size of a walnut, which severely restricts food intake.
By itself, this procedure serves as only a short-term solution, so the second step of the surgery involves rerouting the small intestine to prevent the absorption of most, but not all, of the ingested food.
This combined restrictive and malabsorptive procedure makes the Roux-En-Y bypass the current heavyweight champion of bariatric surgeries, with the best weight loss but also the most complications.
This surgery has “Go big or go home” tattooed on its massive bicep.
In addition to the usual risks of bleeding and infection common to all surgeries, deficiencies of all nutrients, including proteins, vitamins, and
minerals, can lead to lifelong malnutrition after the bypass.
Gastric dumping syndrome, caused when food moves too quickly (is dumped) from the surgically altered stomach to the small intestines, can cause nausea, diarrhea, and facial flushing after meals.
Strictures (abnormal narrowings) due to scar tissue can occur at the surgical site and block the passage to the stomach.
The Roux-En-Y surgery is often reserved for severe cases of obesity, typically patients with a body mass index greater than 40.
The side effects, however, have led to the development of milder forms of bariatric surgery that can also produce spectacular results without the complexity or complications of the Roux-En-Y.
The sleeve gastrectomy THE SLEEVE GASTRECTOMY simply removes a large portion of the healthy stomach without altering the intestines, making it a purely restrictive form of weight-loss surgery.
It dramatically reduces the stomach’s capacity for holding food.
More than a thimbleful of food causes severe gastric distention, ballooning of the miniature stomach, and persistent nausea and vomiting.
Over time, the remaining stomach stretches until it becomes possible to eat small meals.
Since this procedure may be done laparoscopically, through a series of small incisions, there tend to be fewer acute surgical complications such as bleeding and infection.
Although gastric dumping syndrome is rare after this procedure, strictures are common.
More importantly, perhaps, compared to the Roux-En-Y surgery, it leads to less weight loss and less durable results.