Living Low Carb (12 page)

It talks to the kidneys.

Insulin’s message to the kidneys is this:
hold on to salt
. Insulin makes the kidneys do this even if the kidneys would much prefer not to. Since sodium, like sugar, is controlled by the body within a very tight range, the kidneys figure, “Listen, if we have to hold on to all this salt, we’d better bring on more water to dilute it so that it stays in the safe range.” And that’s exactly what they do. Increased sodium retention results in increased water retention. More fluid means more blood volume, and more blood volume means higher blood pressure. Fully 50% of people with hypertension have insulin resistance.
¹³

Insulin will also ultimately raise adrenaline, and adrenaline will raise both blood pressure and heart rate. We’ll discuss the insulin–adrenaline axis a little more, under the topic of obesity in the next section.

How Does a Low-Carb Diet Lower Your Risk of Hypertension?

Lowering insulin levels will intercept the message to the kidneys to hold on to salt. You will almost immediately lose water weight, and bloat and blood pressure will go down. Lowering insulin is actually such an effective strategy for lowering blood pressure that it sometimes works too well too fast. In rare cases, your blood pressure might dip too low, and you may experience lightheadedness or dizziness upon standing up. This is why some clinicians recommend increasing salty foods or adding a teaspoon of salt to your food on a daily basis if you find this happening to you.
¹⁴

When the kidneys dump excess sodium, potassium sometimes gets caught in the crossfire and you wind up dumping potassium as well. This is even truer if you exercise and sweat a lot. You don’t want to lose too much potassium, because that can cause muscle cramps, fatigue, and breathlessness. This is why I always recommend potassium supplements, especially during the first week of a low-carb diet, and particularly when you are on one of the very restricted carbohydrate plans such as the induction phase of Atkins or the first two weeks of Protein Power. Potassium supplements come in 99-milligram tablets, and you can get them at any drugstore or healthfood store. Take one or two at each meal. Foods rich in potassium, such as liver, broccoli, and avocados, are also a good idea, as is using over-thecounter salt substitutes like Morton’s Lite Salt or NoSalt, which are both potassium salts.

Insulin and Obesity

The connection between a high-sugar diet, high levels of insulin, and becoming overweight or obese should be painfully obvious by now. The more sugar—i.e., carbohydrates—you take in, the more sugar you need to store and the more your insulin levels rise. The more your insulin levels rise, the less fat you burn and the more sugar you store in fat cells, along with those extra triglycerides that the liver made from excess sugar. The more you store, the fatter you get. The fatter you get, the more insulinresistant you become.

When there are consistently high levels of insulin floating around, the body will put out more cortisol and adrenaline (the “breakdown” hormones) to counteract the “building-up” effects of insulin and to attempt to bring the body back into balance. Cortisol in part breaks down muscle, further reducing your metabolic rate. Too much adrenaline can eventually lead to even
more
insulin, as insulin will eventually be secreted to combat the effects of too much adrenaline! The interaction of insulin and cortisol/adrenaline is the particular aspect of low-carbohydrate dieting central to the metabolic healing work of Diana Schwarzbein, who feels that this kind of constant imbalance—often brought on by yo-yo dieting, high levels of stress, and a diet high in sugar—ultimately damages the metabolism. If getting off this particular seesaw sounds interesting to you, be sure to read about the
Schwarzbein Principle
in
chapter 7
.

Even if you don’t remember the basic biochemistry discussed here, tattoo the following on the inside of your eyelids:
insulin is the fat-storage hormone.
It is also the hunger hormone. When it finally does its job of lowering blood sugar, it causes blood sugar to go really low, setting you up for a cycle of craving (and eating) more high-carb foods. Result: higher blood sugar, more insulin, and more fat storage as the cycle continues.

How Does a Low-Carb Diet Help You Lose Weight?

When you eat a lower-carb diet, you stimulate less insulin but you also stimulate more glucagon, its sister hormone, which responds more to protein (remember that neither hormone is stimulated by fat). Glucagon liberates the fat from storage sites and gets it ready to burn for energy. Meanwhile, since you no longer have elevated levels of insulin, you are not suppressing carnitine, which, you may remember, is the compound in the body responsible for escorting fat into the central furnaces of the cells, where it can be burned for fuel.

Along with insulin and glucagon, a pair of enzymes plays a major role in the whole fat-storage/fat-release equation: lipoprotein lipase and hormone-sensitive lipase. Lipoprotein lipase is responsible for storing fats: it breaks down triglycerides in the bloodstream and shoves the fatty-acid parts into fat cells. People who are trying to lose weight are not fond of this enzyme. It’s very persistent; in fact, when people lose weight, the activity of lipoprotein lipase is ramped up, almost as if the body is fighting to hold on to fat. This is one of the reasons it’s so difficult to keep weight off. (Lipoprotein lipase is also suppressed when you smoke and increases when you stop smoking, one of the reasons people usually put on a few pounds when they first give up cigarettes.)

Hormone-sensitive lipase, on the other hand, reaches into fat cells and releases fatty acids into the bloodstream when they are needed—for example, if you’re doing a long aerobic exercise session and your legs need some fuel. Its ability to liberate fat is really intense. Consider this: there’s a protein called perilipin that shields fat from the fat-burning effects of hormonesensitive lipase. Mice that don’t have any perilipin to protect their fat from hormone-sensitive lipase don’t get fat, no matter what they eat!
¹⁵
The fatburning effect of hormone-sensitive lipase is that intense.

Insulin and glucagon have profound effects on both lipoprotein lipase and hormone-sensitive lipase. Can you guess what effects they have? By now it should come as no surprise: insulin
stimulates
lipoprotein lipase (the fat-storing enzyme) and
inhibits
hormone-sensitive lipase (the fat-releasing enzyme). If you want your fat cells to let go of fat, you want all the hormone-sensitive lipase activity you can scrounge up—you certainly don’t need high levels of insulin turning down the volume. Glucagon, on the other hand, has exactly the opposite effect on these enzymes. It
inhibits
the fatstoring enzyme and
stimulates
the fat-releasing one. This is just one more way that restoring a healthy balance between insulin and glucagon helps you to lose weight.

Fat Cells Know How to Protect Their Existence!

When you do lose weight, you stack the hormonal deck in your favor even more. We used to believe that fat cells were inert little sacks of blubber that basically didn’t do anything metabolically—they just took up space and held on to a gazillion calories’ worth of energy that never got burned up fast enough. We now know that fat cells are anything
but
inactive. They are actually endocrine glands that release a host of hormones—including estrogen—and other substances that can have a profound effect on our weight.

Many of the hormones that are released by the fat cells have one major purpose—to keep those fat cells in business! In this way, you might say that fat actually perpetuates its own existence by releasing hormones that make it harder for the body to get rid of it.

One of the hormones released by fat cells is
resistin
. The more fat cells you have, the more resistin gets released into your body. Mice given extra dosages of resistin develop insulin resistance in two days;
¹⁶
and, as we’ve just seen, insulin resistance is a major obstacle to fat loss. Another substance released by the fat cells is TNF-alpha 1, also known as tumor necrosis factor. This is a good guy: it’s part of the immune system’s arsenal, and, as you can tell by the name, it’s involved in destroying tumors. But TNFalpha 1 is also found in fat tissue, and in the circulatory system it appears to act like a hormone. In low amounts, it
inhibits
the ability of insulin to lower blood sugar, essentially making insulin’s job harder to accomplish and thereby forcing the pancreas to put out even more insulin to get the job done.
¹⁷
Once again, a hormone-like compound released by the fat cells raises insulin and makes fat loss difficult. As you can see, the fat cells
themselves
contribute to the difficulty in losing weight by releasing substances that offer “fat-protection insurance”—chemicals that, in essence, help your fat cells stay in business. By lowering your fat stores with a low-carbohydrate diet, you will also lower the amounts of these fat-protecting substances in the bloodstream.

A Low-Carb Diet Helps Reduce Insulin Resistance

When you are insulin-resistant, your cells stop making insulin receptors to import sugar and fat into the cells. This process is called down-regulation. Receptors are like job recruiters. When the market is flooded with unemployed workers, companies don’t have to go hunting for job applicants, because there are so many knocking at the door. When you’re insulinresistant, you’ve got a hell of a lot of insulin—applicants—knocking at the cell door. The cells figure there’s enough insulin hanging around, beating on the doors, so they stop sending out “recruiters” to the surface of the cells. When you bring your insulin down with a low-carb diet, suddenly there’s not so much insulin banging at the doors of the cells. Now you begin to lose weight. Eventually, the cells start to send up more receptors to bring in the fuel, a process called up-regulation. The cells are now gradually becoming more insulin-
sensitive
—a condition you most decidedly want. Insulin sensitivity always improves when you lose weight.

There are other ways in which a low-carb lifestyle will help you lose weight. One way has to do specifically with protein itself, which is usually more plentiful on lower-carb diets. Protein has less of an effect on insulin, has a greater effect on glucagon, and increases metabolic rate considerably more than carbohydrates do. Specific amino acids found in protein may also play a role in weight loss. Several papers by D. K. Layman demonstrated greater body-fat loss on a high-protein diet than on a high-carb diet,
¹⁸
and in one paper he argued that leucine—an amino acid—may be one of the reasons.
¹⁹
Other studies have also suggested the possible role of specific amino acids in weight loss. In one animal study, a diet deficient in the amino acid lysine resulted in the accumulation of larger amounts of fat both in the bodies of the animals and in their livers.
²⁰
Increasing the proportion of protein to carbohydrates appears to be more
satiating
during weight loss—it makes you feel fuller.
²¹
And metabolic rate, technically called thermogenesis—the heat production in our bodies from burning calories—is turned up after eating protein. In one study, thermogenesis was 100% higher with highprotein meals—even 2½ hours after eating—in young, healthy women.
²²

You may have heard that it is easier to stay on a low-carb diet than it is to stay on a traditional high-carb, low-fat diet. Let me say one word about that:
appetite
. A low-carb diet contains built-in appetite controls—it’s like having your own little diet pill built into the meals. Here’s how it works. One of the major hormones involved in telling the brain that you are full is cholecystokinin (CCK), which is secreted in the intestines in response to a meal. (You may have also heard, correctly, that it takes about twenty minutes for this hormone to reach your brain and tell you that you’ve had enough—another reason to listen to your grandmother and eat slowly if you want to lose weight!) But here’s the thing: CCK, being part of our ancient digestive system, recognizes protein and fat very well because they’ve been the mainstay of our diet for as long as the human genus has been on the planet. But CCK does
not
respond very well to carbohydrates. It barely recognizes them! That’s why it is so easy to overeat carbs—you really have no idea when you’ve had enough.

Insulin Resistance and Diabetes

Insulin resistance is a huge risk factor for the development of both heart disease and diabetes.
²³
Eighty percent of the 16 to 17 million Americans who have diabetes are insulin-resistant.
²⁴
Dr. David Leonardi, founder of the Leonardi Medical Institute for Vitality and Longevity in Denver, insists that insulin resistance is reversible and that many type 2 diabetics can be cured. He says: “Diabetics die from
diabetes complications, all of which are a direct or indirect result of high blood sugar
. Normalizing the blood sugar prevents disease, normalizes life expectancy, and profoundly enhances quality of life. Cured or not, they’re winners either way.”

In case you hadn’t noticed by now, low-carb diets are all about normalizing blood sugar. Insulin resistance is reversible. And it’s hardly a rare phenomenon. The prevalence of insulin resistance has skyrocketed 61% in the last decade alone, according to Daniel Einhorn, MD, co-chair of the AACE Insulin Resistance Syndrome Task Force and medical director of the Scripps Whittier Institute for Diabetes.
²⁵
In fact, the prevalence of insulin resistance has probably been underestimated from the beginning. Gerald Reaven of Stanford University did the original work on insulin resistance in the 1980s. Here’s how he approximated the number of people who were insulin-resistant: He divided his test population—nondiabetic, healthy adults—into quartiles and tested their ability to metabolize sugar and carbohydrates. He found that while the top 25% of the population could handle sugar just fine, the bottom 25% could not—they had insulin resistance (or, in the parlance of researchers, impaired glucose metabolism). So for a long time, it was thought that the number of people with insulin resistance was one in four.