Digestive Walk

What about herbal tea? One of the most widely used medicinal plants in the world is chamomile—and for good reason. When people with type 2 diabetes drank a small cup of chamomile tea after each meal for a few months, they achieved a more significant improvement in their long-term blood sugar control than with the same amount of warm water or, in a direct comparison, to black tea. And the side effects? All good—lower LDL cholesterol and triglycerides, less inflammation, better sleep, better mood, and a healthier antioxidant status. Chamomile and green tea appear to regulate blood sugar through the same mechanism: They don’t let the sugar through the intestinal wall.

An enslave to rhythm

In my chronobiology chapter in How Not to Diet, I address how blood sugar control declines over the course of the day. Thanks to our day-and-night rhythm, a meal at eight o’clock in the evening can trigger a blood sugar response twice as high as the same meal at eight o’clock in the morning. Even an earlier lunch acts significantly differently than a later one. So if you absolutely have to eat refined grains and sugar, give in to your cravings in the morning, and then it may do less harm.

Digestive Walk

Since active muscles take up excess blood sugar, planning exercise can complement planning meals. When researchers randomized people with type 2 diabetes to either a 20-minute leisurely walk before or after dinner (at about 3 km/h), they found that the walk after eating blunted blood sugar spikes 30 percent more. With a little tactical timing, the same meal and the same amount and type of exercise can give us a considerable bonus in blood sugar control. Exercise after eating can lower blood sugar as well as some glucose-lowering medications, and even a short, ten-minute walk makes a difference. See my section “Optimizing Exercise” in How Not to Diet for details on optimal timing.

Food for thought

AGEs are considered “gerontotoxins,” which means “aging factors” (from the Greek geron for “old,” as in geriatric), and are linked to a whole range of age-related diseases. In a sense, we are all slowly being boiled alive. AGEs form in us at body temperature, especially with high blood sugar, but their accumulation in tissue is determined to a large extent by the AGEs we eat (or smoke) that are formed at much higher temperatures when food is cooked with high heat (or tobacco is dried).

But rather than dealing with changing eating habits, medicine has focused on developing agents to combat AGEs. It is said that the healthier way of life has “zero economic benefit,” and people cite that “steamed chicken tastes less good than fried ….” Why not calmly eat your Kentucky Fried Chicken and then take Kremezin, the medication that blocks the absorption of AGEs with every meal to reduce uptake of the toxins? As it turns out, the product is just a preparation of activated charcoal, like what is used in drug overdoses or poisoning. I’m sure it would also lower your AGE level if you ate your Kentucky Fried Chicken and washed it down with ipecac! A safe level of AGE intake has not yet been defined, but animal studies show that reducing intake by 50 percent can lead to a longer life.

The best way to reduce AGE intake is not to eat so much of it in the first place.

To help slow this pathway of aging every day, you should:

IGF-1

In the early 1990s, there was a major breakthrough in our understanding of aging. Getting old was generally viewed as a hopelessly unsolvable problem. People thought at the time that we wear out in an arbitrary, passive process of wear and tear. Then, in 1993, it was found that a single gene mutation extends the life span of C. elegans, the roundworm so often used in aging research. Normally, after 30 days all the worms are dead, but in one experiment they all lived 60 days or longer. The study leader Cynthia Kenyon recalls: “The mutants were the most astonishing thing I had ever seen. They were active and healthy, and they lived more than twice as long as normal. It was like a miracle, but also a little creepy: They should have been dead, but they were alive and well.”

This extension of life span was the longest that had ever been reported for an organism up to that point. These Methuselahs among worms were seen as a medical miracle, “the equivalent of a healthy 200-year-old human,” and all thanks to a single mutation. That was especially surprising. It is assumed that numerous processes contribute to aging that are influenced by a whole series of genes. How could shutting off a single gene double life span?

Watch out, Grim Reaper

What is this so-called Grim Reaper gene—that speeds up aging so much that the animals live twice as long when it is switched off? It is the counterpart of the receptor for human insulin-like growth factor 1 (IGF-1), a powerful growth hormone with the same structure as insulin. Mutations of the same receptor in humans could explain why some people live to be 100 and others do not. That was an overwhelming discovery, the first tangible path to life extension. We discovered that aging is determined by hormone signals that have been conserved in evolution from tiny worms all the way to us.

Since then, intervening in IGF-1 metabolic signaling has extended the lives of a number of species. Mice whose IGF-1 was knocked out live 42 to 70 percent longer. Kenyon marveled: “Some of these long-lived mutants are breathtaking; on the human scale, they look like 40-year-olds even though in reality they are 80 or even older.” It is suspected that turning down growth hormone signaling shifts the body’s priorities from growth to maintenance and repair, thereby extending life. The decline in IGF-1 levels with age may be set up by nature to keep us going into old age.