Metabolism Support
Targeted supplementation can also help reverse mitochondrial decay. At the forefront of this research is preeminent biochemist Bruce Ames, PhD, a professor emeritus at the University of California, Berkeley, and senior scientist at Children’s Hospital Oakland Research Institute.
For years now, Ames has been working on ways to protect and restore mitochondria in the brain. His goal is to halt and even reverse the cognitive and neurologic decline that usually comes with age.
Ames’s first line of attack was to try to reverse the mitochondrial deterioration that produces excess free radicals, a process he compares to “an old car engine producing too much smoke,” and thus, not running efficiently.
Aging mitochondria, with their inefficient machinery, damaged DNA, and decaying membranes, can’t clear the smoke, which leads to impaired memory and mental function over time.
The only means Ames knew to slow the process in animals was calorie restriction — flat-out reducing the amount of fuel burned. But it’s hard (and not healthy) to starve humans, so Ames vowed to find another way.
He experimented in the lab, trying out various supplements on a group of aging rats. Acetyl-L-carnitine (ALC), which is known for transporting fatty acids into the mitochondria, shored up the membranes and helped repair the DNA, but it didn’t decrease free-radical production. So, he added alpha-lipoic acid (LA), a mitochondrial coenzyme capable of cleaning up the messes free radicals make.
The result? Ames’s older lab rats — who couldn’t run well on a treadmill and couldn’t navigate in a water pool — were rejuvenated. Their running and swimming improved. Their mitochondria became more youthful, too.
Ames discovered that a host of different micronutrients are involved in mitochondrial health. Looking at human cells, for example, Ames found damage to DNA whenever even one of a number of minerals or vitamins was removed.
To explain the phenomenon, Ames came up with a theory rooted in our hunter-gatherer past, when micronutrient shortages must have been recurrent: To make sure the species was perpetuated, natural selection imposed a “strategic rationing response,” shunting the vital nutrients toward functions essential for short-term survival and reproduction, and away from longevity systems affected by dysfunctional mitochondria.
Although a variety of lifestyle factors contribute to mitochondrial health, says Ames (see below), the single most important thing we can do is to eat a well-balanced, whole-foods diet.
Because research suggests that virtually all U.S. adults are deficient in one or more important nutrients, many experts recommend supplementing with a high-quality multivitamin, vitamin D, essential fatty acids — and perhaps more, depending on your individual profile.
But a cautionary note comes from Bruce Cohen, who points out that many nutrition studies have been done only with mice or cell cultures. “When you try the strategies on humans,” he says, “they don’t always work.”
Wahls is trying to set that right. Her pilot study on the Wahls Protocol, which studied 13 MS patients, was published in The Journal of Alternative and Complementary Medicine earlier this year. Within the study group, six people rigorously adhered to the protocol — including a paleo diet, exercise, meditation, and massage — for a full year. Those patients, who normally would have experienced only further decline, showed clinically significant improvement in fatigue symptoms compared with their baseline assessments.
A great deal more research is necessary, notes Wahls. But eating for your mitochondria, she argues, is almost guaranteed to pay off. “I am the canary in the coal mine, here as a warning to all of you,” Wahls says. “If we don’t care for our mitochondria, we will pay a very high price when it comes to our health.