We are just beginning to understand the biological intricacies of aging. A growing body of research is challenging the belief that aging is beyond your control, prompting scientists to begin thinking about ways we can slow our aging clocks to a slow crawl.

Although this is a relatively new branch of science, there are some factors that appear to be key in controlling how quickly you age. One major factor seems to be insulin signaling and the metabolic “engines” you have running day to day, which are largely controlled by the foods you eat.

In the first featured video, Dr. Peter Attia discusses how a ketogenic diet can optimize your metabolism. But before I discuss the specifics of this, I want to tell you about a remarkable mouse study, presented in the second video. Scientists just accomplished quite a feat: extending the lifespan of mice by 20 percent just by manipulating just one single gene.

The Aging of Mice and Men

In a report published in the August 2013 issue of Cell Reports, scientists discovered that the “mTOR gene” is a significant regulator of the aging process—at least in mice. This gene is thought to be involved, in some capacity, with insulin signaling.

In this study, a drug was used to suppress the action of the mTOR gene by 25 percent in a group of laboratory mice. The drug, rapamycin, is an immunosuppressant used to treat certain cancers and also to prevent organ rejection in transplant patients.

The mice whose mTOR was suppressed lived 20 percent longer than the control mice—which in human terms, equates to an additional 15 years of life! But they had other effects as well—some that were beneficial, and some that were not.

For example, the mTOR-suppressed mice demonstrated improved memory and cognition and had a much lower cancer risk. However, they also developed softer bones, more infections, and more cataracts than normal mice.

The mTOR gene is known to play a role in cellular metabolism and energy balance. Researchers believe it’s also somehow involved in the effects of calorie restriction, which is associated with longevity. It’s been known for nearly a century that animals consuming less food live longer.

Those on restricted calorie diets are living longer probably as a result of improvedinsulin regulation, as insulin resistance is a major factor in many chronic illnesses.2Researchers concluded that mTOR is a significant regulator of aging and are optimistic that targeting this gene may someday be part of an anti-aging strategy.

But mouse studies don’t always translate to humans. There is no guarantee that inhibiting the action of mTOR in humans would produce similar life-extending effects—and it could be harmful in unforeseen ways.

For now, your best bet is to use diet and exercise to optimize your mTOR pathway, which is part of your insulin pathway. You can learn more about this in this previous interview with fitness expert Ori Hofmekler.

The role that insulin plays in longevity was also demonstrated by earlier research involving worms, of all things! By adding just a tiny amount of glucose to worms’ diets, their lifespan was shortened by 20 percent. Believe it or not, when it comes to insulin signaling, there are many similarities between you and those wiggly creatures. Consuming lots of sugar and grains is the equivalent of slamming your foot on your aging accelerator.

A High-Fat Diet May Also Lengthen Your Life

Numerous studies have shown that lowering your caloric intake may slow down aging, help prevent age-related chronic diseases, and extend your life. As you age, your levels of glucose, insulin and triglycerides tend to gradually creep upward.

A 2010 study examined the effects of a high-fat diet on typical markers of aging. Study participants were given a high-fat, low-carbohydrate diet with adequate protein, and the results were health improvements across the board. Serum leptin decreased by an average of eight percent, insulin by 48 percent, fasting glucose by 40 percent, triglycerides by nearly eight percent, and free T3 (thyroid hormone) by almost six percent.

What we know now about calorie restriction is that, in animals, it reduces metabolic rate and oxidative stress, and it alters neuroendocrine and sympathetic nervous system function. We also know that calorie restriction improves insulin sensitivity, and high insulin levels accelerate aging.

Therefore, it is safe to assume that much of the longevity phenomenon can be attributed to improved insulin signaling. What this means for you is that your longevity depends more on whatyou eat than on how muchyou eat.

A Radical Ketogenic Diet Experiment

Now that you have an understanding of how important insulin is to your health and longevity, let’s take a look at Dr. Peter Attia, who presents one of the clearest examples of the effects of diet on overall health markers. Dr. Attia is a Stanford University trained physician with a passion for metabolic science, who decided to use himself as a lab rat—with incredible results.

Although Dr. Attia has always been active and fit, he did not have genetics on his side. His natural tendency was toward metabolic syndrome, in spite of being very diligent about his diet and exercise. So he decided to experiment with a ketogenic diet, to see if he could improve his overall health status.

For a period of 10 years, he consumed 80 percent of his calories from fat and continuously monitored his metabolic markers, such as blood sugar levels, percent body fat, blood pressure, lipid levels and others.

He experienced improvement in every measure of health, as you can see in the table below. An MRI confirmed that he had lost not only subcutaneous fat but also visceral fat, which is the type most detrimental. His experiment demonstrates how diet can produce major changes in your body, even if you are starting out relatively fit. And if you’re starting out with a low level of fitness, then the changes you experience may be even more pronounced.

What is a Ketogenic Diet?

Dr. Attia consumed what is known as a ketogenic diet, which is one that shifts your body’s metabolic engine from burning carbohydrates to burning fats. Your cells have the metabolic flexibility to adapt from using glucose for fuel to using ketone bodies, which come from the breakdown of fats—hence the name “ketogenic.” Another term for this is nutritional ketosis. As an aside, many types of cancer cells do NOT have this adaptability and require glucose to thrive, which makes the ketogenic diet an effective therapy for combating cancer.

A ketogenic diet requires that 50 to 70 percent of your food intake come from beneficial fats, such as coconut oil, grass-pastured butter, organic pastured eggs, avocado, and raw nuts (raw pecans and macadamia nuts are particularly beneficial). One of the fastest ways to prevent nutritional ketosis is by consuming sugar or refined carbohydrates.

Besides restricting carbs and limiting protein, you can also strengthen your ketone engine with intermittent fasting, which is what Dr. Attia did. He restricted his sugar intake to about five grams per day, which is quite extreme and much lower than I recommend for most people. He consumed a moderate amount of protein, and the rest of his foods—80 percent of them—were fats. But his approach, as radical as it was, really proves that a ketogenic diet can have profound health benefits—not to mention blowing thesaturated fats theory of heart disease out of the water, once again.

Please note that I have recently revised my position on using low carb long term and now believe that the low carb, low to moderate protein, high healthy fat diet is appropriate for most who are insulin or leptin resistant. Once that resistance resolves, then it likely becomes counterproductive to maintain a low-carb approach. Once your weight, blood pressure, sugar, and cholesterol normalize, you can increase your carbs. Personally, I now consume several pieces of fruit a day and have two dozen fruit trees in my yard, but my body weight, fat, and insulin resistance are all optimized.

Your Heart LOVES Ketones

Your heart, as well as other muscles, operates quite efficiently when fueled by ketones. Your muscles can store more glucose (as glycogen) than your brain because they have an enzyme that helps them maintain their glycogen stores. But your brain lacks this enzyme, so it prefers to be fueled by glucose. When your blood glucose levels are falling, your ketone levels are typically rising, and vice versa. You might be wondering, then, how your brain is able to function when you’re in a state of ketosis.

It turns out that your body has a mechanism for providing your brain with a fuel source it CAN use when glucose is in short supply. When your glucose is low, your brain tells your liver to produce a ketone-like compound called beta-hydroxybutyrate (or beta-hydroxybutyric acid). This compound is able to fuel your brain very efficiently, especially with “practice.”

The more efficient your body is at burning fats, the more easily it can move seamlessly between its fat-burning and carbohydrate-burning engines, and the more stable your blood sugar will be. Your body will be able to save its glycogen stores for when they are critically needed, such as when you’re engaged in intense physical activity.

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