Before this last year, you could walk into any nursing home in the world and find most people there weren’t actually sick.
They’re in there because of a medical condition that’s made them so weak from musculoskeletal loss, they can no longer care for themselves.
I’m talking about sarcopenia, a slow and creeping loss of muscle that strikes so gradually, you don’t even notice it happening. Simply put, sarcopenia is to muscle what osteoporosis is to bone.
But doctors don’t realize or acknowledge that muscle loss accelerates aging. They simply see it as a risk factor for falls and loss of mobility.
A recent population study reveals that sarcopenia is also a major contributor to accelerated telomere shortening. In other words, muscle loss itself actually causes aging.
If you’re a regular reader, you’ll know telomeres are the protective caps at the ends of each of your chromosomes.
The longer your telomeres are, the younger your cells behave; the shorter they get, the more vulnerable you are to “old age” and the so-called “diseases of aging.”
Most conventional doctors will tell you that muscle loss is an inevitable and irreversible part of the aging process.
I couldn’t disagree more.
Sarcopenia Isn’t Inevitable – And Neither is Telomere Shortening
The good news is that both can be prevented and reversed.
What most doctors don’t know is that sarcopenia is a modern condition largely caused not by age – but by a lifetime of eating an unnatural diet and a lifestyle of little physical activity.
Your ancient ancestors enjoyed strong, lean bodies throughout their lives. Their physical needs were perfectly matched to their environment, activity level and diet.
In our modern era, humans get sarcopenia for the same reason that gorillas – immensely strong and active in the wild – become weak and old before their time in captivity.
We don’t live in our native environment any longer either, and we don’t eat the native diet we evolved to eat. Grains and insane amounts of sugar have overwhelmed our bodies. Now we have diseases and conditions that didn’t even exist before.
I recommend a three-step approach to reversing muscle loss…
- Get more protein: Protein is the wisdom of our ancestors, backed up by multiple scientific studies. A protein-rich diet builds muscle mass that helps you stay mobile, healthy and independent far into old age.
All the best sources of protein come from animals – organic eggs, grass-fed beef, wild-caught fish and whole milk. Focus all your meals around high-quality protein.
- Ursolic acid and tomatidine: Muscle loss is triggered by the protein ATF4, which reduces the level of protein synthesis in your muscles. Research from the University of Iowa reveals that two tiny, overlooked natural molecules, ursolic acid and tomatidine, block ATF4 activity in the skeletal muscle.
Tomatidine is found in green tomatoes. And you can find ursolic acid naturally in apple peel, cherries, prunes, holy basil, lavender, oregano, sage and thyme. Supplements are also available online and in health food stores.
- Use PACE: Exercise is a vital component of rebuilding muscle mass. I recommend the PACE exercise program, because it’s effective at any age and whatever physical condition you’re in. And it can also extend telomere length.
It works with any exercise, but shifts the focus of your workout from “how long” to “how intensely” you exert yourself. You’ll find good PACE exercises to get started with on my YouTube channel: https://www.youtube.com/user/AlSearsMD/videos.
 Lingzhi C, et al. “Association between appendicular skeletal muscle index and leukocyte telomere length in adults: A study from National Health and Nutrition Examination Survey (NHANES) 1999e2002.” Clinical Nutrition. November 2020.
 Ebert SM, et al. “Identification and Small Molecule Inhibition of an Activating Transcription Factor 4 (ATF4)-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy.” Journal of Biological Chemistry. Vol 290, Issue 42, pp 25497-25511. 2015.
 Cherkas LF, et al. “The association between physical activity in leisure time and leukocyte telomere length.” Arch Intern Med. 2008;168(2):154-8.