The New Science of Aging Well, Understanding Cellular Nutrition & Natural Age-Associated Cellular Decline (AACD).
Welcome to MyAACD.org, a dedicated source for learning about the evolving science of Age-Associated Cellular Decline, or AACD.
AACD is the time-related deterioration in the way our cells function as we age, which often begins in our 40s and accelerates in our 60s.
Signs of AACD may include lower levels of daily energy, a decline in strength and stamina, decreased immune function, or reduced resilience.
Major cellular processes have now been identified which play an important role in AACD.
Explore how cellular changes can impact aging, and follow the latest scientific developments in cellular nutrients which can help to address key drivers of AACD.
Learn More About the New Science of Aging: Explore www.myaacd.org
The New Science of Aging: What is Age-Associated Cellular Decline?
Age-Associated Cellular Decline (AACD) is the natural, time-related deterioration in the way our cells function as we age, which often begins in our 40s and accelerates in our 60s.1,2
While aging is a complex process involving many physical changes, new advances in science have brought a wealth of understanding about why we age, what natural cellular processes change with age, and the important role cellular health plays in how we age.
Research on aging continues to describe what mechanisms relate to the health of our cells and how these mechanisms change over time and contribute to cellular decline and the process of aging. What has become increasingly evident is the importance of mitochondrial health for proper cellular function and the significant impact this can have on energy, endurance, strength and stamina after middle age.3
As the “powerhouse” of the cell, mitochondria are primarily responsible for producing cellular energy (ATP).4 However, a variety of cellular mechanisms decline and mitochondria become less efficient, which gradually impairs cellular function as we age. Current evidence points to mitochondrial dysfunction as a factor commonly driving accelerated cellular aging and Age-Associated Cellular Decline.5
In light of this growing understanding, three major mechanisms of cellular decline have now been identified as playing important roles in accelerating the declines associated with aging. These mechanisms include:
1. A decline in mitochondrial health, which reduces efficiency in cellular energy production, mitochondrial function, and cellular function.6
2. A decline in NAD+ (nicotinamide adenine dinucleotide), which impairs the natural process for producing cellular energy (ATP).7 NAD+ is a coenzyme, which is essential to turn nutrients into energy and is critical for energy production.
3. A decline in levels of glutathione, a “master antioxidant,” which must be continuously produced by the body for proper cellular protection from oxidative stress and damage.8 Glutathione is also essential for healthy immune.
Collectively, these mechanisms of decline contribute to accelerated cellular aging. The progressive decline of mitochondrial function, decreased levels of NAD+ and increased oxidative stress within cells cascade throughout the body. This may have noticeable effects on a loss of cellular protection, daily energy levels, and muscle and organ function.5-11
Although the speed of aging may be different for each individual, partly because of lifestyle and genetic factors, the decline in these important cellular mechanisms are linked with declining health. This includes reduced immune response, loss of muscle strength and function, metabolic disorders, and chronic diseases including cardiovascular and cognitive conditions.3
Given the pivotal role mitochondria play in our cellular health and all organs throughout the body, the ability to maintain mitochondrial health after middle age may help to support healthy cellular aging.
Research and new interventions that target the health of mitochondria may show significant promise for restoring cellular processes that decline with age and improving Age-Associated Cellular Decline.6