Life Extension Magazine®
A nutrient called PQQ (pyrroloquinoline quinone) restores youthful cellular function and extends the lifespan of worms.1,2
PQQ helps mitochondria—the “powerhouses” of the cell—work more efficiently.
It also promotes formation of new mitochondria in aging cells. Dysfunctional mitochondria contribute to body-wide degeneration. 2-9
But it turns out PQQ does much more.
A team of researchers from China and Italy found that when PQQ was applied to human cells in culture, it delayed cellular senescence.10
A growing body of research suggests that reducing cellular senescence may lead to increased healthspan and lifespan.
This one-two punch—promoting mitochondrial health and slowing cellular senescence —explains why PQQ has powerful potential to slow aging processes.
In fact, in those recent worm studies, PQQ increased lifespan by roughly 30%.1,2
Stopping Cellular Senescence
Low-level chronic inflammation is a key contributor to aging of the human body.
As we age, levels of inflammation-stoking messenger molecules called cytokines increase, contributing to greater risk of cardiovascular disease, neurodegenerative diseases, diabetes, cancer, and more.
This phenomenon, known as inflammaging, is a major factor in the aging process itself.11,12
In a preclinical cell study, the nutrient PQQ (pyrroloquinoline quinone) showed the ability to block the effects of these harmful molecules by interfering with the signaling pathways they provoke to induce cellular senescence and inflammaging.10
Testing PQQ in Human Cells
A team of scientists recently set out to determine whether PQQ could slow cell aging caused by inflammatory signaling, and reduce the number of senescent cells.10
Researchers first grew human lung cells in a nutrient broth, and added inflammaging-associated proteins, including TNF-alpha, to some of the cell samples.10
TNF-alpha promoted senescence and inflammaging in the treated cells. But when cells were pre-treated with PQQ before the TNF-alpha, the numbers of senescent cells in the culture dropped to significantly less than those in the untreated group.
Other signs of inflammaging were also reduced in PQQ-treated cells.
This study shows that PQQ can inhibit cellular aging by reducing TNF-alpha’s ability to stimulate senescence. This is a promising finding for PQQ’s ability to slow aging throughout the body and help prevent age-related disease.
Protecting the Heart
In energy-consuming cells like those in the heart, PQQ functions almost like a “fuel additive”, helping to burn fuel more efficiently.
In animals suffering heart attacks, insufficient PQQ contributes to worse outcomes.13
Animal studies show that increasing PQQ in models of heart attack can:14-17
- Shrink the size of the infarct, or damaged area, in the heart muscle,
- Improve cardiac function following loss of blood flow (ischemia) to the heart muscle,
- Boost the function of mitochondria in ailing heart cells subjected to ischemia, and
- Prevent heart muscle death after ischemia.
These benefits are likely attributable to PQQ’s ability to combat oxidative stress and its effects on signaling pathways.17,18
Benefits for Diabetes
PQQ was shown in a cell culture study to block oxidative stress and cell death caused by high glucose, through an effect on signaling pathways.19
By battling oxidative stress and modulating insulin signaling pathways, PQQ has been shown in diabetic animals and in lab studies to:19-23
- Lower blood sugar,
- Decrease lipid abnormalities,
- Activate insulin signaling to increase glucose tolerance,
- Reduce glucose-induced oxidative stress in brain tissue, a contributor to neurodegenerative diseases, and
- Protect kidney cells against events leading to diabetic kidney disease.
PQQ also increases production of the “longevity protein” Sirt3, a longevity-associated factor that supports healthy mitochondrial function.24,25
Building Stronger Bones
In aging bone, senescent cells accumulate, pouring out damaging pro-inflammatory signaling molecules.26 This is yet another mechanism involved in the destructive effects of inflammaging.
Over time, inflammaging contributes to lower rates of new bone formation and higher rates of bone breakdown. The result: weaker, fracture-prone bones.27
Animal studies have shown that PQQ can promote bone formation and prevent bone degradation. It accomplishes this through multiple, different pathways, including oxidative stress, hormonal, and complex signaling pathways.28-32
In these studies, PQQ’s effects included the ability to:
- Strengthen and thicken healthy bone,
- Rescue weakening bone from further breakdown,
- Inhibit inflammatory secretions from senescent cells,
- Prevent bone loss related to low levels of estrogen (like that seen in menopause) and testosterone,
- Stimulate new bone formation,
- Slow the development of bone-depleting osteoclasts, and
- Promote formation of bone-producing osteoblasts.
WHAT YOU NEED TO KNOW
Fight Aging with PQQ
- Damaged, aging cells called senescent cells give off age-promoting signaling molecules.
- These harmful molecular signals promote inflammation and are a major driver of aging and age-related disease.
- PQQ (pyrroloquinoline quinone) is a vitamin-like nutrient that is known for its ability to protect the mitochondria and promote the formation of new mitochondria.
- A new cell-based study shows that PQQ can also reduce senescent cells and block the harmful signals they give off.
- PQQ may also slow the overall aging process itself, and has been shown to extend lifespan by 30% in animal studies.
Help for the Aging Brain
The brain consumes more energy than any other organ in the body.
That makes brain tissue especially vulnerable to disruptions in its energy supply.
In fact, aging mitochondria are known to contribute to many age-related brain disorders, including Alzheimer’s and Parkinson’s disease.33,34
By helping mitochondria perform more efficiently and by promoting the development of new mitochondria, PQQ may help prevent these diseases.23,35,36
Studies in rats show that increasing PQQ can minimize brain injury induced by rotenone, a neurotoxin that causes Parkinson’s-like symptoms.36 Rats receiving rotenone and then being treated with PQQ suffer less loss of brain cells and perform better on lab tests afterward compared with untreated animals.
PQQ also protects brain cells against excitotoxicity, which is believed to be one cause of Alzheimer’s disease.37 Excitotoxicity occurs when nerve cells are damaged or killed by overactivity of the neurotransmitter glutamate.38
In a cell culture study, PQQ countered glutamate’s destructive effects by stimulating growth of neural stem cells and reducing damage to brain cells.39
Extending Lifespan
When senescent cells accumulate, it accelerates aging processes.12 By reducing the number of senescent cells, PQQ may increase lifespan.
Two different research groups evaluated PQQ’s life-extending effects on a type of roundworm, C. elegans, which is commonly used to study longevity.
The findings were nearly identical. In one study, giving the animals PQQ increased lifespan by an average of 30%. In the other study, the animal models lived an average of 31% longer.1,2
Summary
PQQ (pyrroloquinoline quinone) is a compound that protects mitochondria, the “powerhouses” of our cells.
It promotes the formation of new, healthy mitochondria. This has anti-aging benefits throughout the body.
Recent studies have shown a way that PQQ may be able to slow aging even more, by reducing the activity of certain age-accelerating signaling pathways.
This can help lower chronic inflammation and aging-promoting senescent cells.
By slowing cellular aging, PQQ can help lower risks of cardiovascular disease, diabetes, osteoporosis, and neurodegenerative disorders.
Since PQQ has effects on so many aging pathways, it is a prime candidate for targeting the aging process itself and extending healthy lifespan.
If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.
References
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- Wu JZ, Huang JH, Khanabdali R, et al. Pyrroloquinoline quinone enhances the resistance to oxidative stress and extends lifespan upon DAF-16 and SKN-1 activities in C. elegans. Exp Gerontol. 2016 Jul;80:43-50.
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