Chronic Inflammation Speeds Aging

Chronic Inflammation Speeds Aging

Lab study affirms prior evidence that chronic, “silent” inflammation drives aging at the DNA level

Dr. Nicholas Perricone is best known as the creator of anti-aging skin creams. But he was perhaps the first bestselling author to stress the role of chronic inflammation in aging.

In his books, Dr. Perricone highlights the pro-inflammatory effects of sugars and refined starches on our genes, which leads to this same kind of “silent” inflammation.

And he stresses the inflammation-moderating “nutrigenomic” effects of omega-3 fats from fish and the “antioxidants” that abound in whole plants foods. (See our sidebar, “The truth about antioxidants in plant foods”)

Perricone and other scientists cite growing evidence that chronic inflammation is responsible for the apparently unrelated degenerative diseases of aging, and may shorten people’s lifespans.

It’s been hard to unravel the causes of aging from its consequences, and the role of inflammation in aging has remained a controversial mystery.

But a growing steam of evidence now links chronic, symptom-free, “silent” inflammation to everything from aging and weight gain to stress, depression, and loss of strength.

Aging begins with our DNA
The rate at which we age is governed in part by our genes … with lifestyle playing a big role.

The speed with which our cells age is partly a function of the health of the genetic material carried within our cells’ chromosomes.

Chromosomes are single pieces of coiled DNA that hold genes and various protein “switches” (transcription factors) needed to carry out gene-drive commands.

(In his books, Dr. Perricone focuses great attention on the helpful or harmful effects that different foods exert on inflammation-regulating transcription factors.)

For a human cell to divide, it must first replicate its chromosomes, so that your hereditary genetic material (DNA and RNA) passes on to new cells.

Telomeres (“end parts” in Greek) are like disposable “caps” that protect the ends of chromosomes undergoing replication.

Any loss of or damage to DNA during replication can lead to serious problems, and recent research shows that telomere durability plays a key role in aging (Hewitt G et al. 2012; Baylis D et al. 2014; Wong JY et al. 2014; Rode L et al. 2014; Zhang L et al. 2014).

For example, see “Omega-3s’ DNA-Telomere Effects vs. Heart Disease and Aging”, “Omega-3s May Slow Aging”, “Tea May Yield Younger Cells… and Longer Lives?”, “Vitamin Studies Paint a More Positive Prevention Picture” (read the section titled “Recent vitamin-health studies: a summary”), and “Magnesium Shortage Speeds Aging of America”.

UK mouse study mice found that inflammation sped aging
British researchers report results that strongly support the idea that inflammation is a key factor in the aging process … a concept some scientists now call “inflammaging”.

A team from Newcastle University studied otherwise healthy mice in which a gene that normally limits the inflammatory response was switched off.

This gene change led to the kind of chronic, progressive, low-grade inflammation seen in humans who eat junky diets, lead sedentary lifestyles, and/or suffer from undue stress.

As study leader professor Thomas von Zglinicki, said, “People age differently, some much faster than others. We know already that faster aging is often associated with activated markers of chronic inflammation.”

And he added two important observations:
“While we become older, a mild form of inflammation without any obvious cause becomes increasingly frequent and ultimately chronic.”
“While this chronic inflammation doesn’t obviously hurt, it still releases the same powerful messenger molecules that cause the pain and fever in [produced by the immune system response to infection or injury].”
His colleagues’ findings suggest that inflammation accelerates the aging of cells via the release of larger amounts of the unstable oxygen molecules called “free radicals”, which are linked to the aging process.

In addition, the genetically altered mice accumulated “telomere-dysfunctional” cells in which DNA was not being protected during replication.

Importantly, mice treated with anti-inflammatory or antioxidant drugs regained their ability to regenerate tissue in a healthy fashion … which confirmed that inflammation (and the uncontrolled oxidation it causes) was damaging the animals’ DNA-protective telomeres.

The genetically altered mice displayed almost all aspects of normal aging … but they did it twice as fast as those that still possesses the gene that moderates inflammation.

Finally, the mice lacking their inflammation-control gene died sooner than their normal peers.

As the Brits wrote, “These data indicate that systemic chronic inflammation can accelerate aging”, and that is does its damage by generating free radicals that cause “telomere dysfunction”, leading to premature cell aging.

Dr. Von Zglinicki noted that, “With these results we can now seriously start thinking about inflammation as a potential driver of accelerated aging and how we might be able to delay it.”

Co-author Diana Jurk, who did most of the experiments, said this: “The most important result of the study is that treatment with a simple and cheap anti-inflammatory drug, ibuprofen, could reverse the progression of cell senescence and restore the ability of tissues to regenerate.”

While she might be right, synthetic non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin and ibuprofen (Advil) are blunt instruments that, over time, can cause serious adverse side effects.

We hope that scientists instead focus on the known benefits of inflammation-moderating nutrients like omega-3s (see our Omega-3 Facts & Sources page) and the antioxidants in whole plant foods.

To learn more about this promising area of food-as-medicine research, see “Fighting Internal Fires with Fish Fats”, “Aspirin Mimics a Fishy Omega-3”, “Omega-3 DHA Derivative May Replace Opiates”, and “Omega-3s May Help Deter Gum Disease”.

And people need to understand the damaging, pro-inflammatory role played by the gross excess of omega-6 fats in the standard American diet. (See Know Your Omega-3/6 Numbers, America’s Sickening “Omega Imbalance”, and the Omega-3 / Omega-6 Balance section of our news archive.)

The truth about
“antioxidants” in plant foods
The polyphenol and carotenoid compounds in whole plant foods are commonly called “antioxidants” because they behave that way in test tube experiments.

But in general, these health allies do not exert direct antioxidant effects in the body… at least not to a very substantial extent.

Instead, polyphenols appear to exert strong indirect effects on oxidation and inflammation via so-called “nutrigenomic” effects on gene switches (e.g., transcription factors) in our cells.

Polyphenols’ nutrigenomic effects tend to moderate inflammation and stimulate the body’s own antioxidant network … which includes enzymes, lipoic acid, CoQ10, melatonin, and vitamins C and E.

The richest known food source of polyphenols are raw (non-alkalized / non-“Dutched”) cocoa, berries, plums, prunes, tea, coffee, extra virgin olive oil, beans, and whole grains.

(Highly beneficial procyanidin-type polyphenols abound in cocoa, dark-hued berries – e.g., blackberries, blueberries açaí berries – grapes, red wine, and tea. Comparably beneficial anthocyanin-type polyphenols abound in cherries and most berries.)

Extra virgin olive oil is uniquely rich in hydroxytyrosol, oleuropein, oleocanthal, and other tyrosol esters … a particularly potent class of polyphenols with clinically documented vascular and brain benefits.

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Hewitt G, Jurk D, Marques FD, Correia-Melo C, Hardy T, Gackowska A, Anderson R, Taschuk M, Mann J, Passos JF. Telomeres are favoured targets of a persistent DNA damage response in aging and stress-induced senescence. Nat Commun. 2012 Feb 28;3:708. doi: 10.1038/ncomms1708.
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Newcastle University. Chronic inflammation accelerates aging. June 25, 2014. Accessed at Click Here
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Rode L, Nordestgaard BG, Weischer M, Bojesen SE. Increased body mass index, elevated C-reactive protein, and short telomere length. J Clin Endocrinol Metab. 2014 Apr 24:jc20141161. [Epub ahead of print]
Wong JY, De Vivo I, Lin X, Fang SC, Christiani DC. The relationship between inflammatory biomarkers and telomere length in an occupational prospective cohort study. PLoS One. 2014 Jan 27;9(1):e87348. doi: 10.1371/journal.pone.0087348. eCollection 2014
Zhang L, Hu XZ, Li X, Li H, Smerin S, Russell D, Ursano RJ. Telomere length – A cellular aging marker for depression and Post-traumatic Stress Disorder. Med Hypotheses. 2014 Aug;83(2):182-5. doi: 10.1016/j.mehy.2014.04.033. Epub 2014 May 9.