The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 20 No. 1 • February 2017


ASSOCIATION OF FEAR OF TERROR WITH LOW-GRADE INFLAMMATION

The fear of terror from terrorists could be processed in the brain like fear from many severe sources of unpredictable danger. In each case, there are similar mechanisms, one of which is inflammation.

Israel is a place where the fear of terror is chronic, present on a day-to-day basis. Scientists from Tel-Aviv University and other Israeli institutions studied the effect of the fear of terror in 1,152 apparently healthy employed adults (721 men and 431 women aged 20-70) to test the hypothesis that “chronic fear of terror may be associated with low-grade inflammation” by measuring high sensitivity C-reactive protein (CRP), a commonly used indicator of inflammation (Melamed, 2004). (Chronically high levels of inflammation, as indicated by increased C-reactive protein, are associated with an increased risk of cardiovascular disease.)

The results were sexually dimorphic: “Chronic fear of terror in women, but not in men, is associated with elevated CRP levels, which suggests the presence of low-grade inflammation and a potential risk of cardiovascular disease.” “They [the women] not only appraised the situation as more threatening and expressed higher fear of terror, but this also appears to have negative implications to their physical health.” “Elevated CRP levels (>3.0 mg/L) were found in 24.5% of the men and 31.1% of the women.”

Since there is no way for an individual to control the uncertain occurrence of terrifying incidents, preventing the low-grade inflammation that mediates much of the negative health aspects of chronic fear is a possible way to maintain health while living in a state of fear. As noted above, EGCG has been shown in a study to reduce the level of CRP, C-reactive protein, in old rats.

A TERRORIZED POPULATION MAY HAVE A HIGHER LEVEL OF C-REACTIVE PROTEIN

As mentioned above, a recent study found that a “highly traumatized civilian population” had elevated levels of C-reactive protein, an inflammatory marker associated with high levels of stress and a biomarker for increased risk of cardiovascular and metabolic diseases. The “highly traumatized civilian population” were 2692 men and women who were recruited from an inner city hospital (Grady Memorial Hospital in Atlanta, GA) that treated primarily African Americans (Michopoulos, 2015).

Increased CRP was associated with PTSD (posttraumatic stress disorder) symptoms and fear physiology, including “hyperarousal” symptoms, all sounding very much like a “highly traumatized” population. “Individuals with PTSD show elevated levels of the inflammatory cytokines IL-6, IL-1beta, and IL-2...[and] peripheral levels of inflammatory molecules correlate with PTSD symptomology (Michopoulos, 2015).”

A second paper (Shenhar-Tsarfaty, 2014) also studied the relationship between C-reactive protein (CRP) and physiological correlates of chronic fear in a highly traumatized population, 17,380 apparently healthy adult volunteers in Israel. While average maximal pulse values tend to decrease with age (Shenhar-Tsarfaty, 2014), here they found 4.1% of the volunteers had annual pulse increases. Moreover, the observed pulse increases were correlated with elevated CRP levels. The authors concluded: “...consistent exposure to terror threats ignites fear-induced exacerbation of preexisting neuro-immune risks of all-cause ­mortality.”

They explain these results, in part, by noting that pulse is controlled by a number of genetic, environmental and other endogenous factors that “include excessive inflammation, shown to associate with pulse increases [and] to be controlled by cholinergic imbalance (decreased vagal tone or increased sympathetic activity), and to increase mortality (Shenhar-Tsarfaty, 2014).”

References

Melamed et al. Association of fear of terror with low-grade inflammation among apparently healthy employed adults. Psychosom Med. 66:484-91 (2004).

Michopoulos et al. CRP genetic variation and CRP levels are associated with increased PTSD symptoms and phy siological responses in a highly traumatized civilian population. Am J Psychiatry. 172(4):353-62 (2015).

Shenhar-Tsarfaty et al. Fear and C-reactive protein cosynergize annual pulse increases in healthy adults. Proc Natl Acad Sci U S A., published online Dec. 22, 2014, pp. E467-71.

C-REACTIVE PROTEIN LEVELS INCREASED IN THOSE WITH PTSD (POSTTRAUMATIC STRESS DISORDER)

Increased systemic inflammation has been linked to certain stress-induced psychopathologic disorders, such as posttraumatic stress disorder. In a recent paper (Michopoulos, 2015), researchers found that increased CRP (C-reactive protein) levels were associated with fear-related psychopathology and PTSD in subjects recruited from an inner city public hospital (Grady Memorial Hospital, Atlanta, GA) that primarily served African Americans.

(In addition, CRP levels were found to differ depending upon CRP gene variants, single nucleotide polymorphisms (SNPs). One particular SNP, rs1130864, was found to be significantly associated with increased PTSD symptoms.)

Since C-reactive protein is increased under inflammatory conditions and is itself a promoter of inflammation, a substance that can reduce the levels of C-reactive protein could possibly be beneficial to those under extreme stress or who have a stress-related disorders such as PTSD.

Delayed inhibition of stress or its prolongation can increase susceptibility to many conditions, including cardiovascular disease, diabetes, allergy, immune system disorders, cancer, schizophrenia, Alzheimer’s disease, and depression (Wong, 2010). In fact, C-reactive protein is considered a marker for increased risk of cardiovascular disease and is included in most lab test panels to evaluate CVD risk.

As mentioned above, EGCG was shown to reduce C-reactive protein levels in old rats.

References

Michopoulos et al. CRP genetic variation and CRP levels are associated with increased PTSD symptoms and physiological responses in a highly traumatized civilian population. Am J Psychiatry. 172(4):353-62 (2015).

Wong et al. Stress and adrenergic function: HIF1alpha, a potential regulatory switch. Cell Mol Neurobiol. 30:1451-7 (2010).

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