4 replies to this topic

[HighDesertWizard]

There are studies that provide evidence associating Inflammation with Telomere Length Shortening. To date, as far as I know, there are none that provide evidence of a causal relationship between Inflammation and Telomere Shortening.

 

This study, published in July 2014, appears to provide evidence of a causal relationship, although, without access to the full study text, it's impossible to tell.

 

Among the questions I have is this... Are there more Inflammatory Cytokines that were found to shortern telomeres than just IL-1B?

 

Thoughts?

 

Inflammation, Telomere Length, and Grip Strength: A 10-year Longitudinal Study

 

Abstract

Telomere attrition has been associated with age-related diseases, although causality is unclear and controversial; low-grade systemic inflammation (inflammaging) has also been implicated in age-related pathogenesis. Unpicking the relationship between aging, telomere length (TL), and inflammaging is hence essential to the understanding of aging and management of age-related diseases. This longitudinal study explored whether telomere attrition is a cause or consequence of aging and whether inflammaging explains some of the associations between TL and one marker of aging, grip strength. We studied 253 Hertfordshire Ageing Study participants at baseline and 10-year follow-up (mean age at baseline 67.1 years). Participants completed a health questionnaire and had blood samples collected for immune–endocrine and telomere analysis at both time points. Physical aging was characterized at follow-up using grip strength. Faster telomere attrition was associated with lower grip strength at follow-up (β = 0.98, p = 0.035). This association was completely attenuated when adjusted for inflammaging burden (p = 0.86) over the same period. Similarly, greater inflammaging burden was associated with lower grip strength at follow-up (e.g., interleukin [IL]-1β: β = −2.18, p = 0.001). However, these associations were maintained when adjusted for telomere attrition (IL-1β, p = 0.006). We present evidence that inflammaging may be driving telomere attrition and in part explains the associations that have previously been reported between TL and grip strength. Thus, biomarkers of physical aging, such as inflammaging, may require greater exploration. Further work is now indicated.

Edited by wccaguy, 28 October 2014 - 08:02 PM.

[HighDesertWizard]

Found the complete text of the study for free here.

[GreenPower]

If inflammation drives telomere shortening, you might want to avoid eating food which cause chronic low-grade inflammation. According to Wikipedia this includes stuff like sugar, white rice, corn and alcohol. Instead you would probably want to eat a Mediterranean diet or LCHF.

 

[Darryl]

There haven't been any studies on white rice and inflammation, per se, only some ecological studies that indicated a dietary pattern with lower glycemic load was associated with lower hsCRP. Not surprising since a lot of things in typical high GL diet are crappy, like sugar sweetened drinks and pizza, with few of the compounds known to supress inflammatory response. And the best study to date actually found no effect of GL on hsCRP, indeed an inverse relationship among the obese.

 

I'd hesitate to recommend LCHF diets to any longevity practitioners. But if you must, pay attention to the fat content, as higher dietary and membrane saturated fat, as well as a poor ω-3 to ω-6 ratio among PUFAs, are consistently associated with markers of inflammation. 

 

So far, the studies that associate telemere length and diet indicate a protective role for vegetable, fruit, and fiber intake, and accelerated attrition with higher processed meat, dairy fat (butter, cheese, whole milk), and linoleic acid intake.

 

Noto, H., Goto, A., Tsujimoto, T., & Noda, M. (2013). Low-carbohydrate diets and all-cause mortality: a systematic review and meta-analysis of observational studies. PloS one, 8(1), e55030.

Griffith, J. A., Ma, Y., Chasan-Taber, L., Olendzki, B. C., Chiriboga, D. E., Stanek III, E. J., ... & Ockene, I. S. (2008). Association between dietary glycemic index, glycemic load, and high-sensitivity C-reactive protein. Nutrition,24(5), 401-406.

Galland, L. (2010). Diet and inflammation. Nutrition in Clinical Practice, 25(6), 634-640.

Nettleton, J. A., Diez-Roux, A., Jenny, N. S., Fitzpatrick, A. L., & Jacobs, D. R. (2008). Dietary patterns, food groups, and telomere length in the Multi-Ethnic Study of Atherosclerosis (MESA). The American journal of clinical nutrition,88(5), 1405-1412.

Cassidy, A., De Vivo, I., Liu, Y., Han, J., Prescott, J., Hunter, D. J., & Rimm, E. B. (2010). Associations between diet, lifestyle factors, and telomere length in women. The American journal of clinical nutrition, ajcn-28947.

Marcon, F., Siniscalchi, E., Crebelli, R., Saieva, C., Sera, F., Fortini, P., ... & Palli, D. (2012). Diet-related telomere shortening and chromosome stability.Mutagenesis, 27(1), 49-57.

Song, Y., You, N. C. Y., Song, Y., Kang, M. K., Hou, L., Wallace, R., ... & Liu, S. (2013). Intake of small-to-medium-chain saturated fatty acids Is associated with peripheral leukocyte telomere length in postmenopausal women. The Journal of nutrition, jn-113.

[Darryl]

Another study:

 

Lian F et al. 2015. Effect of vegetable consumption on the association between peripheral leucocyte telomere length and hypertension: a case–control study. BMJ open, 5(11), e009305.

In normotensive controls (n=455), higher vegetable intake was associated with longer age-adjusted RTL (p=0.01), while regular consumption of soya milk (p=0.01) and regular consumption of fried food (p=0.045) were associated with shorter telomere length. We did not observe significant associations between other dietary factors (fruit, meat, poultry, fish/seafood, milk, dessert and salt) and telomere length.