Sex-specific effects of tea consumption on methylation

Research out of Uppsala by Ek et al. showed an effect of tea consumption on methylation patterns in women, not in men. Coffee had no effect on methylation in either sex. While not a randomized trial, four large scale cohort data sets were used, giving the findings substantial weight.


Lifestyle factors, such as food choices and exposure to chemicals, can alter DNA methylation and lead to changes in gene activity. Two such exposures with pharmacologically active components are coffee and tea consumption. Both coffee and tea have been suggested to play an important role in modulating disease-risk in humans by suppressing tumour progression, decreasing inflammation and influencing estrogen metabolism. These mechanisms may be mediated by changes in DNA methylation. To investigate if DNA methylation in blood is associated with coffee and tea consumption, we performed a genome-wide DNA methylation study for coffee and tea consumption in four European cohorts (N = 3,096). DNA methylation was measured from whole blood at 421,695 CpG sites distributed throughout the genome and analysed in men and women both separately and together in each cohort. Meta-analyses of the results and additional regional-level analyses were performed. After adjusting for multiple testing, the meta-analysis revealed that two individual CpG-sites, mapping to DNAJC16 and TTC17, were differentially methylated in relation to tea consumption in women. No individual sites were associated with men or with the sex-combined analysis for tea or coffee. The regional analysis revealed that 28 regions were differentially methylated in relation to tea consumption in women. These regions contained genes known to interact with estradiol metabolism and cancer. No significant regions were found in the sex-combined and male-only analysis for either tea or coffee consumption.

Tea and coffee consumption in relation to DNA methylation in four European cohorts

Weronica E. Ek
Elmar W. Tobi
Muhammad Ahsan
Erik Lampa
Erica Ponzi
Soterios A. Kyrtopoulos
Panagiotis Georgiadis
L.H. Lumey
Bastiaan T. Heijmans
Maria Botsivali
Ingvar A. Bergdahl
Torgny Karlsson
Mathias Rask-Andersen
Domenico Palli
Erik Ingelsson
Åsa K. Hedman
Lena M. Nilsson
Paolo Vineis
Lars Lind
James M. Flanagan
Åsa Johansson
on behalf of the Epigenome-Wide Association Study Consortium

Hum Mol Genet ddx194.

An evergreen of human aging: Is there an upper bound to human lifespan?

Some very good points for the existence of an upper limit to how old humans can get are given in this paper by Dong, Milholland & Vijg in Nature (but see critique of stats and statements, linked below).

Vaupel and colleagues had argued previously that there was no such limit, based on analyses of Swedish cohorts that showed a steady increase of of maximum lifespan over the last 100 years up to the 1990s. In their paper, Dong et al. argue that this increase peaked in the mid 1990s, coincidentally that time when the world record holder of oldest age, Jeanne Calment, died at 122 years of age.

The authors close with these statements:

“To further extend human lifespan beyond the limits set by these longevity-assurance systems would require interventions beyond improving health span, some of which are currently under investigation. Although there is no scientific reason why such efforts could not be successful, the possibility is essentially constrained by the myriad of genetic variants that collectively determine species-specific lifespan.”


Evidence for a limit to human lifespan (Nature article)

First reactions can be found here:


Fun links (and data that was actually used in this paper):

The Human Mortality Database:

Supercentenarian (>110 years of age) List of the Gerontology Research Group:

Dietary restriction: a mechanism behind its lifespan extension effect

Vermeij et al. show that dietary restriction delays aging and extends lifespan in two mouse models of progeroid human aging, by alleviating DNA damage.

Progeroid syndromes are relatively rare genetic disorders that show premature aging-like symptoms, for example Werner’s syndrome, Cockayne syndrome, and Hutchinson-Gilford progeria syndrome.

Restricted diet delays accelerated ageing and genomic stress in DNA-repair-deficient mice

Nature 537 (427–431), 15 September 2016

IL-33 protein injection reverses Alzheimer’s symptoms in mice in just one week

“Mice bred to develop a progressive Alzheimer’s-like disease as they aged (called APP/PS1 mice) were given daily injections of the protein, and it appeared to not only clear out the toxic amyloid plaques that are thought to trigger Alzheimer’s in humans, it also prevented more from forming.‌‌” (original PNAS article)

Reversed antagonistic pleiotropy

Mitochondrial-targeted catalase (mCAT) has a negative effect on ROS levels, and overexpression of mCAT might therefore be beneficial in diminishing the negative effects of ROS on health and lifespan. This study on th effects of mCAT on teh proteome shows that overexpression of mCAT in early life might actually not be beneficial. (free full text)