Global warming, brown fat and diabetes

In 2009 three influential back-to-back papers appeared in the renowned New England Journal of Medicine which conclusively demonstrated that even mild cold exposure could activate brown adipose tissue, thereby dramatically increasing resting energy expenditure in humans:

  1. Cypess AM, Lehman S, Williams G, Tal I, Rodman D, Goldfine AB et al. Identification and importance of brown adipose tissue in adult humans. N Engl J Med 2009; 360(15):1509-1517.
  2. Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, Drossaerts JM, Kemerink GJ, Bouvy ND et al. Cold-activated brown adipose tissue in healthy men. N Engl J Med 2009; 360(15):1500-1508.
  3. Virtanen KA, Lidell ME, Orava J, Heglind M, Westergren R, Niemi T et al. Functional brown adipose tissue in healthy adults. N Engl J Med 2009; 360(15):1518-1525.

This fascinating finding immediately prompted me to write a letter, together with my colleague Hanno Pijl, in response in which I postulated that based on these findings global warming might actually worsen the obesity pandemic (bearing in mind Newton’s law of cooling). However, our letter was unfortunately rejected without peer-review. Seven years later (!) another study was published by Hanssen et al. which prompted me again to contact Hanno Pijl, who brought me into contact with Patrick Rensen and Lisanne Blauw, and together we finally managed to conduct a more thorough examination of the relation between rising global temperatures and the incidence of diabetes in the United States, as well as the prevalence of glucose intolerance worldwide. And the results were fascinating indeed as you can read here.  The article was widely covered in the international media and has already been downloaded more than 13500 times!  So a happy end after all you might think, but unfortunately I don’t think so as long as some lunatic ‘world leaders’ are just flatly denying the very concept of global warming (very, very, very sad…)

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Pokémon Go, nudge theory and infectious diseases

Here is how we think that Pokemon Go might be utilized to prevent infectious diseases spread: Please bear in mind that it is hypothesis!

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“Reducing the connectivity of the Pokémon Go network to limit transmission of infectious diseases. A) In a normal situation, players of Pokémon Go interact in a “small world network”, in which players (blue dots) battle each other at PokéGyms (red dots). Some players become “hubs” in the network by visiting multiple PokéGyms (green dots). B) If an infectious disease breaks out in a specific part of the city (green area), a virtual quarantine could be instituted by strategically modifying which PokéGyms are visible to individual players.”

 

 

The role of DNA repeats in depression

Please check our recent paper published in Translational Psychiatry in which we showed that DNA repeat polymorphisms in two particular genes, i.e. ATXN7 and TBP, were associated with the risk of lifetime depression in two large and well-characterized Dutch cohorts — the Netherlands Study of Depression and Anxiety (NESDA) and the Netherlands Study of Depression in Older Persons (NESDO) —including 2165 depressed and 1058 non-depressed individuals. We found that carriers of either ATXN7 or TBP alleles with relatively large CAG repeat sizes in both alleles had a substantially increased risk of lifetime depression. I believe that these as well as many other DNA repeat polymophisms could actually account for a substanial degree of ‘missing heritability’, and not only of depression. The paper is open access, so please feel free to disseminate!

Gardiner SL, Van Belzen MJ, Boogaard MW; Van Roon-Mom WM, Rozing MP, Van Hemert AM, Smit JH, Beekman AT, Van Grootheest G, Schoevers RA, Oude Voshaar RC, Comijs HC, Penninx BW, Van der Mast RC, Roos RA, Aziz NA (2017). Large normal-range TBP and ATXN7 CAG repeat lengths are associated with increased lifetime risk of depression. Translational Psychiatry. 7(6): e1143. doi: 10.1038/tp.2017.116.

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Brain and Nature…

Recently our research letter was accepted for publication in Brain. In this paper we show for the first time that CAG repeat length variations in genes other than the HTT gene may also affect phenotype in patients with Huntington disease. Interestingly, only two weeks after our paper was accepted for publication, another intriguing paper was published in Nature by David Rubinsztein’s group which could provide a mechanistic basis for interactions among polyglutamine-disease associated genes through polyglutamine-length dependent competitive interactions among the encoded proteins and regulators of autophagy. Fascinating!

Entropy and epidemiology…

A few days ago I posted a preprint of a methodological paper in which I examine the potential value of a new measure grounded in information theory called ‘transfer entropy’ for analyzing observational epidemiological data (Transfer entropy as a tool for inferring causality from observational studies in epidemiology. ). I posted it on ‘bioRxiv’ (dubbed ‘The Preprint Server for Biology’ by the makers) which is a new website very similar to ‘arxiv’ but with a focus on life sciences. I think that the paper needs more polishing for final publication, so please feel free to comment! That is the whole idea behind publishing preprint: To allow peers to review a piece before it gets eternalized.

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