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We are interested in the intersection of aging, obesity, diabetes and cardiovascular disease. These are progressing phenomena that affect all of us directly or indirectly through family and friends and account for the majority of deaths and chronic disease burden in the world. They are also difficult to treat and prevent in the obesogenic environment we are living in. Indeed, it would be easy to blame people for the food they eat and the lack of exercise but from an evolutionary point of view this is what we are supposed to do; eat as much as possible with the least effort possible. If you happen to be one of those people who has genetic susceptibility to gain excessive weight or get type 2 diabetes, the environmental exposure enables and escalates the pathogenesis and serious complications follow.

Luckily there are also people who are remarkably resilient against severe complications of metabolic diseases. For instance, Elisabeth Hughes Gossett was an adolescent with type 1 diabetes, and one of the first patients to receive insulin in the early 1920s. In light of modern standards, the treatment available during most of the 20th century was poor and outright dangerous, yet she lived into her seventies, had children, and even hid her disease from most people. Even without access to her medical files, it is all but certain that she had abnormal blood glucose levels throughout her adult life. A typical patient would have suffered from eye and kidney diseases, and probably died decades earlier due to a heart attack. Why did she survive? Was it something in her genetic make-up that protected her eyes and kidneys? Maybe it was something she ate or did? What if we figured out the molecular pathways involved, could we then reproduce her resilience in other people?

In March 2014, I was very fortunate to be placed into a position where I could connect a few of the dots on why some people get diseases while others do not. EMBL Australia and the University of Adelaide joined forces to create an EMBL Group Leader position in the brand new South Australian Health and Medical Research Institute (SAHMRI). We are still a very small group with myself and two postdocs Song Gao and Stefan Mutter (May 2015), but more people are already coming and we are actively seeking to expand our funding beyond the admittedly generous EMBL package. Current projects involve a fair bit of basic methodology to get things going especially on new areas such as dynamic big data analyses of large human cohorts, and we are heavily involved in network biology. We are also venturing into the wet lab with innovative study designs to bridge some of the gaps between mouse models and human biomedicine.

Today, many of the big chronic diseases such as diabetes and atherosclerosis are intertwined and the molecular risk factors are difficult to separate in the traditional reductionist ways; we postulate that systems biology and multimorbidity are the most effective paradigms for the discovery of new therapies and effective translation into interventions for the mosaic of phenotypic subgroups we see in human populations.

Ville-Petteri Mäkinen presenting a workshop to students on the 2019 PhD Course.

Highlight publications

Published In

Wang Q, Jokelainen J, Puukka K, Keinänen-Kiukaanniemi S, Järvelin MR, Kettunen J, Mäkinen VP, Ala-Korpela M

BMC Medicine (2019)  volume 17, Article number: 217.

Song G, Mutter S, Casey A, Mäkinen V-P

Int J Epidemiology (2018) 48:369-374.

Song G, Mutter S, Casey A, Sargeant T, Mäkinen V-P

Brain (2018) 144:2711-2720.

Shu L, Zhao Y, Kurt Z, Byars SB, Tukiainen T, Kettunen J, Orozco L, Pellegrini M, Lusis AJ,  Ripatti S, Zhang B, Inouye M,  Mäkinen VP & Yang X 

BMC Genomics 17:874.

Lithovius R, Toppila I, Harjutsalo V, Forsblom C, Groop PH, Mäkinen V-P

Diabetologia (2017) 60:1234-1243.


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A full list of Ville-Petteri Mäkinen's publications can be viewed on PubMed.