About Me

I am an Assistant Professor in the Department of Epidemiology at Columbia University Mailman School of Public Health and the Robert N Butler Columbia Aging Center. I was a Jacobs Foundation Research Fellow  from 2016-2018.

I work at the intersection of genetics, the social and behavioral sciences, and public health.  My work brings together discoveries from the cutting edge of genome science and longitudinal data from population-based cohorts to identify mechanisms that cause accelerated health decline in older age. I take a life-span approach that encompasses research on cohorts of children, young and middle-aged adults, and older adults. My goal is is to understand why socioeconomically disadvantaged populations suffer increased morbidity in older age and earlier mortality, and to devise strategies for intervention to mitigate these health inequalities.

Research Areas of Interest

  • Aging
  • Health disparities and social gradients in health
  • Genetic/Genomic Epidemiology – Life course and developmental approaches

My CV

Papers

Affiliations
Center for the Study of Aging and Human Development
Duke Population Research Institute (DuPRI)

 

 

Contact

Email  daniel.belsky@columbia.edu

Tel. 212-304-7580

 LinkedIn

Research Gate

19 thoughts on “About Me

  1. The biological aging study is super freaking cool. I had a question – what’s the breakdown of aging effects by race? I saw that only 7% of the population had “partial non-Caucasian” ethnicity so maybe it’s not very significant but I was curious nonetheless. Thanks!

  2. Dear Prof Belsky,

    I read your Quantification of biological aging in young adults paper with great interest and wanted to share with you an idea I have had for some years now about a possible mechanism for aging that might warrant investigation.

    It has always intrigued me that as people age the amount of slow wave sleep that they get declines. SWS is of course associated with growth and repair of the body’s cells and more recently been shown to be necessary for the formation and consolidation of memory.

    It seems to me that it is possible that the decline in SWS perhaps has some causal role in aging, and perhaps could explain to some extent the different rates of aging that you observe in your research as SWS decline doe not progress at a universal speed.

    A cross sectional correlation study looking at the relationship between the nature of sleep, (specifically total SWS time) and indications of relative age would be an interesting way to initially investigate this relationship.
    The relationship between aging and memory decline could also be partly explained be the loss of SWS again a cross-sectional study looking at the relationship between total average SWS time and age related memory decline would be an interesting start point.
    If a relationship could be established then therapeutic applications based on increasing total SWS could be developed?
    I am a secondary school psychology teacher and have no way of investigating any of these ideas, if you like them or know anybody who might be interested in them I’d be happy to just get my name on any paper that was published!
    Kind regards
    Peter Ions
    Head of Psychology
    Kingsdale School
    London

  3. Hi Dan,

    You have done a very interesting study. Here are some points I would make, after spending 25 years studying diseases, nutrition and ageing:

    1. Your markers of ageing are more likely to be markers of pre-clinical disease: we badly need genuine age-markers–even telomere length has been related to anxiety, rather than ageing per se.

    2. The above diseases, like vascular disorders and diabetes, have their own specific causes, and are not age-related: they simply take time to develop, like any chronic, slow-onset disease. If they were truly age-related, then all old folks would get them eventually–but they don’t.

    3. I strongly suspect that faster-ageing folks are simply anxious people suffering chronic effects of stress hormones–I would expect such folks to also show fatigue, declining grip strength, cognitive problems, and reduced libido and immunity. In addition, all these problems would be worse in anxious folks eating a pro-inflammatory fatty diet [or smoking], which converts straight anxiety to clinical depression.

    4. Anxiety disorder affects a third of Americans [and 1 in 4 Australians], and is now known to arise pre-natally, when the mother eats a fatty diet [Dr Elinor Sullivan, monkeys, Oregon; Dr Staci Bilbo, mice, N Carolina]. Fatty diet causes slight inflammation in all tissues, and an inflamed placenta allows the maternal stress hormone [cortisol] to reach and re-programme the unsuspecting foetal brain. Anxious offspring are at risk of diabetes, vascular disease, depression, osteoporosis, cravings and addictions etc., and so forth.

    5. Therefore, to ensure a long healthy life, we must start with nutritional midwives. And for existing cases of anxiety, there is a very simple answer [which ALSO restores restorative slow-wave sleep!!]. In grains, nuts, beans and citrus, we find the glucose isomer Myo-Inositol, an effective serotonin 2A receptor inhibitor, that is known to reverse anxiety, panic disorder, depression, obsessions etc.. I give 5 gm/day to my anxious worriers, and invariably they report calmness, enhanced energy, libido and immunity–and even their hair and nails grow faster [and stronger too].

    6. As an encore, the very same Myo-Inositol inhibits the pro-growth, pro-ageing Insulin-like Growth Factor-1 [IGF-1] signalling pathway–a sure route to both anti-cancer and anti-ageing benefits. I figured this out by studying the diets of unusually long-lived healthy and energetic oldsters, about 10 years ago. They often eat oat porridge, or legumes, all their life.

    7. At Albert Einstein College, in the Bronx, Prof Nir Barzilai studies Jewish centenarians in Manhattan: a few have IGF-1 receptor mutations, that suppress cellular IGF-1 pathway enzyme activity. He tests these enzymes in extracted white blood cells, and finds that the wonky receptor does indeed suppress pathway enzyme activation [reduced phosphorylation was observed].

    8. I suggest that this test may be the very best way to assess the rate of ageing, since high animal protein diets will activate the Growth Hormone/IGF-1 signalling axis [accelerating ageing], while plant-based diets rich in grains, beans etc., would reduce IGF-1 signalling, thereby activating 100s of longevity genes via FOXO and Nrf2 transcription factors.

    9. Even without any such formal testing, one may safely forecast a very long and energetic life, in any folks eating Myo-Inositol-rich foods regularly.

    10. I estimate the anti-ageing dose of Myo-Inositol to be about 2 gm daily, as from a serve of oat porridge, plus a large drink of orange juice. But anxiety suppression needs 3.0 to 5.0 gm a day, which requires powder supplement. High anxiety, panic and self-harm need about 10 gm a day, for 100% effect. Poor folks are lucky that grain and beans and citrus are very cheap foods, and they won’t be sorry if they eat them regularly.

    • Hi Robert,

      Thanks for your interest in our study.

      I agree with you that animal experiments suggest promise to slow aging through dietary modification. Now that measures like ours that track the aging process in real time in young, free living humans are becoming available, I hope we can soon see tests in humans.

      PS: You may be interested in my co-author Morgan Levine’s recent article on protein intake and aging — http://www.cell.com/cell-metabolism/abstract/S1550-4131(14)00062-X.

      Best wishes,

      Dan

  4. Dear Dan,

    Your paper “Quantification of biological aging in young adults” is very interesting. I was wondering if you or others are planning or executing validation studies to make this algorithm available as a predictive tool for ageing. Are there any such activities?

    Best regards,
    Tomris Cesuroglu

    • Hi Tomris,

      Thanks for your interest! We are definitely interested in this kind of possibility. If you are interested in clinical tools to measure aging that are available today, you might check out the folks at InSilico Medicine (http://insilicomedicine.com/). They have a tool called Aging.ai that uses clinical blood biomarker data to estimate biological aging (http://aging.ai/).

      Best wishes,

      Dan

  5. Hi Professor Belsky,

    I found your comments in the article from the January-February Harvard Business Review by Alison Beard fascinating and a very interesting read. To the best of your knowledge, is there any literature that you’d recommend for someone looking to educate themselves on this new field of ‘sociogenomics’? How do you see this niche field developing?

    Thanks for your thoughts!

    Peter

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  13. To the best of your knowledge, is there any literature that you’d recommend for someone looking to educate themselves on this new field of ‘sociogenomics’? How do you see this niche field developing? Thank you for sharing this post.

    • Hi Jasmine,

      Thanks for your interest!

      Here are some links to resources you may find of interest:

      Our 2016 article in Psychological Science might be one point of entry if you are interested in what to make of GWAS discoveries for educational attainment (link).

      I’ve written a bit about that study and why, more generally, it’s important to study genetics linked with educational and socioeconomic attainment. This post on the Jacobs Foundation’s BOLD Blog Why should we study the genetics of success? and this one on the NIH OBSSR Edge Blog might be helpful. Ed Young probably did a better job of it in the Atlantic. Carl Zimmer’s NYT piece is also a must-read.

      The Social Science Genetic Association Consortium (thessgac.org) is also a great resource. They conducted the original genetic studies of educational attainment and age-at-first-birth that we followed up. Their FAQs are a great resource for understanding what these new genetic discoveries do and do not mean. See also this post I co-wrote with Paige Harden about their recent GWAS of educational attainment. It discusses the recent GWAS findings as well as a follow-up analysis we did investigating how these genetics are related to patterns of social mobility.

      For thinking through moral and political implications, I recommend Paige Harden’s NYT Op Ed and also her posts on the Genetics of Human Agency Project website. Her blog there is called Fortune’s Favor.

      As for where the field is going, I would look to the new studies of “genetic nurture“. (see also this excellent editorial). This type of work opens a range of opportunities for using genes to better understand how social environments shape human health and behavior. Much of the work is focused on families (see Bates et al., Liu et al., and Wertz et al.). But there are also opportunities to study other types of social units. For example my colleague Ben Domingue has been looking into genetic influences operating at the level of peer and school networks. We wrote a piece about this type of work that provides a bit of an overview of the opportunities in this area that might be a place to start.

      A second research direction is work to map connections between genetic influences on different characteristics and behaviors. There is a surprising (or maybe not so surprising) amount of overlap between genetics discovered in studies of social attainments and behaviors and genetics discovered in studies of chronic disease and longevity. What genetic links between these outcomes means is a critical question for research integrating genetics and social sciences and, I would argue, for public health more generally.

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