The range of people who are genetically XY include those who are born with an external female genital appearance and never, even at puberty, are exposed to male levels of androgen as they are either unable to respond to or synthesise potent androgens. There are no issues/

https://twitter.com/drmjoyner/status/1819839017564746093

Of unfairness or XS risk in such people being allowed to participate in competitive, even combative, female sports. This is not the case with 5 alpha reductase deficiency where pubertal development of skeleton and musculature occurs in response to testosterone levels 10 to 20/

Yesterday , at Memorial Sloan Kettering I met very successful young clinician scientist and medical oncologist. Having graduated from the Cambridge MBPhD programme she took one look at UK post grad training and left. In the USA after 1 yr internship, 2 years residency and 1 yr/

https://twitter.com/bykatewomersley/status/1761405479912128872

full time clinical fellowship and 3 as 20% + 80% research she is practising as an independent specialist in her discipline and leading a growing and increasingly successful lab. This is not a unique case. the American Board of Internal Med. has created/abim.org/certification/…

Delighted to see our work on post-prandial insulin resistance published nature.com/articles/s4158… Its the result of a great collaboration with, among others, #ClaudiaLangenberg @omicscience, @DPhaz @klmohlke, #EleanorWheeler and #NickWareham The first author is Alice @ AC_Williamson, a terrific PhD student with Claudia and me. In 2000 with @satya Dash009 , #David Savage we described a family where a mutation in a Rab-GAP for GLUT4, TBC1D4, impaired GLUT4 translocation in response to insulin in muscle and fat/2.

As a young teenager growing up in Ireland in the early 1970s, when daily news was a torrent of identity politics fuelling hatred and violence, the copies of Scientific American @sciam that my father regularly bought for me were like refreshing draughts of sanity. It was clear

https://twitter.com/doctorveera/status/1476493953616596992

that the elegant beauty of biology and the potential usefulness of its ingenious application transcended any racial or religious boundaries and held out the hope of helping all of humanity. How depressing to read in the pages of this once inspiring journal that "empiricism" is

There's no doubt that biology strongly influences the risk of becoming obese. Evidence for reduced energy expenditure being involved is much weaker than for variation in control of appetite. Not sure that the results of the fasting studies cited below support the latter /

https://twitter.com/AbdTahrani/status/1360711433739243521

e.g. Take an obese person with 60Kg lean and 40kg fat and a lean person with 60kg lean and 10 kg fat and deprive them of all calories. Glycogen will disappear rapidly and they will both burn fat (9 kCal/G) at rate determined by the largely by their lean mass /

Before I go off Twitter for a week or so to get on with proper work it might be helpful, at least for some correspondents, to review a few pretty well established facts
1. Obesity has become more common in the recent past (precise trajectories depend on which country) \ 2 This is very unlikely to have anything to do with genetics
3. This is most likely to do with an obesogenic food environment combined with a reduced need to expend energy in work and domestic life
4. In all societies, and at all times, some people have been obese and some not

Here is a testable hypothesis for why male sex, BMI, ethnicity and T2D status are related to COVID 19 mortality. Unlike ppl with hypertension, T2D pts who die get ventilated more frequently (recent NYC JAMA paper). The infection obviously impairs their alveolar function. For any given BMI, males and ppl of sth asian ethnicity tend to have more ectopic lipid. Women/Caucasians store more in sub. cut. adipocytes. Lung alveolar cells can accumulate lipid pathologically in overnourished states (PMID 20061442). Could impair their response/survival.