Pregnancy in women after undergoing bariatric surgery are by no means uncommon. There is even some evidence from case series to suggest that babies born to mothers, who have undergone surgery may be less likely to become obese or experience the cardiometabolic complications of obesity.
This risk needs to be balanced against potential risks the known adverse effects of gastric bypass surgery on the metabolism of iron, vitamin B12, and folate,
Now a paper by Karl Johansson and colleagues, published in the New England Journal of Medicine, suggests that this may well be the case.
The researchers identified 627,693 singleton pregnancies in the Swedish Medical Birth Register from 2006 through 2011, of which 670 occurred in women who had previously undergone bariatric surgery and for whom presurgery weight was documented.
They found that pregnancies after bariatric surgery, as compared with matched control pregnancies, were associated with lower risks of gestational diabetes (1.9% vs. 6.8%; odds ratio, 0.25) and a lower incidence of large-for-gestational-age infants (8.6% vs. 22.4%; odds ratio, 0.33).
These potentially beneficial outcomes for the infant were counterbalanced by a two-fold increase in the likelihood of having a small-for-gestational-age infants (15.6% vs. 7.6%; odds ratio, 2.20) and a somewhat shorter gestation (mean difference -4.5 days)
Also, the risk of stillbirth or neonatal death was 1.7% versus 0.7% (odds ratio, 2.39).
No differences were found in the frequency of congenital malformations.
Bariatric surgery was associated with reduced risks of gestational diabetes and excessive fetal growth, shorter gestation, an increased risk of small-for-gestational-age infants, and possibly increased mortality.
Thus, the authors conclude that,
“…a history of bariatric surgery was associated with reduced risks of gestational diabetes and large-for-gestational-age infants.”
Nevertheless, they do recommend increased surveillance during pregnancy and the neonatal period, as bariatric surgery may also be associated with small-for-gestational-age infants, a shorter length of gestation, and potentially an increased risk of stillbirth or neonatal death.
For all my Canadian readers (and any international readers planning to attend), here just a quick reminder that the deadline for early bird discount registration for the upcoming 4th Canadian Obesity Summit in Toronto, April 28 – May 2, ends March 3rd.
To anyone who has been at a previous Canadian Summit, attending is certainly a “no-brainer” – for anyone, who hasn’t been, check out these workshops that are only part of the 5-day scientific program – there are also countless plenary sessions and poster presentations – check out the full program here.
To register – click here.
Researchers from the University of Alberta are conducting a short online survey to get a better understanding of the barriers and challenges you may experience related to gestational weight gain, and about what may help and support them to help women achieve healthy weights during pregnancy.
The researchers are also asking you to assess the strengths and limitations of the 5As of Healthy Pregnancy Weight Gain, a new resource from the Canadian Obesity Network.
This information will help to inform the development of universal strategies that promote healthy dietary intake and appropriate weight management in pregnancy and postpartum.
Your participation in this short survey is much appreciated.
Last week, Edward Archer from the University of Alabama at Birmingham (UAB), published a paper in the Mayo Clinic Proceedings (to much media fanfare), suggesting that the primary driver of childhood obesity is the shifting of nutrient energy to fetal adipose tissue as a result of increased maternal energy availability paired with decreased maternal energy expenditure, resulting in fetal pancreatic b-cell and adipocyte hyperplasia – a theory, which Edwards labels the “maternal resource hypothesis”.
The primary process for these changes, as readers of these pages will have read before, is through epigenetic modification of DNA, which, together with other non-genetic modes of transmission including learned behaviours and environmental exposures (socioenvironmental evolution), leads to “phenotypic evolution”, which Edward describes as,
“…a unidirectional, progressive alteration in ontogeny that is propagated over multiple successive generations and may be quantified as the change over time in the population mean for the trait under examination (eg, height and obesity).”
Since the beginning of the 20th century, socioevironmental factors have significantly altered the energy balance equation for humans
“Socioenvironmental evolution has altered the evolution of human energy metabolism by inducing substantial decrements in EE imposed by daily life while improving both the quality and the quantity of nutrient-energy availability.”
“For example, as thermoneutral environments became ubiquitous, the energy cost of thermoregulation declined, and improved sanitation (eg, clean water and safer food) and vaccinations decreased the energy cost of supporting parasites (eg, fleas) and resisting pathogens (eg, communicable diseases and diarrheal infections).”
Over the past century, these developments have led to profound phenotypic changes including,
“progressive and cumulative increases in height, body stature and mass, birthweight, organ mass, head circumference, fat mass/adiposity as well as decreases in the age at which adolescents attain sexual maturity…”
Archer goes on to describe some of the many factors that may have changed in the past century, whereby, he singles out sedentariness as one of the key drivers of these developments (not surprising given Archer’s background in exercise science).
Thus, although one could perhaps make very similar arguments for any number of factor that may have changed in the past century to, in turn, affect insulin resistance and ultimately energy partitioning (change in diet, sleep deprivation, increasing maternal age, endocrine disruptors, antibiotic use, gut microbiota, medication use and many other factors I ca think of), Archer chooses to elevate sedentariness to being the main culprit.
While this may or may not be the full story, it does not change the thrust of the paper, which implies that we need to look for the key drivers of childhood obesity in the changes to the maternal-fetal (and early childhood) environment that have put us on this self-perpetuating unidirectional cycle of phenotypic evolution.
Ergo, the solution lies in focussing on the health behaviours (again, Archer emphasizes the role of physical activity) of moms.
While Archer largely focusses on maternal transmission, we should perhaps not forget that there is now some also evidence implicating a role for epigenetic modification and intergenerational transmission through paternal DNA – yes, dads are getting older and more sedentary too (not to mention fatter).
I do however agree with Edward, that this line of thinking may well have important implications for how we approach this epidemic.
“…the acknowledgment that obesity is the result of non-genetic evolutionary forces and not gluttony and sloth may help to alter the moralizing and demoralizing social and scientific discourse that pervades both public and clinical settings.”
“Future research may be most productive if funding is directed away from naive examinations of energy balance per se and redirected to investigations of interventions that alter the competitive strategies of various tissues.”
“From the standpoint of the clinician, accurate patient phenotyping (inclusive of family obstetric history and metabolic profiling) may allow the targeting of women most likely to be a part of populations that have evolved beyond the metabolic tipping point and therefore require significant preconception intervention.”
While none of this may be easier or more feasible than other current efforts, they may well point us in a different direction than conventional theories about what is driving childhood obesity.
If you have a professional interest in obesity, it’s your #1 destination for learning, sharing and networking with experts from across Canada around the world.
In 2015, the Canadian Obesity Network (CON-RCO) and the Canadian Association of Bariatric Physicians and Surgeons (CABPS) are combining resources to hold their scientific meetings under one roof.
The 4th Canadian Obesity Summit (#COS2015) will provide the latest information on obesity research, prevention and management to scientists, health care practitioners, policy makers, partner organizations and industry stakeholders working to reduce the social, mental and physical burden of obesity on Canadians.
The COS 2015 program will include plenary presentations, original scientific oral and poster presentations, interactive workshops and a large exhibit hall. Most importantly, COS 2015 will provide ample opportunity for networking and knowledge exchange for anyone with a professional interest in this field.
Abstract submission is now open – click here
- Notification of abstract review: January 8, 2015
- Call for late breaking abstracts open: Jan 12-30, 2015
- Notification of late breaking abstracts and handouts and slides due : Feb 27, 2015
- Early registration deadline: March 3, 2015
For exhibitor and sponsorship information – click here
To join the Canadian Obesity Network – click here
I look forward to seeing you in Toronto next year!