Does Extreme Obesity in Pregnancy Affect Baby's Health?

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The new study reveals the optimal weight gain for women that would give them a balanced risk of having a very small or very large baby. The findings will enable healthcare providers to give their patients more personalized recommendations. The team has developed an online calculator that can advise women on their ideal weight gain for the safest birth outcome, based on the research.

"The results of our research provide a solution to the conundrum affecting the 135 million pregnancies per year on this planet," said lead author Dr. Pierre-Yves Robillard. "Women want to know what their optimal weight gain should be to have their baby as safely as possible, and their maternity care providers want to know what advice they can give women throughout their pregnancy. While our results show the recommendations are fine for women in the normal weight range, we have shown they are not ideal for very underweight and very overweight women."

There is a strong link between the weight of mother and baby: very underweight mothers tend to have smaller babies – called small for gestational age (SGA) babies – and morbidly obese mothers tend to have more large for gestational age (LGA) babies. These babies are at higher risk of conditions like heart attacks, hypertension, obesity and diabetes as adults than babies born at normal weight.

In order to ensure babies have the safest births and healthiest lives possible, there are guidelines recommending the ideal weight gain during pregnancy based on body mass index (BMI). These guidelines, set by the US Institute of Medicine in 2009, have been subject to some controversy: in countries where women are generally smaller, such as Japan and Korea, healthcare providers have suggested the weight gain at the lower end of the spectrum is not sufficient. With the increasing burden of obesity in many countries, it has been suggested that very obese women should in fact lose weight during pregnancy.

To test these claims, Dr. Robillard and the team carried out a 16.5-year observational study. They recorded the pre-pregnancy BMI, weight gain, and weight of the baby of 52,092 women who gave birth at full term. The first finding was that only women with a normal BMI had a balanced risk of having an SGA or LGA baby (both 10 percent risk); they call this crossing point the Maternal Fetal Corpulence Symbiosis (MFCS).

They then looked at how this MFCS shifted with BMI and weight gained during pregnancy. They pinpointed for each BMI category what the optimal weight gain should be for a balanced risk of having an SGA and LGA baby. This revealed that although the current recommendations are correct for women with a normal BMI, they are not correct for underweight or obese women.

According to the study, a woman with a BMI of 17 should gain about 22kg instead of the recommended 12.5-18kg. An obese woman with a BMI of 32 should gain 3.6 kg instead of the recommended 5-9kg. And a very obese women with a BMI of 40 should actually lose 6kg.

"We were surprised to find such a linear connection between BMI, weight gain and MFCS," said Dr. Robillard. "The results will greatly facilitate an individualized approach when advising women about their optimal weight gain during pregnancy without having to put them into fixed categories – using the equation we uncovered, it's possible to give specific advice based on the exact BMI of the woman."

The results have already led to an online calculator in which a woman can enter their height and weight to get a specific recommendation for her optimal weight gain, based on the research results. This could be developed into an app for women and their healthcare providers. 

Source: medicalexpress.com

Combating childhood obesity by preventing 'fatty liver' in fetus

Fat content in fetal livers at the end of pregnancy from, A) fetus of a normal weight mother during pregnancy and B) fetus of an obese, overweight mother during pregnancy. The red stain represents fat. Credit: Edward Dick

 "New research published in The Journal of Physiology indicates that an obese pregnant mother and exposure to a high fat, high sugar diet during pregnancy produces a "fatty liver" in the fetus, potentially predisposing children to obesity, metabolic and cardiovascular disorders later in life. The research aims to understand the cellular mechanisms involved in laying down fat in the liver of a fetus - leading to a "fatty liver". This knowledge is essential to developing strategies to combat childhood obesity.

Throughout the world over fifty percent of women of reproductive age are either overweight or obese. Obesity in pregnant women, combined with intake of high-fat, high-sugar diets during pregnancy predisposes their children to obesity and other chronic metabolic and cardiovascular diseases. These complications probably account for a significant proportion of the current epidemic of childhood obesity.

This research aimed to shed light on the mechanisms underlying this link between obese pregnant mothers and obesity in their child, called developmental programming, which is currently poorly understood. This study found that when a fetus develops in an obese pregnant mother, fat accumulates in its liver and many metabolic pathways are disturbed. This is the first study to report that important recently discovered microRNAs (a DNA product which modifies protein synthesis) play a role in this increased deposition of fat in the liver in our closest relatives, the nonhuman primates. The observations of this study may explain why children of obese mothers live shorter lives than the offspring of normal weight mothers.

While there is always some fat in the liver, when the liver fat increases above normal an individual is said to have a "fatty liver". As the amount of liver fat increases, troubles begin. If this is dealt with early, it can be reversed, however if fat deposition persists, the damage can lead to liver scarring and even later life liver cancer. Therefore it is important to understand the early cellular mechanisms involved in laying down the fat early in life while the fetus is developing.

The research was a joint collaboration between University of Wyoming at Laramie Wyoming, the Texas Biomedical Research Institute, San Antonio, Texas, Wake Forest Baptist Medical Centre, Indiana University School of Medicine and the University of Texas Health Science Center. In order to determine which genes were changed in the fetal liver of obese pregnant monkeys and to identify which microRNAs regulate these genes, genomic and epigenomic methods were used. The altered cellular signalling pathways were identified using bioinformatics approaches, and microscopic studies were conducted to quantify the amount of stored fat and sugar present in the liver cells, as well as assessing their shape, which is an indicator of liver cell health..."

Learn more:

https://medicalxpress.com/news/2018-03-combating-childhood-obesity-fatty-liver.html

Inflammation in testes could explain link between obesity and reduced fertility

image credit: news.com.au

"A new study sheds light on how obesity may contribute to male infertility. Published in open-access journal Frontiers in Physiology, the study reports that obese men have increased levels of inflammatory markers in their seminal fluid and lower sperm quality, both of which correlate with their body mass index (BMI). The findings suggest that chronic inflammation in male reproductive organs explains the link between obesity and reduced fertility.

Obesity is a significant global health issue and is on the increase. In addition to variety of chronic illnesses, such as diabetes and cardiovascular disease, obesity is also linked to reduced sperm quality and male infertility. Scientists have also linked obesity to increased inflammation. Obese people can experience chronic inflammation in various tissues, and previous studies show that fat cells can produce and release specific signaling proteins that cause inflammatory responses.

Some studies have linked chronic inflammation to impaired sperm production and function -- however it was unknown whether obesity-related inflammation could influence fertility. Researchers from China hypothesized that the chronic inflammation associated with obesity might affect the male genital tract, which includes reproductive organs including the testes, providing a potential mechanism to explain the link between obesity and male infertility.

To investigate this, the researchers compared the level of inflammatory markers in the genital tracts of normal male mice and those fed a high fat diet to become obese. They found that the obese mice showed structural changes in their testes and changes in sex hormone expression. This included decreased levels of testosterone -- a sex hormone which can help maintain the protective blood-testes barrier, an important shield that protects delicate tissues in the testes from components in the blood..."

Learn more:

https://www.sciencedaily.com/releases/2018/02/180207120642.htm

 

Couples with obesity may take longer to achieve pregnancy

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"Couples in which both partners are obese may take from 55 to 59 percent longer to achieve pregnancy, compared to their non-obese counterparts, according to a study by researchers at the National Institutes of Health.

The findings appear online in Human Reproduction.

"A lot of studies on fertility and body composition have focused on the female partner, but our findings underscore the importance of including both partners," said Rajeshwari Sundaram, Ph.D., a senior investigator in the Division of Intramural Population Health Research at NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development. "Our results also indicate that fertility specialists may want to consider couples' body compositions when counseling patients."

The couples in the study were part of the Longitudinal Investigation of Fertility and the Environment (LIFE) Study, which examined the relationship between fertility and exposure to environmental chemicals. The study enrolled 501 couples from Michigan and Texas from 2005 to 2009. The women ranged from 18 to 44 years of age, and the men were over 18 years old. Women kept journals to record their monthly menstrual cycles, intercourse and the results of home pregnancy tests. The couples were followed until pregnancy or for up to one year of trying to conceive..."

Learn more: 

https://www.sciencedaily.com/releases/2017/02/170203085147.htm

Nature and nurture work in unexpected ways to determine obesity and diabetes risk even before birth

via americanpregnancy.com

"Few too many sugary treats during pregnancy put children at higher risk of becoming overweight, A*STAR research shows, but only if their mothers are not already obese. "It is interesting to see how nature and nurture interact to affect a child's outcomes," says principal investigator Yung Seng Lee, from the A*STAR Singapore Institute for Clinical Sciences (SICS).

"Excessive and rapid growth during infancy is a risk factor for obesity, and could lead to comorbidities such as diabetes and cardiovascular disease," adds SICS research fellow Izzuddin Aris.

One of the first studies to look at the role of maternal nutrition in child development was the Dutch famine study. In 1944–1945, Germany's occupation of the Netherlands resulted in food shortages and rationing to less than a quarter of the recommended daily caloric intake for an adult. Babies born during this period had higher rates of diabetes, cardiovascular disease and obesity later in life.

Izzuddin and Lee wanted to investigate this mother–child relationship in an Asian population. "Asians are at higher risk of diabetes at a lower body mass index compared to Caucasians," says Lee. "We have to conduct our own studies to look at the determinants and risk factors, which might be different—we can't take data from the West wholesale for our public health decisions."

The source of their analysis came from GUSTO (Growing Up in Singapore Towards healthy Outcomes); a SICS-led long-term study of pregnant mothers and their babies visiting KK Women's and Children's Hospital and the National University Hospital in Singapore.

The researchers analyzed the body fat and blood sugar levels of more than 900 mothers during their pregnancies and the size and weight of their children (from newborns up to three year olds). Obese mothers were found to have heavier children compared to non obese mothers, but the two groups' sugar levels showed a different story..."

Learn more:

http://medicalxpress.com/news/2016-06-nature-nurture-unexpected-ways-obesity.html

New links between heart hormones, obesity and diabetes new research reveales

via recoverwellness.com

"A new research study has revealed an important relationship between proteins secreted by the heart and obesity, glucose intolerance, and insulin resistance. The findings, published today in Obesity, offer a new approach to treating metabolic disorders, including type 2 diabetes, by targeting the pathway that controls the proteins' concentration in the blood.

"Our results illustrate how the regulation of cardiac natriuretic peptides (NPs) is altered in obesity, insulin resistance, and type 2 diabetes," said study co-author Sheila Collins, Ph.D., professor in the Diabetes and Obesity Research Center at Sanford Burnham Prebys Medical Discovery Institute (SBP). 

"When we examined fat (adipose) tissue from patients with these metabolic conditions, we found higher levels of the receptor that clears NPs from circulation, suggesting that if we can boost NP levels and/or reduce the level of its clearance receptor, we may be able to correct some of these conditions."

The double life of NP hormones

NPs are hormones produced by the heart that are primarily known for their ability to influence blood pressure. When the heart senses elevated pressure, it releases NPs, which go to the kidneys, triggering the body to release salt and water from the bloodstream to lower blood pressure. NPs prompt the response to blood pressure by signaling through an active receptor (NPRA), and are removed from the blood by a clearance receptor (NPRC). Both receptors contribute to the level of NP activity..."

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