Breastfeeding Babies Exposed To Diabetes In Utero Protects Against Childhood Obesity

Breastfeeding a baby exposed to diabetes in utero may help protect that infant from becoming obese during childhood, according to a study published in the February issue of Diabetes Care and an accompanying editorial, which noted that population-wide detection and treatment of gestational diabetes takes on even greater importance due to these findings.

Babies that were breastfed for six months or more, after exposure to maternal diabetes in utero, were no more likely to put on extra weight as children (ages 6-13) than those who were not exposed to diabetes, the study found. This effect was not realized, however, for babies breastfed less than six months. The results were consistent across ethnicities.

"Our data suggest that breastfeeding promotion may be an effective strategy for reducing the increased risk of childhood obesity in offspring of mothers with diabetes during pregnancy," said Dr. Dana Dabelea, Associate Professor in the Department of Epidemiology, Colorado School of Public Health, and lead researcher on the study. "Since childhood obesity and in utero exposure to maternal diabetes have both been associated with later development of type 2 diabetes, it follows that breastfeeding these children may also help reduce their future risk for developing type 2. However, further research would be needed to confirm that added protection."

The study also suggests that the early postnatal period may be a critical period for determining future obesity and diabetes risk, the researchers concluded. "The macronutrient composition of breastmilk (i.e. protein, fat, carbohydrate) and bioactive substances not present in formula may influence metabolic programming and regulation of body fatness and growth rate," they wrote.

Previous research has shown that children born to mothers who had diabetes during pregnancy are more prone to childhood obesity than those who are not, perhaps because they are "programmed" to put on extra weight due to exposure to their mother's excessive glucose levels during these critical stages of prenatal development.

In an editorial accompanying this study, Dr. Andreas Plagemann, of the Clinic of Obstetrics, Division of Experimental Obstetrics, Charite-University Medicine Berlin, wrote that the study reinforced the importance of breastfeeding and of testing and treating pregnant women for diabetes "to enhance not only the prenatal but also the neonatal nutritional environment of the offspring."

"Beyond its important role for mother-child binding, breastfeeding as compared to formula has a considerable number of positive short and long term effects on human development, such as a decreased incidence of high respiratory infections, a lower risk of asthma and atopy, and a decreased risk of high blood pressure, type 2 diabetes as well as type 1 diabetes," he wrote. "Moreover, profound evidence exists that breastfeeding has the potential to permanently decrease the long-term risk of developing obesity, as shown by the results of at least for meta-analyses on this issue."

 

Obesity And Diabetes May Be A Downside Of Human Evolution

New research in the FASEB Journal suggests that a gene called CMAH has been lost during the course of recent evolution, and may lead to an increased risk of Type 2 diabetes in humans

As if the recent prediction that half of all Americans will have diabetes or pre-diabetes by the year 2020 isn't alarming enough, a new genetic discovery published online in the FASEB Journal provides a disturbing explanation as to why: we took an evolutionary "wrong turn." In the research report, scientists show that human evolution leading to the loss of function in a gene called "CMAH" may make humans more prone to obesity and diabetes than other mammals.

"Diabetes is estimated to affect over 25 million individuals in the U.S., and 285 million people worldwide," said Jane J. Kim, M.D., a researcher involved in the work from the Department of Pediatrics at the University of California, San Diego in La Jolla, CA. "Our study for the first time links human-specific sialic acid changes to insulin and glucose metabolism and therefore opens up a new perspective in understanding the causes of diabetes."

In this study, which is the first to examine the effect of a human-specific CMAH genetic mutation in obesity-related metabolism and diabetes, Kim and colleagues show that the loss of CMAH's function contributes to the failure of the insulin-producing pancreatic beta cells in overweight humans, which is known to be a key factor in the development of type 2 diabetes. This gene encodes for an enzyme present in all mammalian species except for humans and adds a single oxygen atom to sialic acids, which are sugars that coat the cell surface.

To make their discovery, the researchers used two groups of mice. The first group had the same mutant CMAH gene found in humans. These mice demonstrated that the CMAH enzyme was inactive and could not produce a sialic acid type called NeuSGc at the cell surface. The second group had a normal CMAH gene. When exposed to a high fat diet, both sets of mice developed insulin resistance as a result of their obesity. Pancreatic beta cell failure, however, occurred only in the CMAH mutant mice that lacked NeuSGc, resulting in a decreased insulin production, which then further impaired blood glucose level control. This discovery may enhance scientific understanding of why humans may be particularly prone to develop type 2 diabetes. Results may also suggest that conventional animal models may not accurately mirror the human situation.

"The diabetes discovery is an important advance in its own right. It tells us a lot about what goes wrong in diabetes, and where to aim with new treatments," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "but its implications for human evolution are even greater. If this enzyme is unique to humans, it must also have given us a survival advantage over earlier species. Now the challenge is to find the function of CMAH in defending us against microbes or environmental stress or both. This evolutionary science explains how we can win some and lose some, to keep our species ahead of the extinction curve."

Details:
Sarah Kavaler, Hidetaka Morinaga, Alice Jih, WuQiang Fan, Maria Hedlund, Ajit Varki, and Jane J. Kim. Pancreatic ß-cell failure in obese mice with human-like CMP-Neu5Ac hydroxylase deficiency. FASEB J. fj.10-175281; doi:10.1096/fj.10-175281.

Evolution Led To Genetic Variation That May Affect Diabetes, Stanford Scientist Says

The root causes of complex diseases such as type-2 diabetes and obesity have been difficult to identify because the diseases are, well, complex. They occur at the dicey biological intersection of genes and environment, and, because they arose in our relatively recent past, it's not easy to simply compare DNA sequences from "then" and "now" to pinpoint likely genetic culprits.

Now researchers at the Stanford University School of Medicine have identified genetic variations in a hormone involved in the secretion of insulin - a molecule that regulates blood sugar levels - that occur more frequently in some human populations than others. People with the "new" variants, which are thought to have first occurred 2,000 to 12,000 years ago, have higher fasting levels of blood glucose than those with the more traditional, or ancestral, form of the gene. High blood glucose levels are associated with the development of diabetes, which occurs when the body is unable to produce or respond properly to insulin.

The finding may help scientists better understand the subtle changes in human metabolism, or "energy balance regulation," that occurred as our species shifted from being primarily hunter-gatherers to a more agriculturally based society. It may also help clinicians identify individuals likely to develop diabetes, and direct the development of new therapies for diabetes and obesity.

"These studies are fascinating because it shows how much the selection process has affected human energy-balance regulation in just a few thousand years and how complex it could be for the future practice of personalized medicine," said Sheau Yu "Teddy" Hsu, PhD, assistant professor of obstetrics and gynecology and senior author of the study.

The research was published online Feb. 7 in Diabetes. It follows a similar paper in the January issue of Genome Research that also explored the recent evolution of energy balance regulation, or how humans choose whether and how to store excess calories, among populations.

In the new paper, Hsu and his colleagues at Chang Gung Memorial Hospital in Taiwan and Texas A&M University first identified 207 genetic regions that have been associated with diabetes or obesity. They then looked to see which of these had increased in prevalence in the time since humans began to move out of Africa about 60,000 years ago. They identified 59 genetic regions of particular interest, and homed in on those that occurred in at least 30 percent of people in the HapMap project - a worldwide survey of genetic differences among populations. (Restricting their search to relatively common variants ensured that their findings would be widely applicable and would provide a more powerful tool to identify any associated phenotype differences.)

The researchers identified five genes with genetic differences that occurred frequently in Asians and/or Europeans, but infrequently in Africans. (These groups were pre-identified as part of the HapMap project, which sampled people of Nigerian, Chinese, Japanese and European ancestry.) Hsu's team selected GIP, one of the five genes, for further study because the GIP protein was known to be involved in stimulating insulin secretion in humans after a meal.

"We thought GIP was the most interesting because the newly selected form occurs in about 50 percent of people from Europe or Asia, but in only about 5 percent of Africans. That indicates this gene is highly adaptable to new environments," said Hsu.

He and his colleagues identified three individual changes in the regulatory region of GIP - that is, the DNA adjacent to the GIP gene that affects when and how it is translated into protein - that reduced the levels of the hormone. What's more, these three also tended to occur with another mutation in the coding region that results in a slightly different form of the protein. This alternate form is degraded more slowly in human blood.

"So now we know there are two different forms of the protein, which allowed one form to be selected in one population, and the other in a different population," said Hsu. "But we still needed to show that these variants led to phenotypic differences in modern humans."

Because previous studies of GIP variants hadn't showed any conclusive differences among their human carriers, Hsu and his colleagues focused their study more narrowly on a population that is not only metabolically challenged, but also critical to evolutionary success: pregnant women. They found that, out of 123 East Asian pregnant women, those who carried two copies of the newly evolved variant had significantly lower levels of GIP circulating in their blood. These women were also at a significantly increased risk to have fasting blood glucose levels that exceeded the recommended threshold of 140 mg/dL (48.3 percent vs. 20.9 percent of those who carry the ancestral variant).

The finding is particularly interesting because it may help clinicians identify pregnant women likely to develop gestational diabetes, according to Hsu. But it also gives a glimpse into our not-so-distant past and the ways our ancestors grappled with environmental change.

"Like other humans at the time, the Eurasian population really had to fight for survival," said Hsu. "Now we're starting to pinpoint how they did that on a molecular level. These gene variants, and the resulting higher blood sugar levels it fostered, may have helped women maintain successful pregnancies in the face of the inevitable famines that occur in an agriculturally based society. Now, in a more food-secure environment, variations in GIP could contribute to the development of diabetes or obesity."

Notes:

In addition to Hsu, James Cai, PhD, a former Stanford postdoctoral scholar in biology, was also involved in the study. He is now an assistant professor at Texas A&M University.

The research was funded by the National Institutes of Health, the Avon Foundation and Chang Gung Memorial Hospital. Stanford's Department of Obstetrics and Gynecology supported the work.

Source:
Krista Conger
Stanford University Medical Center

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3,000 Steps Five Days A Week Wards Off Diabetes

If you walk three thousand steps a day, five days each week, your chances of developing diabetes and becoming obese are significantly reduced, Australian researchers report in the BMJ (British Medical Journal). Increase your daily steps over a five year period to 10,000 steps a day, and the benefits skyrocket. This is the first study to assess the impact of doing a daily step count on insulin sensitivity, the authors claim.
Previous studies have demonstrated how physical activity can reduce insulin resistance and BMI (body mass index), both indicators of looming diabetes. However, none had clearly shown how adding a certain number of steps each day to your physical activity can significantly improve your chances of remaining obese- and diabetes-free.
Most experts advise people to walk 10,000 steps daily. However, doing 3,000 steps five times a week can also work. Also, you don't have to start off with the 10,000 steps - you can gradually build up over a five year period.
Scientists from the Murdoch Children's Research Institute, Melbourne, Australia, gathered data on 592 adults, all of them middle-aged. They had taken part in a nationally representative study aimed at gauging diabetes rates throughout Australia between 2000 and 2005.
The participants underwent a comprehensive health check, and then completed a questionnaire that revealed details on their eating habits and lifestyle. Each adult was given a pedometer and shown how to use it.
A pedometer, also known as a step counter is a portable electronic device that counts each step you take by detecting the motion of your hips - you attach it to your side. It is usually worn on the belt and you keep it on all day - it records how many steps you have walked during the day.
The participants were followed-up again five years later. The researchers also took into account other lifestyle factors, such as smoking status and alcohol intake.
The investigators found that those with a higher daily step count over the five year period generally had a lower BMI, lower waist to hip ratio, and superior insulin sensitivity, compared to individuals with a low daily step count - regardless of what their dietary energy intake was. They added that the more active individuals enjoyed the above-mentioned benefits mainly because of a change in fatness (adiposity) over the five years.
The researchers worked out that sedentary individuals who gradually increased their daily step count to 10,000 over a five-year period would enjoy a threefold improvement in insulin sensitivity compared to those who managed to reach 3,000 steps a day (five days a week) at the end of five years.
It is important to remember that staying at 3,000 steps a day does have its benefits, compared to remaining completely sedentary.
The authors concluded:

"These findings, confirming an independent beneficial role of higher daily step count on body mass index, waist to hip ratio, and insulin sensitivity, provide further support to promote higher physical activity levels among middle aged adults."

According to the American Diabetes Association: 18 million Americans are diagnosed with diabetes5.7 million Americans have diabetes but don't know it (undiagnosed)57 million individuals in the USA have pre-diabetes186,300 people under the age of 20 years have diabetes in the USA2 million US teenagers have pre-diabetes10.7% of Americans over the age of 20 have diabetes11.2% of American adult males have diabetes10.2% of American adult females have diabetesType 1 Diabetes is an autoimmune disease - the person's body has destroyed his/her own insulin-producing beta cells in the pancreas. A person with Type 2 Diabetes does not produce enough insulin, or suffers from 'insulin resistance' (the insulin is not working properly). Type 1 Diabetes is unavoidable and is not caused by lifestyle. Type 2 Diabetes is usually caused by being overweight and having a sedentary lifestyle.
"Association of change in daily step count over five years with insulin sensitivity and adiposity: population based cohort study"
T Dwyer, A-L Ponsonby, O C Ukoumunne, A Pezic, A Venn, D Dunstan, E Barr, S Blair, J Cochrane, P Zimmet, J Shaw
BMJ 2011; 342:c7249 doi: 10.1136/bmj.c7249
Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today


Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
posted by W D Clark on 13 Jan 2011 at 8:55 pm
How much trouble would it have been for you to just tell me approximately how far 10,000 steps is?
Now I have to go see if I can look it up somewhere.
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posted by Me on 14 Jan 2011 at 6:49 am
Average stride 2-3 feet.
Mile 5280 feet.
(3,000 steps * 3 foot stride) / 5,280 feet = approx 1.7 miles
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posted by anon on 14 Jan 2011 at 6:54 am
Stride length depends on height.
Note a starting spot, take 10 normal steps, measure the distance in feet with a tape measure or yardstick, and write it down. Do this several times during the day and several places, average the distances and divide by 10 and you will have a good estimate of your stride length in feet over the day. Or, if you regularly do one long walk, do it several times at the beginning and the end.
(No. Feet/step)*(Number steps/day)*(mi/5280 feet)= No. miles/day
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Taking More Steps Every Day Can Help Ward Off Diabetes

Simply taking more steps every day not only helps ward off obesity but also reduces the risk of diabetes, finds a study published on bmj.com today.

While several studies have shown that physical activity reduces body mass index and insulin resistance - an early stage in the development of diabetes - this is the first study to estimate the effects of long-term changes in daily step count on insulin sensitivity.

A popular guideline is to do 10,000 steps every day, though a more recent recommendation is 3,000 steps, five days a week.

The research, by the Murdoch Childrens Research Institute, Melbourne, involved 592 middle aged adults who took part in a national study to map diabetes levels across Australia between 2000 and 2005.

At the start of the study, participants completed a detailed diet and lifestyle questionnaire and underwent a thorough health examination. They were also given a pedometer and instructed how to use it. Participants were monitored again five years later.

Other lifestyle factors, such as diet, alcohol and smoking were taken into account.

A higher daily step count over five years was associated with a lower body mass index, lower waist to hip ratio, and better insulin sensitivity.

These associations were independent of dietary energy intake and appeared to be largely due to a change in adiposity (fatness) over the five years, say the authors.

The authors estimate that, in their setting, a sedentary person who takes a very low number of daily steps but who was able to change behaviour over five years to meet the popular 10,000 daily step guideline would have a threefold improvement in insulin sensitivity compared with a similar person who increased his or her steps to meet the more recent recommendation of 3,000 steps for five days a week.

They conclude: "These findings, confirming an independent beneficial role of higher daily step count on body mass index, waist to hip ratio, and insulin sensitivity, provide further support to promote higher physical activity levels among middle aged adults."

Click here to view paper

Source: British Medical Journal

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View the original article here