Archive for November, 2012
November 28th, 2012
Breastfeeding has long been considered to be protective against the development of adult obesity in the child but a causal relationship has been difficult to establish. Early Life Determinants Evidence from epidemiological research indicates that overweight and obese women are less likely than normal weight women to initiate breastfeeding or maintain it for shorter durations. However, whether this is due to biological, psychological or cultural reasons is unclear. Systematic Review of maternal obesity and breastfeeding The Growing Up Today Study of 15,000 children showed that, if breastfed longer than seven months, a child was less likely to be obese. Overweight Adolescents and breastfeeding More recent studies appear to mute the benefit of breastfeeding vis a vis child’s adult weight. A study of over 7,000 children found the effects vanished when other factors, such as parental smoking, education and age were analyzed. Exclusive breastfeeding of Swedish children Most recently, a randomized trial of breast feeding promotion in Belarus of 17,000 infants raised the rates of breastfeeding but had no effect on weight. Randomized breast-feeding trial in Belarus
However, reliance on this advice may be misplaced. According to an update of a Cochrane Review, Optimal Duration of Breastfeeding. http://www.ncbi.nlm.nih.gov/pubmed/22895934
“Exclusive breastfeeding for six months versus three to four months, with continued mixed breastfeeding thereafter) reduces gastrointestinal infection and helps the mother lose weight and prevent pregnancy but has no long-term impact on allergic disease, growth, obesity, cognitive ability or behavior. ..A reduced level of iron has been observed. ..
The epidemiologic evidence is now overwhelming that, even in developed countries, breastfeeding protects against gastrointestinal and (to a lesser extent) respiratory infection, and that the protective effect is enhanced with greater duration and exclusivity of breastfeeding. Prolonged and exclusive breastfeeding has also been associated with a reduced risk of the sudden infant death syndrome and, in preterm infants, necrotizing entrerocolitis. Breastfeeding is life-saving in developing countries; a meta-analysis reported markedly reduced mortality (especially due to infectious disease) with breastfeeding even into the second year of life…
The evidence of long term effects of breastfeeding on obesity and mean body mass index (citations omitted) or blood pressure, type 1 or type 2 diabetes, or ischemic heart disease is also weak.
Importantly, they comment on the possibilities of bias in the scientific evidence, stating,
Most of the scientific evidence on the health effects of breastfeeding has been based on observational studies, with well-recognized sources of potential bias. Some of the biases tend to favor exclusively breastfed infants, while others favor those who receive earlier complimentary feeding. Reverse causality is an important potential source of bias. Infants who continue to be exclusively breasted tend to be those who remain health and on an acceptable growth trajectory; significant illness or growth faltering can lead to interruption of breastfeeding or supplementation with infant formula or solid foods. Infants who develop a clinically important infection are likely to become anorectic (loss of appetite) and to reduce their breast milk intake, which can in turn lead to reduction in milk production and even weaning. The temporal sequence of the early signs of infection and weaning may not be adequately appreciated; infection may be blamed on the weaning, rather than the reverse. Advanced neuromotor development may also lead to earlier induction of solid foods, which could then receive ‘credit’ for accelerating motor development. Poorly-growing infants (especially those in developing countries) are likely to receive complementary feedings earlier because of their slower growth. In developing countries, however, rapidly-growing infants may require more energy than can be met by the increasingly spaced feedings typical of such settings. This may result in crying and poor sleeping, supplementation with formula or solid foods, or both, reduced suckling, and a vicious cycle leading to earlier weaning. ..
Finally, the underlying assumption in this field has been that ‘one size fits all’, i.e. that average population effects can be applied to individual infants. There has been little discussion of the fact that all infants, regardless of how they are fed, require careful monitoring of growth and illness, with appropriate interventions undertaken whenever clinically indicated.”
In case you haven’t noticed, our pubic health leaders push policies which are virtually 180 degrees away for the Cochrane conclusion. Why such a discrepancy between the highly-regarded Cochrane review and US public health authorities
In May 7, 2012, Health and Human Services Secretary Kathleen Sebelius told the audience at the Weight of the Nation conference, that, in regard to obesity, “ We know that a mother’s health during pregnancy and decisions like whether or not to breastfeed, can have a huge impact on both the mother and child’s health. And these impacts last a lifetime.” HHS:Speeches:Sebelius: Weight of the Nation
Genetic studies may clarify the mixed outcomes of many studies. Laurent Briollais and colleagues in Canada and Australia have studied 1,096 Australian children from birth to 14 years of age. They found that the presence of the risk allele of the FTO gene, SNP rs9939609. In girls, exclusive breastfeeding for three months interacts with the SNP at baseline and can reverse the increase in BMI. In boys, exclusive breastfeeding reduces BMI in both carriers and non-carriers of the SNP. Six months of exclusive breastfeeding put the boys’ BMI growth curves back to the normal range. If validated by other studies, this finding could bring a new dimension to the breastfeeding and obesity issue.Impact of breastfeeding on FTO-related BMI
November 28th, 2012
Anis Larbi, Iftikhar Alam and Tze Pin Ng have produced a truly provocative review article, Does Inflammation Determine Whether Obesity is Metabolically Healthy or Unhealthy? The Aging Perspective in Mediators of Inflammation. They start by addressing the fact that not all obesity is the same. Some adults with obesity can be metabolically healthy (MHO) while others are metabolically unhealthy (MUHO). The difference is the presence or absence of impaired glucose tolerance, dyslipidemia, hypercuricemia and hypertension. They note that obesity has spread around the world even as the exact causes of the obesity ‘pandemic’ are still in doubt. Additionally, they view obesity as a form of chronic inflammation. The inflammatory response is due to a number of components, including cytokines and adipokines.
The authors posit that, theoretically, metabolically healthy obese (MHO) and metabolically unhealthy obese (MUHO) humans “may represent distinct subtypes of obesity that were predetermined genetically to confer different metabolic and cardiovascular risks. Another theoretical possibility is that MHO and MUHO represent transitions phases from nonobesity in the development and natural history of obesity, with MHO individuals eventually turning into MUHO. It is tempting to think over the possibility of the other way round, that is, the possibility of converting MUHO into MHO. Whether MHO or MUHO is sustained or not for substantially a longer period may depend upon a number of factors, including the levels of cytokines and/or adipokines.” They call for studies to investigate of this transition from MHO to MUHO. “The answer to this question,” they note, “may have paramount clinical and public health implications. Once the temporal is established, the course of obesity can be stopped or delayed at some stage in its natural history before it becomes “metabolically unhealthy.”
They suggest that the elderly be the focus of such studies for a number of reasons, while noting that the BMI alone, as a sole indicator of obesity, is responsible for discrepant findings. (No argument here). They also point out that in one study, inflammation could be a key factor in causing obesity-induced type 2 diabetes. Gestational diabetes is also associated with chronic subclinical inflammation.
November 28th, 2012
Aetna, the nation’s third largest health insurer, has announced that it will provide reimbursement coverage for Vivus Inc’s obesity treatment, Qsymia, and Arena Pharmaceutical’s Belviq, which will go on the market next year.
No details are available yet on the duration of coverage or any requirements to show weight loss. Nevertheless, this is a major breakthrough in the resistance of the insurance industry to cover drugs to treat obesity.
November 28th, 2012
In the essay, she recounts the frustration at her clinic with a single-Mom and her two daughters who were morbidly obese and developing serious health problems. Eventually, she referred the family to Child Protective Services, a step recommended by Dr. David Ludwig last year. Dr. Cheng writes, “Children with obesity severe enough to warrant a report for medical neglect and invariably come from impoverished families with chaotic lives fraught with social difficulties, including unfilled basic needs. She recounts that the mother dropped out of school, was never taught how to cook and had depression, trying to keep her impoverished family together. She often did not pay the phone bill and did not understand how Medicaid worked. But the Child Protective Service did not help. She cites a study of 595 high risk children reported for intervention showing no significant improvements in family functioning, social support, maternal education or child behavior problems. So, while calling for state intervention in cases of childhood obesity may get headlines, it certainly lacks evidence that it makes anyone better.
November 28th, 2012
The Center for Disease Control and Prevention (CDC) has reported that the prevalence of diagnosed diabetes has increased in all US states, the District of Columbia and Puerto Rico between 1995 and 2010. The prevalence increased by 50% or more in 42 states and by 100% or more in 18 states. The states with the largest increases were Oklahoma, Kentucky, Georgia, Alabama and Washington. According to the CDC press release, in 1995 only 3 states had diagnosed diabetes prevalence of 6% or more; by 2010, all 50 states had a prevalence over 6%.
The press release, (rather amazingly to my point of view) states, “Type 2 diabetes, which may be prevented through lifestyle changes, accounts for 90 percent to 95 percent of all diabetes cases in the United States. CDC and its partners are working on a variety of initiatives to prevent type 2 diabetes and to reduce complications in those already diagnosed. CDC leads the National Diabetes Prevention Program, a public-private partnership that brings evidence-based programs for preventing type 2 diabetes to communities. The program is helping to establish a network of lifestyle-change classes for overweight or obese people at high risk of developing type 2 diabetes.” Of course the evidence-based program they refer to are the Diabetes Prevention Program, which found lifestyle prevention was only effective in young retirees and the Look AHEAD trial, which was terminated prematurely because the lifestyle group had no better outcomes than the control group. Why does the CDC continue to hype bang-the- lifestyle-drum when they know it doesn’t work?