Addressing Rising Childhood Obesity: Strategies Beyond Nutritional Deficiency

Ultra-processed foods might contribute to the growing obesity epidemic in children

UNICEF/UN0846048/Florence Gou

For the first time, a significant number of children worldwide are experiencing obesity rather than malnutrition. This trend signifies a critical shift in childhood nutrition. While many strategies exist to combat hunger, few address obesity specifically.

“Despite years of attempts to prevent obesity, particularly in children and adolescents, we are not achieving satisfactory outcomes,” notes Andrea Richardson from RAND, a California-based nonprofit research organization.

A new report by Harriet Torres from UNICEF Belgium and her team utilized data from a comprehensive study to evaluate the nutritional status of children aged 5 to 19. This initiative, called the Collaboration of Non-Communicable Disease Risk Factors, encompasses over 160 countries and territories, representing more than 90% of the global child population.

The findings indicate that global childhood obesity rates have nearly tripled since 2000, with around 9.4% of children classified as obese versus 9.2% who are undernourished. This marks a significant moment, as obesity now outnumbers nutritional deficiencies in children.

Most troubling is the sharp increase in obesity rates in low- and middle-income nations. “Over 80% of children facing overweight and obesity globally are from these regions,” highlighting that this is no longer merely a high-income issue; it’s a pervasive global concern.

This situation necessitates that governments and organizations rethink their strategies regarding childhood malnutrition. “We are observing not just nutritional deficiencies but all forms of malnutrition,” asserts Shivani Ghosh from Cornell University, New York. Unfortunately, effective methods to combat obesity are still lacking, unlike those available for hunger.

The UNICEF report criticizes the prevalence of ultra-processed foods in contributing to rising obesity rates among youth. These foods, made using industrial processes, typically contain additives and preservatives and are high in fats, sugars, and salts. Common examples include packaged snacks, candies, chips, and sodas. The report claims that ultra-processed foods contribute to at least half of the calorie intake for children in Australia, Canada, the U.S., and U.K., and about a third in some low- and middle-income countries such as Argentina and Mexico.

Numerous studies indicate that ultra-processed foods correlate positively with obesity rates. However, the policies aimed at reducing their consumption have seldom led to significant declines in obesity.

For instance, Mexico was the first country to impose a tax on certain high-calorie foods and sugar-sweetened drinks in 2014. Following this, sales for these items decreased, particularly among lower-income families. Adolescent obesity rates experienced only minimal change, notably impacting only teenage girls, similar to the outcome in the U.K. after a tax was levied on sugary drinks in 2018.

Conversely, Chile has implemented some of the strictest regulations regarding ultra-processed products. In 2016, it limited marketing for these foods and mandated warning labels for those high in calories, salt, saturated fats, and sugars. As a result, obesity rates among children aged 4-6 decreased by 1-3 percentage points within a year. However, the figures reverted to baseline by 2018, and in 2019, obesity rates in 14-year-olds rose by 2 percentage points, underlining the ineffectiveness of these measures.

Torless provides a different perspective, stating, “No single intervention is sufficient. Some countries are imposing soda taxes, others are labeling foods. While these efforts are commendable, a comprehensive, multi-faceted approach is essential for meaningful change.”

Thus, the report advocates for policies that enhance the availability and affordability of nutritious food, including grants and school meal programs. Furthermore, it highlights the critical role of nutritional education and poverty alleviation. “The same factors contributing to undernutrition parallel those causing overnutrition,” Richardson elaborates. “These issues stem from unsafe drinking water, lack of financial resources, and inadequate access to nutritious food.”

No nation has fully adopted all of UNICEF’s recommendations, leaving the question of their effectiveness in reducing obesity unanswered. “The underlying assumption is an increased consumption of unhealthy foods correlating with rising overweight and obesity rates,” remarks Ghosh. “This could partially explain the trends we’re seeing.”

However, other factors may also play a role, including stress, pollution, and even genetic factors.

“This truly needs to be seen as a major public health crisis,” concludes Richardson. “Our children are our future, and they deserve to be healthy. If they are not thriving, our future looks bleak.”

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Source: www.newscientist.com

CDC Finds Risk Factors for Congenital Deficiency in Women Under 50 Can Be Mitigated

In the United States, one in 33 infants is born with a birth defect. New research from the Centers for Disease Control and Prevention highlights methods to mitigate that risk.

The study identifies five risk factors that public health officials, and even the women themselves, can address: obesity, diabetes, tobacco exposure, food insecurity, and insufficient folic acid levels (a crucial vitamin for cell production).

The findings indicate that 66% of women aged 12 to 49 possess at least one of these risk factors, with 10% having three or more. The CDC’s discovery, published on Tuesday in The American Journal of Preventive Medicine, is based on data from 5,374 women surveyed as part of the National Health and Nutrition Examination Survey from 2007 to 2020.

“It’s vital to raise awareness about these risk factors and encourage women to consult their healthcare providers if they have any concerns or questions before pregnancy,” stated Arick Wang, a CDC health scientist and lead author of the study.

She further noted, “The risk can be mitigated through measures such as daily intake of 400 micrograms of folic acid, maintaining a healthy diet and exercise routine, and managing blood glucose levels.”

Congenital abnormalities are significant causes of infant mortality, according to CDC statistics. Risks often begin before women even realize they are pregnant. While the causes of birth defects remain largely unknown, experts typically acknowledge that various combinations of genetic, environmental, and lifestyle factors contribute.

“This should serve as a wake-up call for all of us,” remarked Dr. Michael Warren, chief medical and health officer at March of Dimes, a nonprofit organization focusing on maternal and infant health.

“We aim to ensure that nutritious foods are accessible,” added Warren, who was not involved in the research. “We want to guarantee that individuals have a secure environment for physical activity.”

Individuals experiencing food insecurity may lack essential nutrients for the healthy development of their fetal organs, including folic acid. For instance, low blood levels of folic acid are linked to neural tube defects—issues impacting the brain or spine that occur during the first month of pregnancy. Healthcare professionals recommend that those who are pregnant or planning to conceive take folic acid, a synthetic version of the vitamin.

Since 1998, the Food and Drug Administration has mandated the fortification of enriched grain products with folic acid. CDC scientist Wang mentioned in a press release that this policy is likely to prevent over 1,300 annual cases of babies born with neural tube defects.

“The majority of birth defects still remain unexplained,” Nembhard stated. “Even when women make all the right choices—avoiding smoking, abstaining from alcohol during pregnancy, monitoring caffeine intake, and staying active—they may still face challenges.

Warren, who previously served as the pre-administrator of HHS’s Maternal and Child Health Department until June, highlighted that many women may not recognize obesity and food insecurity as risk factors.

Obesity, which impacted approximately one-third of the surveyed women, was identified as the most prevalent modifiable risk factor in CDC studies. While the reasons behind its association with birth defects are not entirely understood, it seems that altered metabolic processes (like how a woman’s body regulates insulin and glucose) can lead to abnormal fetal development.

“When our cells grow and develop into organs, they depend on precise conditions and functions. Disrupting these processes can lead to complications,” Warren explained.

He noted that elevated blood sugar levels from diabetes can also contribute to abnormal organ development. Additionally, certain chemicals found in tobacco smoke, including nicotine, can diminish oxygen supply to the fetus.

Warren emphasized the need for ongoing efforts. He referenced Mississippi’s recent declaration of a public health emergency, which aims to address the “Care Desert,” where women struggle to access obstetric services due to high infant mortality rates.

External researchers commended the release of the study amidst budget cuts and proposed reductions in funding for agencies.

“We are pleased to see this research continue, even amidst questions about its future,” remarked Wendy Nenberd, director of the Center for Research and Prevention at the University of Arkansas for Medical Sciences.

In March, the Department of Health and Human Services announced layoffs of 2,400 CDC employees. However, a federal judge issued a preliminary ruling on August 12, which blocked layoffs for specific CDC programs, including the National Center for Congenital Deficiency and Developmental Disorders, the team behind the current study. At least 600 CDC employees are still expected to receive permanent termination notices.

Source: www.nbcnews.com

The correlation between vitamin B12 deficiency and multiple sclerosis

A groundbreaking study focused on astrocytes in the brain has uncovered a new molecular link between vitamin B12 and multiple sclerosis (MS). This study demonstrates that his FDA-approved MS treatment drug, fingolimod, can modulate the B12 transmission pathway, highlighting the potential of B12 supplementation in MS treatment. Credit: SciTechDaily.com

Study results identify molecular signaling pathways that have the potential to enhance current MS treatments.

Scientists have noted interesting similarities between vitamin B deficiency and B vitamins for decades.12 – Essential nutrients that support the healthy development and function of the central nervous system (CNS) – and Multiple Sclerosis (MS) is a chronic disease in which the body’s immune system attacks the CNS, causing neurodegeneration.

Both are vitamin B12 (also known as cobalamin) deficiency and multiple sclerosis cause similar neurological symptoms, including numbness or tingling in the hands and feet, loss of vision, difficulty walking or talking normally, and cognitive impairment such as memory loss .

New research reveals molecular connections

In a new study published online on December 8, 2023, cell reportSanford Burnham Prebys researchers are working with other collaborators to describe a new molecular relationship between B vitamins.12 The other is MS, which occurs in astrocytes, which are important non-neuroglial cells in the brain.

The findings of the study’s senior authors Jerrold Chun, MD, PhD, professor and senior vice president for neuroscience drug discovery, and Yasuyuki Kihara, PhD, associate research professor and co-corresponding author, and their colleagues, open new ways to conduct research. It suggests. Improving MS treatment through CNS-B12 Replenishment.

“Covalent molecular bonds of vitamin B in the brain”12 A carrier protein known as transcobalamin 2 or TCN2 and the FDA-approved MS drug fingolimod provide a mechanistic link between B and B.12 “Signal transduction and MS lead to reduced neuroinflammation and possibly neurodegeneration,” Chun said.

“Strengthen Brain B”12 When used in combination with fingolimod or potentially related molecules, it could potentially enhance both current and future MS treatments. ”

Study details and impact

In their paper, the Sanford Burnham Prebys team, along with collaborators from the University of Southern California, Japan’s Juntendo University, Tokyo University of Pharmacy, and the State University of New York, focused on the molecular function of FTY720, or fingolimod (Gilenya®). . ), a sphingosine 1-phosphate (S1P) receptor modulator that suppresses the distribution of T and B immune cells that mistakenly attack the brains of MS patients.

Using animal models of MS and postmortem human brains, researchers found that fingolimod suppresses neuroinflammation by functionally and physically modulating group B.12 Enhance communication channels, especially B12 A receptor called CD320 must take up and use the necessary B12 If bound to TCN2 distributing B12 throughout the body, including the CNS. This known process was newly identified through interaction with fingolimod within astrocytes. Importantly, this relationship was also observed in human MS brains.

Of particular note, the researchers reported lower levels of CD320 or dietary B;12 The restriction worsened the disease course and reduced the therapeutic efficacy of fingolimod in animal models of MS.This occurred through a hitchhiking mechanism in which fingolimod binds to TCN2-B.12 This complex allows delivery to all astrocytes via interaction with CD320, and loss of the component disrupts the process and exacerbates the disease.

These new findings further support the use of B .12 It turns out that supplements, particularly fingolimod, can correct astrocyte B disorders in terms of delivering vitamins to astrocytes in the brain.12 Pathways for MS patients.

Scientists say other commercially available S1P receptor modulators, such as Mayzent®, Zeposia® and Ponvory®, may be able to access at least part of this CNS mechanism.This study supports B12 Supplementation with S1P receptor modulators aimed at improving the efficacy of this class of drugs.

This study also opens new avenues for how B functions.12The -TCN2-CD320 pathway is regulated by sphingolipids, specifically sphingosine, an endogenous structural analog of naturally occurring fingolimod, for future improvements in MS treatment, Chun said.

“We support the creation of B that targets the brain.”12 formulation. In the future, this mechanism may be extended to new treatments for other neuroinflammatory and neurodegenerative diseases. ”

Reference: “FTY720 requires astrocyte vitamin B12-TCN2-CD320 signaling to reduce disease in animal models of multiple sclerosis” (Deepa Jonnalagadda, Yasuyuki Kihara, Aran Groves, Manisha Ray, Arjun Saha, Clayton Ellington, Hyeon-Cheol Lee-Okada), Tomomi Furuhata, Takehiko Yokomizo, Edward V. Quadros, Richard Rivera, Jerrold Chun, December 7, 2023. cell report.
DOI: 10.1016/j.celrep.2023.113545

Additional authors of the study include Sanford Burnham Prebys, Alan Groves, Sanford Burnham Prebys, Deepa Johnnalagadda, Manisha Ray, Clayton Ellington, and Richard Rivera of the University of California, San Diego . Arjun Saha, University of Southern California. Juntendo University, Hyeon-Cheol Lee-Okada and Takehiko Yokomizo. Tomomi Furuhata (Tokyo University of Pharmacy) Edward V. Quadros, Downtown Medical Center, New York.

This research was supported by a grant from the National Institute of Neurological Disorders and Stroke. National Institutes of Health (R01NS103940), Novartis, Ministry of Education, Culture, Sports, Science and Technology/JSPS KAKENHI (18H02627, 19KK0199, 21H04798, 18K16246 and 21K08565). Additional support was provided by the Uehara Memorial Foundation, Kanae Medical Foundation, Mochida Memorial Medical and Pharmaceutical Research Foundation, Human Frontier Science Program, and the University of California, San Diego Medical Scientist Training Program and Pharmacology Training Grant (T32GM007752). . ).

Source: scitechdaily.com