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Fatty Acids Linked to Bone Density Development in Children

by Dr. Michael Lee – Health Editor September 9, 2025

written by Dr. Michael Lee – Health Editor

Blood Fatty ⁣Acid Profile Linked to Bone Growth in Children & Adolescents

A new study from the University of Eastern Finland reveals a connection between the composition of ⁤fatty acids in blood and bone mineral density development during childhood and adolescence. Researchers followed 480 ‌children (227 girls and 253 boys) over⁣ an eight-year period,finding that specific fatty acids circulating in the blood could predict changes in bone density. The ‍findings, published in the journal of Bone and Mineral Research,⁢ suggest that fatty acid ⁢metabolism plays a significant role in healthy bone development.

The research demonstrated that higher levels of arachidonic acid were associated with increased bone density during the study period. Furthermore, increased activity of enzymes involved in fatty acid metabolism, specifically delta-6 desaturase, also ⁢correlated with higher bone density. Conversely,a greater proportion of linolic acid in the ⁤blood was linked⁢ to⁢ lower bone density.

Researchers emphasize that simply categorizing ⁤fatty acids into broad groups (saturated, monounsaturated, polyunsaturated) isn’t ⁢sufficient for understanding their impact on bone health. individual fatty acids within these groups can⁢ have differing effects. The study also⁣ acknowledges that muscle and ‍fat mass contribute to these observed associations.

“This is the first study to demonstrate ‌that the fatty acid composition of the blood in childhood can predict ⁣the development of bone density into adolescence,” stated Professor Timo Lakka, Director of the‍ PANIC study. “Our ‌results indicate ⁣that fatty ⁤acid metabolism is an important factor in the healthy development of ⁢bones.”

Associate Professor Sonja Soininen, responsible⁤ for the bone health section of the study, highlighted the complexity of the findings. “Interestingly,not all fatty acids ⁣within the same group are associated with bone health in the same⁢ way – some appear to be positively ⁤associated⁢ with bone development,while others are linked to⁢ less optimal outcomes. This reflects the complexity ‍of metabolism‌ and its significance for bone development.”

The ‍study utilized data from the Physical Activity and Nutrition in Children (PANIC) study, a long-term investigation initiated in 2007. Blood samples were analyzed using gas chromatography to measure fatty acid‍ levels in plasma phospholipids, while bone density and body composition were assessed ‍using a DXA device.⁣ The⁣ PANIC study, which began with over 500 children, is currently in ⁢its 16-year follow-up ⁤phase, continuing until the end‌ of 2026.

These results provide new insights into the relationship between fatty acid metabolism ⁢and bone development in children and may inform future nutritional strategies‍ aimed at‍ promoting bone health.

Source: University of Eastern ⁤Finland ⁢(UEF Viestintä). https://www.uef.fi/en/article/fatty-acid-composition-of-blood-predicts-bone-density-from-childhood-to-adolescence

Journal Reference: Lakka, T.‌ A., et al. (2025). Plasma fatty acid composition predicts bone mineral accrual from childhood to ⁣adolescence: the PANIC study.Journal of Bone ‌and Mineral Research. https://doi.org/10.1093/jbmr/zjaf104

September 9, 2025 0 comments

Health

Honey’s Neuroprotective Potential: Lab Study on Alzheimer’s Disease

by Dr. Michael Lee – Health Editor September 2, 2025

written by Dr. Michael Lee – Health Editor

Can Honey Protect Your Brain?⁢ Study Reviews Its Potential Against Alzheimer’s

A recent ‌review of laboratory studies suggests honey may offer a surprising defense against alzheimer’s ⁣Disease ⁢(AD).Published in Nutrients in 2025, the research, led by M.D. Navarro-Hortal and colleagues,‍ examined a range⁤ of experiments – from⁢ those ⁣using isolated cells to studies involving invertebrates like the ⁤nematode‌ Caenorhabditis elegans and the ⁣fruit ‍fly Drosophila melanogaster, as ⁤well as rodent models – to understand ⁤how different types ‍of honey impact AD pathology. The review⁢ considered the diverse sources and types of honey, ⁢including Manuka, Tualang, Chestnut, and Avocado varieties.

The findings indicate‌ honey combats several⁢ key hallmarks of AD, including oxidative stress,⁢ inflammation, ⁤and ⁤neurotransmitter imbalances. Researchers found honey and its extracts⁤ significantly reduced levels⁣ of ⁣reactive oxygen species (ROS),⁤ damaging molecules linked to cellular harm,⁤ in various models.

For example, chestnut-derived honey demonstrated antioxidative activity by protecting neuronal ‍cells from glutamate-induced damage and preserving mitochondrial function at concentrations between 500 and 750 ⁣μg/mL. In C. elegans engineered to produce human amyloid-beta, both Manuka and avocado honey⁤ (at 100 mg/mL) notably delayed the onset of ‌paralysis ⁤caused by Aβ. This suggests‍ a ⁣potent ⁢anti-inflammatory and anti-Aβ efficacy. Interestingly, the study also revealed a paradoxical effect: in some worm models of tauopathy, honey ⁢ worsened mobility, perhaps due ⁣to its sugar content rather than a direct impact on tau.

These findings were further supported by experiments using murine models. Tualang honey reversed shifts‍ in hippocampal Aβ1-40 and ⁢Aβ1-42 levels ⁢induced by LPS, while Kelulut honey reduced ⁣Aβ1-42 deposition specifically in the dentate gyrus, but not in‍ the CA1 or CA3 regions of the‌ brain. Furthermore, certain⁢ honeys exhibited the ability to inhibit ‍acetylcholinesterase, the⁢ enzyme responsible for breaking down acetylcholine – a ‍neurotransmitter crucial for memory. Acetylcholinesterase inhibitors are⁤ currently used as symptomatic treatments ‌for AD.However, the review authors caution that results ⁤varied significantly depending on the honey type, botanical source, processing methods, and study design. They also noted⁢ that many of the included studies carried a high or unclear risk of ⁤bias.

The review concludes that, in laboratory and non-human models, honey demonstrates meaningful neuroprotective ⁤potential, triggering benefits against the molecular drivers of AD by ‌reducing oxidative stress and inflammation and interfering with‍ toxic protein aggregation. Despite these⁣ promising results, the authors emphasize a “stark lack⁤ of human-derived‌ evidence” and call for clinical trials to determine optimal dosages and establish quality guidelines for honey’s potential use in AD treatment.

Source: Navarro-Hortal, M. D., Romero-Márquez, J. M.,Ansary,J.,‍ Hinojosa-Nogueira, D., Montalbán-Hernández, C., varela-López, A., & Quiles, J.⁣ L. (2025). Honey⁣ as a Neuroprotective Agent: molecular Perspectives on ⁢Its Role in Alzheimer’s disease. Nutrients,⁢ 17(16), 2577. DOI – 10.3390/nu17162577. https://www.mdpi.com/2072-6643/17/16/2577

September 2, 2025 0 comments

Health

PTSD Treatment: New Drug Targets Brain’s GABA Imbalance

by Dr. Michael Lee – Health Editor July 29, 2025

written by Dr. Michael Lee – Health Editor

Here’s a breakdown of the provided text, focusing on the key findings and implications:

The Problem:

Post-Traumatic Stress Disorder (PTSD) is tough to treat.
Current medications (targeting serotonin) offer limited relief for many.

The New Finding:

Brain Region of Interest: Medial Prefrontal Cortex (mPFC) – crucial for fear regulation.
Key Findings in PTSD patients:
Unusually high levels of GABA (a neurotransmitter that inhibits neural activity).
Reduced cerebral blood flow in the mPFC.
GABA’s Role in Recovery: GABA levels decreased in patients who showed clinical betterment, indicating its central role in recovery.
source of Excess GABA:
Not neurons, but astrocytes (a type of glial cell).
Astrocytes produce abnormal GABA via the enzyme monoamine oxidase B (MAOB). Mechanism of Dysfunction: This astrocyte-derived GABA impairs neural activity, specifically blocking the brain’s ability to forget traumatic memories (memory extinction).

The Potential Treatment:

Drug: KDS2010 – a selective, reversible MAOB inhibitor developed at IBS.
How it works:
Inhibits MAOB, reducing GABA production by astrocytes.
Reduces GABA levels.
Restores blood flow in the mPFC.
Re-enables memory extinction mechanisms.
Preclinical Evidence: KDS2010 showed normalized brain activity and allowed mice to extinguish fear responses.

Key Methodological Innovation:

Reverse Translational Strategy: the researchers started with clinical findings in humans (brain scans) and worked backward to identify the cellular source of dysfunction, then confirmed the mechanism and tested drugs in animal models. This approach helped link human symptoms to cellular mechanisms.

Importance and future Implications:

novel Understanding: Identifies astrocyte-derived GABA as a key pathological driver of fear extinction deficits in PTSD.
New Therapeutic Target: MAOB inhibition is a viable therapeutic path.
Broader Impact: Opens a new therapeutic paradigm not only for PTSD but potentially for other neuropsychiatric disorders like panic disorder,depression,and schizophrenia.
Current Status: KDS2010 is currently undergoing Phase 2 clinical trials, suggesting a potential for new treatment options for patients unresponsive to conventional therapies.
Glial Cell Role: Highlights the active role of glial cells in shaping psychiatric symptoms, challenging the previous view of them as merely passive support cells.

Quotes:

Dr.Woojin Won: Emphasizes the study’s novelty in identifying astrocyte-derived GABA as a driver of fear extinction deficit and the preclinical evidence for MAOB inhibitors.
Director C. Justin LEE: Highlights the success of reverse translational research and the potential for a new therapeutic paradigm for multiple neuropsychiatric disorders.

July 29, 2025 0 comments

Health

Study finds past H1N1 exposure shields animals from deadly H5N1

by Dr. Michael Lee – Health Editor July 28, 2025

written by Dr. Michael Lee – Health Editor

Past Flu Immunity Shields Against Bird Flu Dangers
New Study Reveals 2009 H1N1 Protection Against Severe H5N1 Illness
Immunity developed from the 2009 H1N1 pandemic flu may offer significant protection against severe illness from current H5N1 bird flu strains, even after close exposure, a groundbreaking study suggests.

A Surprising Shield Found

Researchers have discovered that a previous infection with the 2009 H1N1 influenza virus can dramatically reduce the risk of serious illness from H5N1 bird flu. This protection was evident even when ferrets, a common model for human influenza, were exposed through close contact with an H5N1 strain originating from dairy cattle.

The study, published in *Science Translational Medicine*, investigated how prior exposure to different influenza A virus subtypes impacts susceptibility to H5N1. The findings are crucial for public health officials and frontline workers dealing with the increasing spread of avian flu among mammals, including a notable outbreak in U.S. dairy herds.

Ferrets Reveal Protective Immunity

In the research, ferrets were pre-conditioned with immunity from either the 2009 H1N1, seasonal H3N2, or influenza B viruses. Those pre-exposed to the 2009 H1N1 strain showed markedly less viral shedding and no signs of illness when later challenged with H5N1. They maintained their body weight and all survived the ordeal.

Conversely, ferrets with only seasonal H3N2 immunity experienced partial protection, with intermediate viral titers and some weight loss, though they also survived. The study highlighted that the H1N1 immunity generated robust cross-reactive antibodies, particularly targeting the neuraminidase enzyme, which effectively inhibited H5N1 neuraminidase activity.

Researchers used a well-established ferret model to test the impact of prior flu immunity on H5N1 infection and disease.

The order of prior infections also proved significant. Any ferret group that had encountered the 2009 H1N1 virus, regardless of sequence, exhibited minimal to no H5N1 shedding and did not develop disease. This suggests that the presence of H1N1 immunity was more critical than the timing of exposure.

Direct Contact Exposure Tests

In a critical direct contact experiment, ferrets naive to any influenza strain transmitted H5N1 to all their cage mates, resulting in universally fatal disease. Prior H3N2 immunity failed to prevent infection, with all contacts shedding virus and only half surviving. However, prior H1N1 immunity significantly improved outcomes. Only half of the H1N1-immune contacts experienced low, transient shedding, none developed clinical disease, and all survived.

These findings strongly indicate that immunity acquired from the 2009 H1N1 pandemic virus acts as a robust defense against contemporary H5N1 strains, suppressing replication and preventing severe disease, even in high-dose exposure scenarios.

Understanding the Mechanism of Protection

The study suggests that the superior protection observed in H1N1-primed animals stems from cross-reactive antibodies, specifically those targeting the N1 neuraminidase found in both H1N1 and H5N1 viruses. Low levels of antibodies targeting the H5 hemagglutinin stem were also present but did not neutralize H5.

Immunity to internal viral proteins appeared comparable between H1N1 and H3N2 groups, implying that the enhanced defense against H5N1 is likely linked to hemagglutinin or neuraminidase cross-reactivity rather than broader immune responses.

The Centers for Disease Control and Prevention reported that as of June 2024, there have been 41 laboratory-confirmed human infections with H5N1 avian influenza in the United States, primarily linked to dairy cattle. Most of these cases have been mild, a trend this study’s findings may help to explain.

Implications for Future Preparedness

The research concludes that preexisting immunity to the 2009 H1N1 pandemic influenza virus offers substantial protection against H5N1 infection, replication, and illness in ferrets, even following direct, high-dose exposure. Immunity to seasonal H3N2 provided some attenuation of illness but did not reliably prevent infection.

The authors noted limitations, including the controlled infection intervals in ferrets and the inability to assess cellular immunity. Nevertheless, these insights are invaluable for developing future preparedness strategies, designing effective vaccines, and informing risk assessment and clinical surveillance policies, particularly emphasizing the role of neuraminidase-focused cross-reactivity.

July 28, 2025 0 comments

Health

Salivary enzyme levels rise with gene variation in diabetics

by Dr. Michael Lee – Health Editor July 8, 2025

written by Dr. Michael Lee – Health Editor

Gene Variation Drives Up Salivary Enzymes in Diabetics

New research indicates a common genetic variation can significantly increase salivary enzyme production, particularly in individuals with diabetes, suggesting a potential biological connection between starch digestion and blood sugar control.

The Role of AMY1 Gene Copy Number

Variations in copy number (CN) signify differences in the number of copies of a specific DNA sequence among individuals. Affecting approximately 10% of the human genome, these variants influence gene expression, thus contributing to varying physical traits and disease susceptibility.

One prevalent CNV involves the AMY1 gene, responsible for encoding salivary amylase, an enzyme that initiates starch breakdown in the oral cavity. In humans, the diploid AMY1 CN spans from 2 to 20, potentially impacting an individual’s metabolic profile.

Study Design and Participant Demographics

The research featured two groups: healthy adults participating in a starch study and individuals aged 45 and older with self-reported prediabetes or type 2 diabetes from a T2D microbiome study. Participants were recruited from the Ithaca, USA area.

Salivary enzyme levels rise with gene variation in diabetics

Saliva samples from 196 participants were analyzed to ascertain AMY1 CN, while samples from a subset of 94 participants were used to measure SAA. Genomic DNA was extracted from saliva to measure AMY1 CN using qPCR and ddPCR techniques.

Key Findings: AMY1 CN and SAA

The median AMY1 CN, as determined by qPCR, was 7.5 (ranging from 2 to 19 copies) and by ddPCR, it was 7.0 (ranging from 2 to 20 copies). A linear mixed model revealed that SAA levels increased as the day progressed, which aligns with previous findings indicating a surge in SAA from morning to midday.

Interestingly, the study found that AMY1 CN could independently account for 18% of the variance in SAA. Researchers suggest that other biological or unexamined factors may contribute to the variance in SAA.

Association with Type 2 Diabetes

A noteworthy association emerged between AMY1 CN and T2D/prediabetes status. For each additional copy of AMY1, SAA increased by nearly 14% in the control group and 43% in the T2D/prediabetes group.

According to the CDC, in 2019, 37.3 million US adults had diabetes; 28.3 million were diagnosed, and 9.0 million were undiagnosed (CDC 2020).

Implications and Future Research

The researchers propose that higher SAA levels might either alleviate or exacerbate glucose dysregulation in individuals with T2D, but emphasize the necessity for longitudinal studies to establish the directionality of this relationship.

Furthermore, the study underscores the importance of consistent saliva collection timing for accurate SAA interpretation as a biomarker, given its natural daily fluctuations.

Conclusions and Considerations

While both qPCR and ddPCR methods proved effective in measuring AMY1 CN, caution is advised when drawing causal inferences due to the study’s cross-sectional design and limited number of participants with T2D/prediabetes.

Ultimately, further investigation is warranted to fully elucidate the role of SAA in glucose homeostasis and its potential health applications. Future studies should prioritize the timing of saliva collection, dietary context, and other relevant factors in establishing SAA as a reliable health biomarker.

July 8, 2025 0 comments

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Prebiotics may boost brain GABA through gut microbiota

by Dr. Michael Lee – Health Editor July 1, 2025

written by Dr. Michael Lee – Health Editor

Prebiotics May Boost Brain Health, Study Suggests

Researchers are exploring how gut health may influence brain function. A recent study discovered that certain dietary additions could potentially elevate brain GABA levels, which play a role in calming the mind. This work could open avenues for treating neurological disorders.

Gut-Brain Connection Explored

GABA, or gamma-aminobutyric acid, is a crucial amino acid that acts as an inhibitory neurotransmitter within the brain. Low levels are linked to conditions like depression and epilepsy. Scientists have been examining the link between gut health, mental well-being, and how specific foods might affect the brain.

In trials conducted on mice, researchers investigated whether brain GABA levels could be enhanced through dietary changes. The goal was to modulate gut bacteria to bypass the blood-brain barrier. The results were published in npj Science of Food in April 2025.

While the gut-brain connection is not novel, it is gaining attention. The study aimed to clarify the direct communication between the two systems: can increased gut-derived GABA directly lead to increased brain GABA levels?

Researchers found a direct link among gut GABA, brain GABA, and the gut microbiota during mouse trials. There are no conclusive results, however, as to whether gut microbiota-derived GABA can cross the blood-brain barrier to increase brain GABA. Further studies point to other possible pathways to increase brain GABA, such as through the Vagus nerve or hormonal pathways.

“Our study suggests that prebiotics have the ability to prevent or treat those brain diseases by increasing brain GABA levels via promoting gut GABA production through modulating gut microbiota.”

—Thunatchaporn Kumrungsee, Study Corresponding Author, Associate Professor at Hiroshima University’s Graduate School of Integrated Sciences for Life

The research team discovered that fructo-oligosaccharides (FOS) and enzymes derived from Aspergillus, like lipase and protease, elevated brain GABA levels in mice. FOS showed a significant increase in brain GABA in both the cortex and hippocampus, areas where GABA reduces excitability and promotes calmness. Additionally, FOS and enzyme supplementation increased homocarnosine levels in the hippocampus.

Food factors such as prebiotics and fungi-derived enzymes with prebiotic-liked effects have an ability to increase brain GABA and homocarnosine, a GABA-containing brain-specific peptide, which can possibly in turn enhance brain health through gut microbiota modulation, said Kumrungsee.

Homocarnosine has links to similar brain diseases. According to a prior study by Kumrungsee, homocarnosine-deficient mice showed depression-like behaviors and hyperactivity.

Despite a lack of proof of direct gut microbiota-derived GABA increases in the brain, the study indicates that prebiotic consumption may boost brain GABA levels. Further research is needed to understand the exact mechanisms by which the gut influences the brain. Ultimately, researchers hope to determine if the prebiotic treatments from this study can treat GABA-related conditions, such as epilepsy and depression.

According to the National Institute of Mental Health, in 2022, an estimated 28.3 million adults in the United States had a major depressive episode Source.

Study Contributors

Researchers contributing to this work included Jason D. Braga, Norihisa Kato, Noriyuki Yanaka, and Thanutchaporn Kumrungsee from the Program of Food and AgriLife Science at Hiroshima University. Also contributing were Jason D. Braga from the Institute of Food Science and Technology at Cavite State University, Yongshou Yang from the School of Life Sciences at Anhui University, and Kyoichi Nishio, Masasumi Okada, Manabu Kuroda, and Shotaro Yamaguchi from Amano Enzyme Inc.

This research was funded by the Japanese Society of Functional Fermented Foods and Enzyme Supplements, the Danone Institute of Japan Foundation research grant, the Japanese Ministry of Education, Culture, Sports, Science and Technology, and Amano Enzyme Inc.

July 1, 2025 0 comments

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