TL;DR:

Higher adherence to BHOD was significantly associated with a lower risk of osteoporosis.

BHOD = moderate intake of:

• Eggs

• Poultry — e.g., chicken and turkey

• Fish and other seafood

• Green leafy vegetables — e.g., spinach and kale

• Red and orange vegetables — e.g., carrots and red peppers

• Potatoes

• Margarine

• Tea

• Fruit juice

Info:

"We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply."

Abstract

Existing dietary patterns were not specifically designed to target osteoporosis and lack the precision required for effective prevention. We aimed to develop a Bone Health Optimized Diet (BHOD) that is tailored to more precisely reduce the risk of osteoporosis. Using dietary data from 183,092 UK Biobank (UKB) participants, we combined food–wide association analysis with machine learning to develop the BHOD. We identified 10 important osteoporosis-related food groups and integrated them to construct the BHOD. The protective association was observed between BHOD and the risk of osteoporosis, which was validated in both the UKB validation set and the NHANES population. Furthermore, the BHOD showed broad protective associations with other musculoskeletal disorders, such as rheumatoid arthritis and osteoarthritis. Importantly, high adherence to the BHOD mitigated the negative impact of genetic susceptibility on osteoporosis, with particularly pronounced benefits observed among individuals at high genetic risk. The multi-omics analysis identified multiple biomarkers (7 proteins, 66 metabolites, and 5 inflammatory markers) jointly associated with BHOD and osteoporosis risk, highlighting immune-inflammatory regulation and lipid metabolism as key biological pathways linking diet to bone loss.

https://www.nature.com/articles/s41538-026-00963-9

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First, during intense physical activity, the body consumes large amounts of oxygen so that the mitochondria (found in all body cells) can produce ATP energy. The problem is that this process is accompanied by the production of toxic, oxidizing gases (free radicals such as O_2^{\bullet-} and OH^{\bullet}). Normally, they are produced in tiny quantities and eliminated, but in intense physical activity, their production becomes very fast and massive to the point where a surplus occurs. When these toxic gases accumulate rapidly, they target the fatty membranes of heart cells and oxidize them (known as lipid peroxidation), leading to a major disruption in the electrical balance of the heart's functioning!

Under normal conditions, when the membrane is intact, there is an electrical balance and precise electronic activity resulting from the regulated passage of calcium and potassium across those membranes. When the membrane is damaged, the passage of these substances (calcium and potassium) becomes random. Therefore: the electrical balance becomes disturbed, a malfunction occurs in the heart's operation and oxygen delivery, the heart muscle experiences fatigue, with the potential occurrence of arrhythmias, heart failure, and perhaps cardiac arrest.

However, with proper nutrition and powerful antioxidants, this issue can be avoided and the heart membrane can be completely protected! Here are the scientifically corrected details of the roles of elements and vitamins:

🍋 Vitamin C: It acts within the water inside cells and in the surrounding fluids (because it is water-soluble), cleaning and ridding the cell of those floating toxic gases.

🥜 Vitamin E: It acts directly within the structure of the cell membrane (because it is fat-soluble), positioning itself in the lipid layer and protecting it by sacrificing itself and confronting free radicals before they can touch the membrane's fats!

🥕 Vitamin A: An important correction here! Unlike Vitamin E, which directly protects the fatty membranes of heart cells, Vitamin A does not protect the heart membrane; rather, it has a completely different essential role. It is involved in protecting and maintaining epithelial cells, mucous membranes, and skin cells, and regulating their growth.

🧪 Selenium: It is not an antioxidant on its own, but rather an essential cofactor that activates the body's antioxidant enzymes (such as glutathione peroxidase) to eliminate those toxic gases.

⚡ Magnesium and Zinc: They act as biological cofactors to activate enzymes (which are proteins produced by the body) such as the superoxide dismutase (SOD) enzyme to remove oxidation and eliminate free radicals.

🛡️ Glutathione: It is the most powerful internal antioxidant produced naturally by the body (specifically the liver is responsible for manufacturing it). When the liver functions well and secretes it, it completely removes oxidation from cell membranes and protects them par excellence!

That is why professional athletes, such as football players, care so much about eating them and their diet... and it made me laugh when the professor said: "Cristiano even knows what he's breathing!" 🤣🤣🤣🤣

Hi Everyone,

I'm a Virginia Tech Researcher who has used my research into the nutraceutical CLA (conjugated linoleic acid) to build a new kind of nutrition bar. CLA appears to work by burning fat and preserving muscle, and people have been taking it as a supplement for years. It is slow working, but appears consistent (recent meta-analysis of 69 studies confirmed fat loss with improved body parameters, increased lean mass/muscle).

Asbaghi O, Shimi G, Hosseini Oskouie F, et al. The effects of conjugated linoleic acid supplementation on anthropometrics and body composition indices in adults: a systematic review and dose–response meta-analysis. British Journal of Nutrition. 2024;131(3):406-428. doi:10.1017/S0007114523001861

My bars contain 4.68 grams of CLA and are under 200 calories. I truly struggle with weight as well, and wanted something to complement my weight loss journal, and I could not tolerate the large, hard-to-swallow pills.

CLAW Bars (for CLA-Weight Bars) are currently in a pre-launch phase on Kickstarter (with some nice incentives when it launches) and on Shopify for immediate sales. Are you interested in a product like this that might not be a main driver of weight loss, but rather a part of the weight/fat loss journal?

https://www.kickstarter.com/projects/goodfamilyfoodsgroup/claw-bar-research-inspired-nutrition-for-everyday-life

https://clawbar.myshopify.com/

Thanks for checking us out!

Debby

Ju, Y., Wright, M., and Good, D.J. (2025) Conjugated Linoleic Acid: a Fatty Acid with Health Benefits, Virginia Cooperative Extension Publication, HNFE-1123P, 1-8. https://www.pubs.ext.vt.edu/HNFE/hnfe-1123/hnfe-1123.html

US Patent application number US-20240238237-A1.

Hi there, been trying to pin point how much protein an average sized egg has. Sources vary from 5.5g to 6g. Same issue with large eggs, 6-7g grams. Since I am consuming around 100 eggs / week would love to know how much exactly protein I'm taking in.

How much protein for an average/large sized egg do you account in your diet?

Abstract:

• PMID: 42460423

A high-fat diet (HFD) with excessive sugar intake contributes to obesity and type 2 diabetes, leading to increased use of non-nutritive sweeteners (NNS). However, evidence on their metabolic effects remains inconsistent, especially between natural and synthetic NNS. This study compared the effects of a natural NNS, monk fruit extract (MFE), with sucrose and synthetic sucralose, at equivalent sweetness on body weight and glucose homeostasis in HFD-induced obese mice. Male C57BL/6 mice were fed an HFD for 8 weeks to induce obesity, then randomized to receive distilled water (control), sucrose (266 g/L), MFE (1.1 g/L; ~50% mogroside V), or sucralose (0.36 g/L) in drinking water for another 8 weeks. Body weight, food and water intake, and oral glucose tolerance tests (OGTT) were assessed. At sacrifice, serum biochemistry, organs, tissues, and duodenal expression of sweet taste receptors (T1R2/T1R3) and glucose transporters (SGLT-1/GLUT2) were analyzed. The results showed that sucralose and sucrose further increased body weight gain, whereas MFE did not promote additional weight gain despite increased food intake. MFE significantly reduced fasting blood glucose, while sucralose impaired glucose tolerance, reflected by increased OGTT area under the curve. No significant differences in visceral adipose tissue weights or duodenal T1R2, T1R3, SGLT-1, and GLUT2 expression were observed among groups. In conclusion, MFE, within ADI-equivalent doses, improved fasting glycemia without promoting further weight gain compared with the HFD-control, whereas sucralose exacerbated obesity-related impaired glucose tolerance. These findings suggest that natural sweeteners such as MFE may represent a safer alternative to added sugars and synthetic NNS for weight management and glycemic control for obese subjects.

Abstract

Background: Evidence is accumulating that gut bacterial communities modulate the outcome of dietary interventions.

Objective: To assess how gut microbial enterotypes correlate with obesity-related outcomes during one month of whole milk consumption.

Methods: This post hoc analysis used data from a previously published trial, which included a lead-in phase during which men with abdominal adiposity replaced habitual dairy product consumption with 400 g/day of whole milk for one month. We compared body weight, urinary metabolites, fecal metabolites, and gut microbiome composition and function based on shotgun metagenomic sequencing at the beginning and at the end of the lead-in phase between individuals with the two most prevalent enterotypes, the Bacteroides1 (B1) enterotype (n = 24) and the Ruminococcaceae (R) enterotype (n = 38).

Results: Individuals with the B1 enterotype, but not those with the R enterotype, exhibited decreases in body weight and the relative abundance of Streptococcus thermophilus. Multiple linear regression analysis identified enterotype as a strong predictor of body weight change (p = 0.0034). In addition, urinary taurine level change was positively associated with body weight change in B1 individuals, not in R individuals.

Conclusions: Our findings reveal an enterotype-specific response to an identical dietary modification, underscoring the value of integrating enterotype information into nutrition-intervention design and personalized nutrition strategies.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12943088/

Abstract

• PMID: 42654240

Background/objectives: Dietary modifiers of the gut ecosystem may influence intestinal and host responses associated with psychological stress. However, it remains unclear whether sucralose, a widely consumed non-nutritive sweetener, alters host-microbiota interactions following chronic stress exposure. We investigated the effects of short-term experimental sucralose exposure in mice previously subjected to chronic restraint stress (CRS).

Methods: Following completion of the CRS protocol, mice received 0.03% or 0.1% sucralose in drinking water for 12 days. Intestinal phenotypes, cecal microbial community structure, microbial metabolites, colonic epithelial gene expression, and epithelial serotonergic responses following allyl isothiocyanate (AITC)-induced visceral stimulation were evaluated.

Results: Colon length was significantly reduced in the 0.1% sucralose group, whereas intestinal permeability remained unchanged. Sucralose selectively altered colonic epithelial gene expression and was associated with changes in cecal microbial community structure without marked changes in alpha diversity. The relative abundance of Bacteroides acidifaciens was significantly reduced, particularly in the 0.1% sucralose group. Fecal acetate and cecal tryptophan concentrations were decreased following sucralose exposure. Following AITC-induced visceral stimulation, the CRS + 0.1% sucralose group exhibited reduced immobility behavior together with increased epithelial serotonin and 5-hydroxyindoleacetic acid concentrations.

Conclusions: In mice previously exposed to CRS, short-term sucralose exposure was associated with colon shortening, differences in cecal microbial community structure, reduced Bacteroides acidifaciens abundance, decreased fecal acetate and cecal tryptophan concentrations, and altered epithelial serotonergic responsiveness following visceral stimulation. The behavioral and epithelial serotonergic findings suggest that prior stress exposure may influence selected host responses to sucralose. These findings provide a basis for future studies examining how dietary sweeteners modify host-microbiota interactions following chronic stress exposure.

Conclusion

Linear trends towards increased bone catabolism among children and accelerated bone turnover among adults following PBDs were observed despite adequate vitamin D status and approximately adequate calcium intake. The role of lower protein intake and calcium bioavailability in PBDs and bone health requires further investigation.

Funding

Open Access funding provided by University of Helsinki (including Helsinki University Central Hospital). The MIRA2 study was supported by the Signe and Ane Gyllenberg Foundation and the Päivikki and Sakari Sohlberg Foundation. The Juho Vainio Foundation and the Foundation for Nutrition Research supported this bone-related sub-study.

ABSTRACT

Purpose

Limited evidence exists on the effects of plant-based diets (PBDs) on bone metabolism, especially in children. We studied bone and mineral metabolism and intakes of bone-related nutrients in 2–7-year-old children and their caregivers who followed vegan, vegetarian (collectively referred to as PBD), and omnivorous diets.

Methods

Blood samples were collected from 29, 18, and 24 children following vegan, vegetarian, or omnivorous diets (mean age 4.5 ± 1.5 years, 51% girls) and from 29, 23, and 24 adult caregivers, respectively (mean age 38.2 ± 4.4 years, 57% women). Serum tartrate-resistant acid phosphatase 5b (S-TRAP5b), bone-specific alkaline phosphatase (S-BAP), 25-hydroxyvitamin D (S-25(OH)D), and plasma parathyroid hormone (P-PTH) were analysed using linear trends by contrast analysis [adjusted for age, sex, and (standardized) body mass index]. Nutrient intakes were calculated from 3-day food records.

Results

Linear trends towards higher concentrations of P-PTH among children and bone resorption marker S-TRAP5b and bone formation marker S-BAP among adults in PBDs were observed (P < 0.05). Mean vitamin D intakes (diet + supplements) were adequate (> 10 µg/d), mean 25(OH)D concentrations were > 70 nmol/l, vitamin D supplement use was common (74–100%), and mean calcium intakes were approximately adequate in all age and diet groups. Protein intake was lower in PBDs (12–14 E%) than in omnivores (16–17 E%) (P < 0.05).

Conclusion

Linear trends towards increased bone catabolism among children and accelerated bone turnover among adults following PBDs were observed despite adequate vitamin D status and approximately adequate calcium intake. The role of lower protein intake and calcium bioavailability in PBDs and bone health requires further investigation.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12426156/

Dear all,                      

We're looking for volunteers to take part in a study exploring the effect of prebiotic supplementation on sleep, mood, cognition and the gut microbiome.

To participate, you must:

• Be 25-50 years old
• Have some mild sleep disturbance
• Not have a diagnosed sleep disorder or major health problems

What’s involved?

• Four visits to the University of Reading, UK (less than 3 hours each)
• Completing cognitive tests, mood, sleep and food questionnaires
• Finger-prick blood samples
• Two stool samples
• Wearing a sleep tracking watch for 4 weeks total

How do I find out more?

To find out more, please contact Gregory Patient at [g.s.patient@pgr.reading.ac.uk](mailto:g.s.patient@pgr.reading.ac.uk).

Alternatively, please follow this link to find out more information: REDCAP link 

This study has received ethical approval by the University of Reading Research Ethics Committee, project UREC 26/16, end date 20-05-2027

Thank you.

A six-month randomized, double-blind trial compared freeze-dried powders equivalent to one cup of blueberries daily, half a cup, or a calorie- and carbohydrate-matched placebo. All 115 completers had metabolic syndrome.

The one-cup group improved flow-mediated dilation (FMD), which measures how well an artery widens in response to increased blood flow. Researchers test this by briefly restricting blood flow with an arm cuff, releasing it, and measuring how much the artery expands.

FMD improved from baseline by 1.45 percentage points with one cup, compared with 0.00 with half a cup and 0.39 with placebo. That puts the one-cup benefit at 1.06 percentage points beyond placebo.

How does that compare with other blueberry studies? A 2024 meta-analysis combined results from six studies involving 276 participants, including this six-month trial. Across those studies, blueberries improved FMD by an average of 1.50 percentage points. The size of the benefit varied considerably between studies.

For scale, if FMD increased from 6% to 7.5%, that would be a 1.5-percentage-point increase and a 25% relative improvement in the artery’s dilation response. This is an illustrative calculation, not the trial’s reported starting and ending values.

The one-cup group also improved augmentation index, a measure related to arterial stiffness. Blood pressure, pulse-wave velocity, and insulin resistance did not improve. Insulin resistance was the trial’s primary outcome; vascular measures were secondary.

Dr. Rhonda Patrick discusses these findings, including the 25% comparison, in her new episode on the science of blueberries. Here's a link to the timestamp

https://doi.org/10.1039/d6fo00807k

Walnut consumption improves mood and is associated with increased urinary excretion of 5-hydroxyindoleacetic acid and urolithins in a randomized crossover trial

Abstract

Walnuts are nutrient-dense and rich in omega-3s, tryptophan, fiber, and ellagitannins, but human evidence tying them to mood outcomes and plausible biological markers has been thin. This open-label randomized crossover trial tested whether daily walnut intake changes mood in young adults and whether those changes track with urinary serotonin metabolism and walnut-derived microbial metabolites. The trial enrolled 31 healthy adults, mean age 24.0 ± 4.2 years, 90.3% female, all normal weight at baseline, and compared an 8-week walnut period with a nut-free control period in an 18-week crossover design.

Compared with control, walnut intake lowered total mood disturbance by -4.85 points (p = 0.030). Anger fell by -1.27 points (p = 0.025) and fatigue by -1.70 points (p = 0.010), but both missed FDR correction (q = 0.075 and q = 0.060). Urinary 5-HIAA rose during the walnut phase by 0.63 (95% CI 0.03 to 1.23, p = 0.038, q = 0.038), while cortisol did not change (-0.14, p = 0.336, q = 0.837). Within-person increases in 5-HIAA tracked with lower fatigue (r = -0.392, p = 0.031) and lower total mood disturbance (r = -0.362, p = 0.049). Urolithins A and B also increased strongly (beta = 1.87, p < 0.001, q < 0.001 and beta = 0.55, p = 0.001, q = 0.001) and correlated with concurrent 5-HIAA changes (r = 0.537 and r = 0.634).

Study Design and Methodology

• Design: 18-week open-label randomized crossover trial
• Sample size: N = 31 completers
• Intervention: 40 g/day walnuts for 8 weeks
• Control: 8-week nut-free period
• Washout: 2 weeks
• Blinding: No blinding
• Metabolic ward: No
• Visits: baseline, week 8, week 18
• Primary outcome: total mood disturbance from the Profile of Mood States (POMS)
• Secondary measures: perceived stress, WHO-5 well-being, trait food cravings, urinary 5-HIAA, urinary cortisol, urinary urolithins A and B
• Biomarker methods: ELISA for 5-HIAA and cortisol, HPLC-QTOF-MS for urolithins
• Analysis: linear mixed-effects models, repeated-measures correlations, FDR correction within outcome families

Key Findings

• Walnuts reduced total mood disturbance by -4.85 points versus control (p = 0.030).
• Anger decreased by -1.27 points (p = 0.025, q = 0.075), and fatigue decreased by -1.70 points (p = 0.010, q = 0.060).
• Perceived stress and well-being did not change significantly.
• Trait food craving domains showed nominal reductions in:
  • anticipation of relief from negative states: -0.76 points (p = 0.035, q = 0.157)
  • guilt over cravings/giving in: -0.72 points (p = 0.017, q = 0.153)
• Urinary 5-HIAA increased by 0.63 (95% CI 0.03 to 1.23, p = 0.038, q = 0.038).
• Urinary cortisol did not change (-0.14, p = 0.336, q = 0.837).
• Higher 5-HIAA tracked with lower:
  • fatigue (r = -0.392, p = 0.031)
  • total mood disturbance (r = -0.362, p = 0.049)
• Urolithin A rose sharply during walnut intake (beta = 1.87, 95% CI 1.49 to 2.26, p < 0.001, q < 0.001).
• Urolithin B also increased (beta = 0.55, 95% CI 0.24 to 0.85, p = 0.001, q = 0.001).
• Changes in urolithins correlated with changes in 5-HIAA:
  • urolithin A: r = 0.537
  • urolithin B: r = 0.634
• BMI, body fat, and physical activity stayed stable across conditions.
• Diet quality was slightly higher during the walnut phase (10.0 ± 1.7 vs 9.2 ± 1.9, p = 0.006).

Limitations

• Small sample size: only 31 completers.
• Open-label design: no blinding, so expectancy effects are possible.
• Short duration: 8-week intervention periods only.
• Crossover gap: no extra assessment right after washout, so carryover can’t be ruled out perfectly.
• Highly skewed sample: young adults, mostly women (90.3% female), limiting generalizability.
• Self-report outcomes: mood, stress, well-being, and cravings relied on questionnaires.
• Control condition differs from usual habits: participants avoided all nuts, which could shift diet beyond walnuts alone.
• Mechanistic inference is indirect: urinary 5-HIAA reflects whole-body serotonin metabolism, not brain serotonin directly.

Discussion and Implications

This paper adds human crossover data showing that a daily walnut serving did more than confirm dietary adherence biomarkers. It was tied to a measurable improvement in total mood disturbance, with the strongest signal sitting in the negative mood domains, especially fatigue. The biomarker pattern matters here: walnut intake increased urinary 5-HIAA and urolithins, and the within-person coupling between those metabolites lines up with the idea that walnut polyphenol metabolism and serotonin-related biology are moving together during the intervention.

The food-craving data fit the same general picture, even though those outcomes didn’t survive FDR correction. People reported less craving-related guilt and less desire to eat for relief from negative states, and those mood-craving links were strong within individuals. That doesn’t prove mechanism, but it does strengthen the case that whole foods like walnuts can influence affective state, not just nutrient intake.

Conclusion

An 8-week walnut intervention improved total mood disturbance in healthy young adults and increased urinary 5-HIAA and urolithins. The signal was strongest for negative mood states like fatigue and anger, while stress and well-being stayed unchanged.

The study adds a useful human link between walnut intake, mood, and urinary metabolite changes, but the sample was small, mostly female, and unblinded, so more work is needed before drawing broad conclusions.

There are already many dietary supplements on the market, including NADH products such as Celfull. So, does NADH actually have anything to do with sleep? The answer is yes, but there's an important distinction.

A more accurate way to put it is that NADH has a biological connection with sleep and circadian rhythms, but we still can't say that taking NADH supplements will necessarily improve sleep.

NAD⁺ and NADH are two interconvertible redox forms of an important coenzyme. Research has found that the redox state of NADH inside cells changes in a circadian pattern, while the NAD⁺/NADH system is also involved in metabolic pathways that regulate the biological clock.

One study directly observed circadian oscillations in the NADH redox state in mammalian cells, suggesting that NADH itself is connected to the cellular mechanisms underlying circadian rhythms. (DOI: 10.1074/jbc.M116.728774)

There also appears to be a two-way relationship between the NAD⁺/NADH system and the core circadian clock. NAD⁺ can influence circadian-related proteins through NAD⁺-dependent pathways such as SIRT1, while the circadian clock can in turn regulate NAD⁺/NADH metabolism. (DOI: 10.1016/j.molcel.2020.04.010, DOI: 10.1016/j.semcdb.2021.07.008)

As for direct NADH supplementation and sleep, there aren't many human studies yet.

One double-blind, placebo-controlled trial gave people with chronic fatigue syndrome 20 mg of NADH per day and also evaluated sleep quality. However, most of the measured outcomes did not differ significantly from placebo. The only changes reported were within the NADH group itself, a decrease in anxiety score and a lower maximum heart rate after an exercise stress test, and neither of those is a sleep outcome, so the study does not provide enough evidence to conclude that NADH improves sleep.(DOI: 10.1016/j.rce.2009.09.015)

Another study used a combination of 20 mg NADH + 200 mg CoQ10 and observed changes in some sleep-related measures. However, because NADH and CoQ10 were taken together, it's impossible to determine whether the effects were specifically caused by NADH. (DOI: 10.3390/nu13082658)

So yes, NADH is connected to sleep, particularly through the relationship between cellular redox status and circadian rhythms. But right now, the human evidence is still limited when it comes to the claim that taking NADH directly can improve sleep in otherwise healthy people. That's why, when I see claims linking NADH and sleep, I think it's important to separate three different things: Mechanistic research on NADH and circadian rhythms, Human trials of NADH supplementation, Sleep studies involving NMN or NR that increase NAD⁺. These are related, but they are not the same thing.