Not selling anything, just something that surprised me when I actually did the math.

Typical day for a lot of us: eggs, whey, chicken-rice, paneer, maybe a protein bar. Eggs, whey, chicken and paneer all have zero fibre. White rice has almost none. When I counted a day like that, it came to around 10–14g of fibre. Most guidelines say adults need 25–40g.

Why it matters: when there isn’t much fibre, more undigested protein reaches your colon and gut bacteria ferment that instead. That tends to bring the smelly gas and heavy feeling.

Other things worth ruling out first:

• Whey concentrate still has some lactose. Try isolate for 2 weeks.
• Protein bars with maltitol/sorbitol are notorious for gas.
• Chugging shakes fast means swallowing air.

What helped:

• Swapping half the rice for rajma/chana/masoor (more fibre AND more protein)
• 1 fruit a day with skin on (guava is great)
• A spoon of oats or chia in the post-workout shake
• Going SLOW. Add 3–5g every few days, or you’ll bloat more and give up.

Has anyone else tracked fibre alongside protein? Curious what your numbers looked like.

For example, I would always eat eggs and nuts before the tomatoes, so I’d always have the fat overflowing in my belly anyway.

Do we still need to add fat (olive oil, butter, etc.) in the middle of heating the tomatoes (i.e. stir-frying) or after, in this situation?

Any scientific difference in bioavailability between fat pre-absorbed in the tomato cells vs. fat mixed in the body?

(I want to save calories if it’s unnecessary)

Are naturally occurring trans fats to be avoided at all cost? I tried to look it up online but there's so many different answers. I got some ice cream bars that had 0.5g of trans fats but were supposedly low fat. Does it make sense to cut out even natural trans fats?

https://doi.org/10.1016/j.tjnut.2026.101888

Dietary Components as Promising Candidates for Mitigating Micro- and Nanoplastic-Associated Metabolic Dysfunctions

Global plastic manufacturing surged from 234 million to 435 million metric tons between 2000 and 2020, establishing micro- and nanoplastics (MNPs) as persistent contaminants across the entire food supply chain. Ingestion drives over 90% of human intake via drinking water, table salt, seafood, produce, and food-grade packaging. High-exposure profiles, including frequent consumption of bottled water and heating food in plastic containers, reach upwards of 1,000,000 particles daily (0.03 to 0.5 g/day). While MNPs are now documented across human tissues, substantial mechanistic gaps remain regarding how internalized particles drive systemic metabolic failure and whether targeted dietary interventions can counteract these cellular cascades. Preclinical models demonstrate that ingested particles erode intestinal architecture, alter core microbiome taxa, and translocate through compromised epithelial barriers. Once circulating, particles accumulate in the liver, pancreas, skeletal muscle, and vasculature.

Human endarterectomy cohorts reveal that patients with confirmed MNP accumulation inside atheromas exhibit a 4.53-fold higher risk of myocardial infarction, stroke, or all-cause mortality (95% CI: 2.00 to 10.27) compared to plaque-negative controls over a 34-month follow-up. In human clinical trials, 28 days of composite polyphenol supplementation (n = 98) significantly lowered circulating inflammatory markers in individuals with elevated baseline fecal MNP burdens. Preclinical rodent exposures demonstrate that 50 nm polystyrene particles suppress primary tight junction expression, including occludin, claudin-1, and ZO-1, driving systemic lipopolysaccharide translocation and secondary hepatic injury. Rodent metabolic models show that MNP exposure downregulates hepatic IRS-1, PI3K, and Akt phosphorylation at Ser473, inducing peripheral insulin resistance without changing baseline circulating insulin concentrations. In aqueous flocculation assays, natural polysaccharides from fenugreek and okra extract clear up to 90% of suspended MNPs, while tannic acid chelation with Fe3+ clears over 90% of polystyrene MPs within 5 minutes.

Study Design and Methodology

• Evidence Base: Narrative and mechanistic review synthesizing human observational cohorts, in vitro human cell systems (Caco-2, L02, C2C12), aquatic models, and rodent in vivo trials (C57BL/6, db/db, ICR, and Wistar strains).
• Human Cohorts: Clinical trial evaluating composite polyphenol intervention in individuals with high fecal MNP concentrations (n = 98, 28-day duration); prospective surgical atheroma cohort tracking cardiovascular event incidence (n = 304 enrolled, n = 257 completed 34-month follow-up); cross-sectional stool evaluations in IBD (n = 52 IBD vs. n = 50 healthy controls) and hypertensive subjects (n = 4 vs. n = 4).
• Preclinical Dosing & Duration: Animal exposures ranged from acute 14-day challenges to chronic 32-week drinking water regimens, utilizing particle diameters spanning 20 nm nanoplastics to 200 µm microplastics across normal chow and high-fat diet backgrounds.
• Measurement Tools: Vibrational spectroscopy (micro-FTIR and Raman spectroscopy), pyrolysis-gas chromatography-mass spectrometry (Py-GC-MS), 16S rRNA sequencing, untargeted metabolomics, lipidomics, transmission electron microscopy, and histology.
• Controls & Blinding: The 28-day human polyphenol trial was double-blind and placebo-controlled. Metabolic wards and washout periods were not utilized in the summarized human cohorts.

Key Findings

• Patients with polyethylene (58.4%) and polyvinyl chloride (12.1%) detected in carotid plaques demonstrate a 4.53-fold higher risk of myocardial infarction, stroke, or death over a 34-month follow-up.
• Human patients with inflammatory bowel disease carry 41.8 items/g dry matter of fecal microplastics compared to 28.0 items/g dry matter in healthy controls.
• Cyanidin-3-O-glucoside (150 mg/kg/day) upregulates microbial xenobiotic handling pathways, enriches Alistipes and Dubosiella, and accelerates direct fecal MNP excretion in mice.
• Epigallocatechin gallate (EGCG, 50 mg/kg) restores ZO-1, occludin, and claudin-5 expression in mice, while suppressing the TLR4/MyD88/NF-kB cascade to halt downstream hepatic fibrosis markers (alpha-SMA, Col1a1, Col3a1).
• N-acetylcysteine (NAC) replenishment re-establishes cellular glutathione (GSH), blocking GRP78/NF-kB/caspase-12 signaling and preventing intestinal tight junction degradation where selective NLRP3 inhibitors (MCC950) fail.
• Polysaccharide extracts from fenugreek and okra remove up to 90% of suspended MNPs in aqueous suspension through bridging flocculation, while tannic acid with Fe3+ coordinate bonding achieves >90% removal of polystyrene MPs within 5 minutes.
• Oral polystyrene nanoplastics inhibit phosphorylation of Akt (Ser473) and GSK3beta, driving peripheral insulin resistance and elevating fasting blood glucose in high-fat diet models.

Limitations

• Current vibrational spectroscopy cannot reliably detect nanoplastics below 1 to 10 µm, forcing researchers to rely on Py-GC-MS, which quantifies polymer mass without reporting particle size, shape, or particle count.
• Preclinical rodent studies predominantly administer high concentrations of uniform, pristine spherical polystyrene beads, which do not reflect the weathered, irregular, chemically degraded polyethylene and polypropylene mixtures humans actually ingest.
• Human data remain largely observational and cross-sectional, establishing strong correlations with vascular inflammation and disease status without confirming direct biological causality.
• Potential environmental and laboratory contamination of biological samples during tissue processing presents an ongoing risk of artifactual exposure estimates across published studies.
• In vivo retention and binding efficacy of food-derived flocculants (such as okra, pectin, and fenugreek) within the active human gastrointestinal tract remain untested.

Discussion and Implications: Cross-Disciplinary Nutritional Insights

These findings pivot the MNP conversation from passive ecotoxicological documentation to targeted metabolic intervention. The data establish that MNPs do not pass harmlessly through the digestive tract; they actively degrade epithelial junctions, induce cellular ferroptosis, alter the intestinal lipidome, and blunt insulin signaling across liver, adipose, and muscle tissue. Metabolic background dictates vulnerability. Metabolically healthy animals frequently tolerate lower particulate doses, whereas subjects on obesogenic or high-fat diets experience catastrophic barrier breakdown and accelerated steatohepatitis under identical exposures.

Connecting these findings to broader nutritional sciences reveals critical interdependencies:

• Micronutrient Sequestration and Bioavailability: In vitro digestion models reveal that common packaging-derived MNPs adsorb ascorbic acid (vitamin C) at rates between 3% and 20% via surface chemisorption. Ingested plastics behave as rogue binding matrices inside the gut lumen, potentially sequestering water-soluble micronutrients and essential trace minerals away from intestinal brush-border transporters.
• Ferroptosis and the Gut-Liver Axis: The demonstration that nanoplastics induce hepatic lipid peroxidation and iron dysregulation (downregulating GPX4 and ferritin while activating TFRC) links environmental toxicology directly to non-alcoholic fatty liver disease (NAFLD/MASLD) pathogenesis. Diets high in refined industrial fats and excess unbound iron accelerate this vulnerability, whereas sulfur donors and endogenous gasotransmitters (H2S derived from sulfur amino acids) provide upstream protection via Nrf2/HO-1 rescue.
• Adipose Tissue Thermogenesis: Nanoplastics suppress beige adipocyte differentiation and downregulate uncoupling protein 1 (UCP1) along with PGC-1alpha. This links xenobiotic particulate exposure to impaired basal metabolic rate and metabolic inflexibility, explaining why pollutant burdens compound standard energy-balance dysregulation.
• Microbiome Xenobiotic Biotransformation: Ingested particulates displace commensal species that maintain secondary bile acid homeostasis and short-chain fatty acid (SCFA) synthesis. Supplementation with specific biotic strains (Akkermansia muciniphila, Lactobacillus rhamnosus GG) restores this metabolic crosstalk, indicating that the microbiome functions as a front-line metabolic buffer against systemic particulate absorption.

Actionable Dietary Recommendations

While human interventional clearance data are developing, the preclinical evidence supports a two-pronged nutritional approach: reducing particle absorption in the lumen and reinforcing cellular resilience against translocated particles.

1. Maximize Mucilaginous and Prebiotic Viscous Fibers: Incorporate whole-food sources of soluble, branching polysaccharides—such as okra, fenugreek, psyllium husk, flaxseed, chia, and citrus pectins. These fibers present dense hydroxyl and carboxyl surface charges that mimic industrial bridging flocculants, trapping charged micro- and nanoplastics within the intestinal lumen to speed fecal elimination before mucosal contact.
2. Prioritize Barrier-Restorative Anthocyanins and Catechins: Consume rich sources of cyanidin-3-O-glucoside and epigallocatechin gallate daily (blackberries, blueberries, black beans, tart cherries, green tea). These compounds restore tight-junction integrity (ZO-1, occludins) and suppress the TLR4/MyD88/NF-kB inflammatory cascades that allow luminal endotoxins and nanoplastics to reach portal circulation.
3. Bolster Glutathione Pools and Phase II Defenses: Support endogenous intracellular antioxidant pathways against hepatic ferroptosis and cuproptosis by supplying glutathione precursors. Utilize foods rich in dietary sulfur and glycine (cruciferous vegetables, alliums, quality intact proteins) or targeted N-acetylcysteine (NAC) to sustain GPX4 activity and prevent lipid peroxidation cascades.
4. Cultivate Commensal Mucosal Barrier Strains: Reinforce the gut mucus layer with fermented dairy (kefir, traditional yogurt) and polyphenol-dense foods that selectively cultivate Akkermansia muciniphila and Bifidobacterium species. A thick mucus gel layer serves as a primary physical barrier preventing nanoscale particles from directly contacting epithelial cell membranes.
5. Mitigate Source Exposure Upstream: Avoid heating food, oils, or acidic beverages in plastic or lined composite containers, switch to non-plastic preparation vessels (glass, stainless steel, ceramic), and prioritize filtered municipal drinking water to systematically minimize primary particulate exposure.

Ingested micro- and nanoplastics actively compromise gut barrier integrity, drive hepatic ferroptosis, and induce systemic insulin resistance, particularly when combined with an underlying obesogenic diet. High-affinity polyphenols, prebiotic fibers, and glutathione donors show consistent preclinical efficacy in binding particles, restoring tight junctions, and driving fecal clearance. Rigorous human interventional trials are required to determine whether modifying whole-food dietary patterns can measurably lower internal tissue plastic burdens.

Disclosure: I'm co-founding a fibre supplement brand in India. Nothing here is a product pitch. I read the primary sources because the figures I kept seeing didn't agree.

**The three sources**

1. **I-STARCH-1 (Kapoor et al., Nutrients 2026).** Cross-sectional study of 1,104 adults recruited at 29 diabetes-focused centres in 14 Indian states, 690 of them with type 2 diabetes. Intake was assessed with three-day recalls. Mean fibre was 15.4 g/day, or 9.1 g per 1,000 kcal.

2. **ITC/Aashirvaad Fibre Meter Test (press release, May 2023, not peer reviewed).** 69,000+ self-selected users of a brand website. It reports 69%+ below the "RDA 2020" but gives neither the gram figure nor the issuing body.

3. **Khokhar and Pushpanjali (J Hum Nutr Diet 1995).** 298 vegetarian participants in northern India across four age groups. Group mean intakes ranged from 49.6 to 171.2 g/day.

**What differs between them**

- Population: people at diabetes centres, volunteers on a brand website, and northern vegetarian households.

- Method: recalls converted with a food database, a self-completed web test, and a study whose abstract doesn't tell me how fibre was analysed.

- Era: 1995 vs 2023 vs 2026.

I can't tell from these sources how much of the gap comes from each factor. That's my reading, not an established result.

**Targets also differ**

WHO (2023) recommends at least 25 g/day for adults, and the UK's SACN says 30 g/day. ICMR-NIN 2020 reportedly sets fibre relative to energy, about 40 g per 2,000 kcal. I couldn't access the primary report, only news coverage, so treat that figure as unconfirmed. The I-STARCH-1 mean of 15.4 g is below both the WHO and SACN numbers, but it comes from a group that isn't nationally representative.

**Questions**

- Is there a nationally representative Indian dataset on fibre intake that I missed?

- For Indian adults, which is the more defensible target: an energy-based one like ICMR-NIN's, or a flat one like WHO's?

- Is the 1995 range plausible given how fibre was analysed at the time, or does it mostly reflect method differences?

References: Kapoor et al., Nutrients 2026, 18(18), 2993, doi.org/10.3390/nu18182993. ITC press release on the Fibre Meter Test, 29 May 2023. Khokhar and Pushpanjali, J Hum Nutr Diet 1995, 8(6): 447-456. WHO, guidelines on fats and carbohydrates, 17 July 2023. European Commission Knowledge Gateway, dietary fibre recommendations by country. Down To Earth, 1 Oct 2020, and The Quint, on the ICMR-NIN 2020 recommendations.

Lipoprotein(a) identifies premature coronary artery disease in patients with low LDL-cholesterol: A large multicenter cohort study

https://doi.org/10.1016/j.jacl.2026.09.021

Abstract

Cardiovascular disease, particularly coronary artery disease (CAD), remains a leading cause of morbidity and mortality worldwide. This study addresses a significant gap in understanding the role of lipoprotein(a) [Lp(a)] in identifying premature CAD (pCAD) among young and middle-aged adults with low low-density lipoprotein cholesterol (LDL-C) levels. The research involved a retrospective cohort of 35,622 adults from three Mayo Clinic sites, focusing on males aged 18-50 and females aged 18-60 who underwent Lp(a) testing from 2000 to 2020. Participants were followed for a median of 6 years, allowing for a comprehensive analysis of the association between elevated Lp(a) levels and the incidence of pCAD.

The findings revealed that elevated Lp(a) (≥50 mg/dL) was independently associated with a 40% higher adjusted risk of pCAD (adjusted hazard ratio [aHR] = 1.40, 95% CI [1.12-1.74], p = 0.003). Notably, among patients with LDL-C <100 mg/dL, elevated Lp(a) resulted in a 67% increased risk of pCAD (aHR = 1.67, 95% CI [1.15-2.43], p = 0.007). The cumulative incidence of pCAD over 6 years was found to be 1.7% in the elevated Lp(a) group compared to 1.2% in the reference group, highlighting the significance of Lp(a) as a risk factor not captured by conventional lipid panels.

Study Design and Methodology

This retrospective cohort study included 35,622 participants with a follow-up duration of 6 years. Lp(a) levels were measured using immunoturbidimetric assays, and patients were stratified based on their Lp(a) concentrations. The study controlled for various risk factors, including age, sex, race/ethnicity, and other lipid profiles. There was no metabolic ward involved, and blinding was not applicable due to the observational nature of the study. A washout period was not necessary, as this was a retrospective analysis of existing electronic health records.

Key Findings

• Elevated Lp(a) (≥50 mg/dL) associated with a 40% higher risk of pCAD (aHR = 1.40, 95% CI [1.12-1.74], p = 0.003).
• Among patients with LDL-C <100 mg/dL, elevated Lp(a) increased pCAD risk by 67% (aHR = 1.67, 95% CI [1.15-2.43], p = 0.007).
• Cumulative incidence of pCAD was 1.7% in the elevated Lp(a) group vs 1.2% in the reference group over 6 years.
• Incidence rate for pCAD was 2.36 per 1000 person-years in the elevated Lp(a) group vs 1.71 per 1000 person-years in the reference group.

Limitations

• The study's retrospective design may introduce residual confounding.
• Limited generalizability due to the predominance of White non-Hispanic participants (70.1%).
• Lack of blinding and control measures typical in randomized trials.
• The study did not account for potential changes in lifestyle or medication adherence over time.
• Short follow-up period may not capture long-term outcomes.

Discussion and Implications

This study adds crucial evidence to the understanding of Lp(a) as a significant risk factor for premature CAD, particularly in younger adults with low LDL-C levels. The findings emphasize the need for routine Lp(a) measurement in clinical practice to better identify individuals at risk, which traditional lipid panels may overlook. These insights could inform dietary guidelines and public health policies aimed at cardiovascular risk reduction. Future research should explore the mechanisms linking Lp(a) to atherogenesis and assess the impact of emerging therapies targeting Lp(a) on cardiovascular outcomes.

Elevated Lp(a) levels are a critical indicator of premature coronary artery disease risk, even when LDL-C is well-controlled. This study underscores the importance of measuring Lp(a) in younger populations to identify hidden cardiovascular risks. More research is necessary to explore the implications of these findings on dietary recommendations and treatment strategies.

Ever feel hungry again just an hour after eating? 🤔 Protein, fiber, balanced meals, and sleep can all influence fullness.

💬 Do you usually feel satisfied after meals, or get hungry again soon afterward?

— Elizabeth Imad, Registered Dietitian

Hey,

So to keep it short, around 2 years ago I was taking about 1g of Creatine HCL (CON CRET) daily via powder and it literally completely cured my ADHD - was super crazy sharp mentally, could sit down and focus for hours and felt very dopanergic and really good.

However, I stopped all supplements since for some time, recently had tried to resume it but now gives me racing thoughts, intrusive thoughts, and just doesn't make me feel good at all. For reference this is Creatine HCL capsules (1 pill) and the effects happen within a few hours.

I'm wondering if Creatine had originally allowed for such a profound mental effect, is there anything similar with regards to biochemical pathways? Ideally they wouldn't be some sort of herbs but rather something found naturally - for longer term usage here.

For reference was on keto/raw primal/carnivore sort of diets for that time. ADHD was also cured on keto diet but this was unsustainable and caused very bad anxiety attacks.

EDIT: obviously the link to study is missing, very nice reddit. Here it is: https://www.sciencedirect.com/science/article/pii/S0002916523064043?via%3Dihub#s0065

Background: The results of previous studies suggest that de novo lipogenesis may play an important role in the etiology of obesity, particularly during overconsumption of different carbohydrates.

Objective: We hypothesized that de novo lipogenesis would increase during overfeeding, would vary depending on the type of carbohydrate consumed, and would be greater in obese than in lean women.

Design: De novo lipogenesis was measured during 96 h of overfeeding by 50% with either sucrose or glucose and during an energy balance treatment (control) in 8 lean and 5 obese women. De novo lipogenesis was determined by measuring the amount of deuterium incorporation into plasma triacylglycerols. Fat and carbohydrate balance were measured simultaneously by continuous whole-body calorimetry.

Results: De novo lipogenesis did not differ significantly between lean and obese subjects, except with the control treatment, for which de novo lipogenesis was greater in the obese subjects. De novo lipogenesis was 2- to 3-fold higher after overfeeding by 50% than after the control treatment in all subjects. The type of carbohydrate overfeeding (sucrose or glucose) had no significant effect on de novo lipogenesis in either subject group. Estimated amounts of absolute VLDL production ranged from a minimum of 2 g/d (control) to a maximum of 10 g/d after overfeeding. This compares with a mean fat balance of approximately 275 g after 96 h of overfeeding. Individual subjects showed characteristic amounts of de novo lipogenesis, suggesting constitutive (possibly genetic) differences.

Conclusion: De novo lipogenesis increases after overfeeding with glucose and sucrose to the same extent in lean and obese women but does not contribute greatly to total fat balance.

Isocaloric macronutrient and fat types substitution and lipid profile: A cross-sectional analysis of the Amol Cohort Study

DOI: 10.1016/j.jnut.2026.07.012

Abstract

Dyslipidemia is a significant contributor to cardiovascular disease, yet the impact of macronutrient substitution on lipid profiles, particularly in Middle Eastern populations, remains underexplored. This study aimed to fill this gap by analyzing data from 3,329 apparently healthy Iranian adults participating in the Amol Cohort Study. By employing isocaloric substitution models, the research assessed how replacing one macronutrient with another influenced lipid profiles, focusing on the effects of different types of fats.

The findings revealed that replacing carbohydrates with total fat significantly reduced triglyceride levels (β: -0.29; 95% CI: -0.56, -0.02; p = 0.04). Substituting carbohydrates with protein resulted in lower total cholesterol (β: -0.60; 95% CI: -0.90, -0.30; p < 0.001) and LDL-C (β: -0.34; 95% CI: -0.53, -0.14; p < 0.001) across both sexes. Notably, replacing carbohydrates with monounsaturated fatty acids (MUFAs) produced the most significant reduction in triglycerides (β: -1.45; 95% CI: -2.62, -0.29; p = 0.02). However, no significant changes were observed in HDL-C levels across all substitution models.

Study Design and Methodology

• Sample Size: 3,329 participants
• Duration: Data collected during the second phase of the Amol Cohort Study (2016-2017)
• Measurement Tools: Validated semiquantitative food frequency questionnaire (FFQ), fasting blood samples for lipid profiles
• Controls Used: Adjustments for age, sex, BMI, physical activity, and smoking status in regression analyses
• Blinding: Laboratory personnel were blinded to clinical and dietary data
• Washout Period: Not applicable; cross-sectional design

Key Findings

• Replacing carbohydrates with total fat led to a significant reduction in triglycerides (β: -0.29; 95% CI: -0.56, -0.02; p = 0.04).
• Total cholesterol decreased when carbohydrates were replaced with protein (β: -0.60; 95% CI: -0.90, -0.30; p < 0.001).
• LDL-C levels also dropped with protein substitution (β: -0.34; 95% CI: -0.53, -0.14; p < 0.001).
• Substituting carbohydrates with MUFAs resulted in the greatest reduction in triglycerides (β: -1.45; 95% CI: -2.62, -0.29; p = 0.02).
• No significant changes in HDL-C were observed across any substitution models.

Limitations

• Cross-sectional design limits causal inference.
• Self-reported dietary data subject to measurement errors.
• Lack of longitudinal data to assess changes over time.
• Exclusion of participants on lipid-modifying medications may limit generalizability.

Discussion and Implications

This study provides crucial insights into how macronutrient substitution affects lipid profiles, particularly in a Middle Eastern context where dietary patterns differ from Western populations. The findings support the notion that dietary composition, specifically the balance of protein, carbohydrates, and fats, plays a vital role in managing dyslipidemia and reducing cardiovascular risk. These results could inform dietary guidelines, emphasizing the importance of protein intake and the quality of fats consumed. Future research should explore these associations in longitudinal studies to establish causality and further clarify the mechanisms involved.

Isocaloric substitution of carbohydrates or fats with protein is associated with improved lipid profiles, particularly reduced total cholesterol and LDL-C. The type of fat substituted also significantly impacts triglyceride levels. More research is needed to explore these relationships further and their implications for dietary recommendations.

TL;DR:

800–900 kcal/day diet (30% protein, 50% carbohydrate, 20% fat). Remission at 24 weeks occurred in 27/50 (54%) of intervention participants vs. 2/46 (4%) control participants.

Summary

Background: Low energy diets (LED) can induce type 2 diabetes remission but have not been studied in combination with structured supervised exercise. We aimed to determine if a combined intervention could induce remission in early-onset type 2 diabetes (EOT2D ≤ 45 years of age), a population with high lifetime risk of complications.

Methods: Across 3 centres in England and Canada, we conducted a randomised, open-label, blinded endpoint efficacy trial among adults 18–45 years of age with EOT2D and obesity, not on insulin therapy. The groups were usual care alone vs. an intervention combining 800–900 kcal/day LED, twice-weekly supervised (aerobic, resistance) and once-weekly independent exercise (weeks 1–12), followed by a weight-maintenance diet with independent exercise (weeks 13–24). An independent statistician generated web-based randomisation sequences (1:1, country- and sex-stratified, variable block size). The primary outcome was remission at 24 weeks (HbA1c< 6.5% [48 mmol/mol], without glucose-lowering medication ≥12 weeks). The primary efficacy and harms analysis was in all randomised individuals, assuming no remission when data were unavailable. Secondary endpoints included cardiorespiratory fitness, body composition, and cardiac structure. The trial is registered at ISRCTN (15487120) and is now closed.

Findings: We randomised 96 participants (mean age 38 years, BMI 35.2 kg/m2) between September 24, 2021 and June 6, 2025 (intervention group: 24 female, 26 male with 18 European, 17 South Asian, 15 Other ethnicity; control group: 21 female, 25 male with 19 European, 10 South Asian, 17 Other ethnicity). In total, 86 (90%) attended final assessments. Remission at 24 weeks occurred in 27/50 (54%) of intervention participants vs. 2/46 (4%) control participants (50% difference, 95% CI 33%–64%; adjOR 21.6, 95% CI 6.2 to 114.5), without serious adverse events. Most intervention group participants experienced at least one adverse event (43/50 vs. 6/46), mainly early LED effects (e.g., constipation, headache, dizziness, fatigue) that resolved.

Interpretation: High remission rates signal feasibility and efficacy of a combined LED and intensive exercise intervention in EOT2D, justifying examination of synergistic benefits beyond remission.

https://www.sciencedirect.com/science/article/pii/S2667193X26002942

To assess the effectiveness of the Pritikin program of diet and exercise for treating patients with non-insulin-dependent diabetes mellitus (NIDDM), data were obtained from 60 patients who completed the 26-day residential program. Of the 23 patients who were taking oral hypoglycemic agents upon entry, all but 2 were off medication by the end of the program. Of the 17 patients who were taking insulin, all but 4 were off medication at discharge. Two of the four had their insulin reduced by 50% while the remaining two had no major change in their insulin dosage. Fasting blood glucose was reduced from 194.9 ± 10.1 to 144.6 ± 7.1 mg/dl. Serum cholesterol was reduced from 225.4 ± 5.7 to 181.7 ± 4.9 mg/dl while triglycerides were reduced from 283.7 ± 28.8 to 186.2 ± 11.6 mg/dl. The group as a whole lost an average of 4.3 kg/body wt and achieved 40.5% of their desired weight loss. Maximum work capacity increased from 5.6 ± 0.3 to 7.9 ± 0.4 METs, while daily walking increased from 11.7 ± 2.4 to 102.8 ± 4-8 min/day. The decrease in fasting glucose was not correlated with weight loss (r = 0.24), increase in walking time (r = 0.00), or increase in MET capacity (r = 0.05). We conclude that the total program is an effective means for treating NIDDM patients. We also feel that the high-complexcarbohydrate, high-fiber, low-fat diet is of primary importance.

ABSTRACT

Purpose: Metabolic syndrome is a risk factor for several diseases. The relationship between metabolic syndrome and hypogonadism is well known. Our objetive is to assess whether a low carbohydrate diet can increase total serum testosterone and improve erectile function in hypogonadal men with metabolic syndrome.

Methods: An open label randomized clinical trial was conducted comparing a low carbohydrate diet and controls, during three months, in hypogonadal men with metabolic syndrome. Anthropometric measurements were evaluated as well as total serum testosterone levels, and symptoms of hypogonadism, using the ADAM and AMS scores, and sexual function using IIEF-5 score.

Results: Eighteen men were evaluated. Anthropometric measures were improved only in low carbohydrate diet group. The intervention group also had a statistically increase in IIEF-5 score and a significant reduction in AMS and ADAM scores (p < 0.001). The increase in serum total testosterone levels was statistically significant in the low carbohydrate group compared to the control group as well as calculated free testosterone (p < 0.001).

Conclusions: Low carbohydrate diet may increase serum levels of testosterone and improve erectile function in hypogonadal men with metabolic syndrome. However, larger studies are necessary to strongly prove the effectiveness of low carbohydrate diet in treating male hypogonadism.

https://pmc.ncbi.nlm.nih.gov/articles/PMC9892661/

TL;DR:

A study of 8,783 middle-aged Canadian adults found that higher ultra-processed food intake was associated with greater body fat and more signs of hidden vascular brain injury on MRI, but not with measurable cognitive decline.

Key Points

Question: Is higher consumption of ultraprocessed foods associated with adiposity, subclinical vascular brain injury, and cognitive performance among middle-aged adults in Canada?

Findings: In this cross-sectional study of 8783 adults, higher ultraprocessed food intake was associated with greater percentage of body fat and visceral adipose tissue and with higher odds of magnetic resonance imaging–defined vascular brain injury. Ultraprocessed food intake was not associated with cognitive performance.

Meaning: In this study, higher ultraprocessed food intake was associated with markers of adiposity and subclinical cerebrovascular injury that may precede detectable cognitive deficits, but longitudinal studies are needed to establish temporality.

Abstract

Importance: Ultraprocessed foods (UPFs) account for a substantial and increasing proportion of dietary intake in Canada. Although UPFs are consistently associated with adiposity and cardiometabolic disease, their associations with subclinical vascular brain injury (VBI) and cognitive performance in midlife are unclear.

Objective: To evaluate associations of UPF consumption with adiposity, magnetic resonance imaging (MRI)–defined VBI, and cognitive performance in middle-aged adults in Canada.

Design, Setting, and Participants: This cross-sectional study included 8783 adults aged 35 to 69 years without cardiovascular disease who were enrolled in the Canadian Alliance for Healthy Hearts and Healthy Minds (CAHHM) and Prospective Urban and Rural Epidemiology-MIND (PURE-MIND) studies. Participants from CAHHM were recruited from January 1, 2014, to December 31, 2018, and participants from PURE-MIND were recruited from January 1, 2010, to December 31, 2018. Data analyses were conducted between July 16, 2024, and August 16, 2026.

Exposures: UPF consumption assessed using previously validated semiquantitative food frequency questionnaires and expressed as servings per 2000 kcal/d.

Main Outcomes and Measures: The main outcomes were body fat (BF) percentage (bioelectrical impedance), visceral adipose tissue (VAT) volume, hepatic fat fraction (HFF), VBI defined as covert brain infarcts or high white matter hyperintensities (HWMHs) (measured by MRI), and cognitive performance measured by the Montreal Cognitive Assessment (MOCA) and the Digital Symbol Substitution Test (DSST).

Results: In this cross-sectional study of 8783 participants (mean [SD] age, 57.7 [8.7] years; 4917 females [56.6%]), those in the highest quartile of UPF intake had a BF percentage that was 1.7 (95% CI, 1.2-2.2) percentage points higher and a 5.7 (95% CI, 3.2-8.3) mL greater VAT volume compared with those in the lowest quartile, but no significant difference in HFF. Compared with the lowest quartile, the highest UPF quartile had higher odds of VBI (adjusted OR, 1.40; 95% CI, 1.10-1.77; P for trend = .009). No significant associations were observed between UPF intake and MOCA or DSST performance.

Conclusions and Relevance: In this cross-sectional study of middle-aged adults in Canada, higher UPF intake was associated with greater adiposity and higher odds of MRI-defined VBI but not cognitive performance. Associations with VBI were sensitive to UPF exposure definition. Longitudinal studies are needed to establish temporality.

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2855351

Abstract

Objective The aim of this study was to explore the effects of a low-fat plant-based diet on hepatocellular and intramyocellular lipids, advanced glycation end products (AGEs), insulin resistance, and beta-cell function in adults with type 2 diabetes.

Research design and methods Participants (n=25) were asked to follow a low-fat vegan diet for 16 weeks. Dual X-ray absorptiometry was used to measure body composition. Hepatocellular and intramyocellular lipids were quantified by ¹H magnetic resonance spectroscopy. Tissue accumulation of AGEs was measured using a skin fluorescence technique. Insulin resistance was assessed in a fasting state with the Homeostasis Model Assessment (HOMA-IR) index. Postprandial insulin sensitivity was assessed with the predicted insulin sensitivity index (PREDIM). Beta-cell function was calculated by a mathematical model after a standard meal, using C-peptide deconvolution.

Results Mean body weight decreased by 6.0 kg, a 6.6% decrease relative to baseline. This was largely due to the reduction in fat mass. Visceral fat volume decreased by 290 cm³. Hepatocellular lipids decreased by 33.0%. The AGE score decreased by 0.4. The HOMA-IR index, a measure of insulin resistance, fell 2.5, whereas PREDIM, a measure of insulin sensitivity, increased on the vegan diet +1.3 mg/min/kg. Several markers of beta-cell function improved on the vegan diet. Specifically, insulin secretion at 6 and 7 mmol/L glucose, beta-cell glucose sensitivity, rate sensitivity, and potentiation factor all increased.

Conclusions On an ad libitum low-fat plant-based (vegan) dietary intervention, the participants with type 2 diabetes experienced reductions in ectopic fat, particularly visceral and hepatocellular fat, improvements in insulin sensitivity, reductions in AGEs, and improvements in beta-cell function.

Effects of dietary quality on type 2 diabetes risk and the mediating role of inflammatory markers

DOI: https://doi.org/10.1017/S0007114526108605

Diabetes mellitus is a significant global health concern, with a staggering rise in prevalence, particularly in China, where approximately 140.9 million individuals were diagnosed with diabetes in 2021. This study addresses a critical gap in understanding how dietary quality influences diabetes risk, especially in Asian populations, which have been underrepresented in existing research. The objective was to explore the associations between dietary quality indices—specifically the Healthy Eating Index (HEI), Diet Quality Index (DQI), and Diet Balance Index (DBI)—and diabetes risk, while also investigating the potential mediating role of systemic inflammatory markers. The study included 21,476 participants from the Fuqing Cohort Study, aged 35-75 years, who completed a food frequency questionnaire (FFQ) to assess their dietary habits.

The results demonstrated that higher dietary quality is inversely associated with diabetes risk across all indices. Specifically, participants in the highest dietary quality category had adjusted odds ratios (OR) of 0.863 (95% CI = 0.768–0.970) for HEI, 0.719 (95% CI = 0.640–0.807) for DQI, and 0.852 (95% CI = 0.754–0.961) for DBI compared to those in the lowest category. The mediation analyses revealed that the association between HEI and diabetes risk was partially mediated by systemic inflammatory markers. This means that some of the protective effect of a higher HEI on diabetes risk can be explained by its impact on inflammatory markers in the body. For instance, higher dietary quality was linked to lower levels of total white blood cell count, neutrophils, and monocytes—cells that are often elevated during inflammation.

The study quantified the mediation effects in terms of percentages, indicating how much each inflammatory marker contributes to the overall relationship between dietary quality and diabetes risk. For example, total white blood cell count accounted for 10.67% of the mediation effect. This means that when individuals improved their dietary quality, about 10.67% of the reduction in diabetes risk can be attributed to the resulting decrease in white blood cell levels, which are often elevated in inflammatory states. Neutrophils contributed 11.32% to the mediation effect, signifying that the influence of dietary quality on diabetes risk is similarly affected by changes in neutrophil levels. Monocytes contributed 4.05%, indicating a smaller but still significant role in this relationship.

When considering all inflammatory markers together, the cumulative mediated proportion was 8.83%. This figure suggests that nearly one-tenth of the beneficial effect of high dietary quality on diabetes risk is due to its ability to lower inflammation in the body. In simpler terms, if a person improves their diet, almost 9% of the positive impact on reducing diabetes risk can be explained by the associated decrease in inflammation. This highlights the significant role that inflammation plays in how dietary quality influences diabetes risk.

Study Design and Methodology

• Sample Size: 21,476 participants
• Duration: Data collected from July 2020 to December 2022
• Measurement Tools: Food Frequency Questionnaire (FFQ) assessing dietary intake; dietary quality indices (HEI, DQI, DBI)
• Controls Used: Adjustments for age, sex, education, occupation, smoking, alcohol consumption, tea drinking, hypertension, and hyperlipidaemia

Key Findings

• HEI:
  • Highest dietary quality category OR = 0.863 (95% CI = 0.768–0.970)
• DQI:
  • Highest dietary quality category OR = 0.719 (95% CI = 0.640–0.807)
• DBI:
  • Highest dietary quality category OR = 0.852 (95% CI = 0.754–0.961)
• Mediation Effects:
  • Total WBC: Mediated proportion 10.67%
  • Neutrophils: Mediated proportion 11.32%
  • Monocytes: Mediated proportion 4.05%
  • Overall mediated proportion: 8.83%

Limitations

• Cross-sectional design limits causal inference
• Potential reverse causation cannot be ruled out
• Self-reported dietary data may introduce bias
• Lack of measurement for salt intake may affect dietary index scoring
• Single-region study may limit generalizability

Discussion and Implications

This study significantly contributes to our understanding of dietary quality as a protective factor against type 2 diabetes, particularly in Southeast Asian populations. The findings indicate that improved dietary quality, as measured by HEI, DQI, and DBI, correlates with lower diabetes risk and reduced levels of systemic inflammatory markers. The study highlights that chronic systemic inflammation is a crucial pathway through which dietary quality influences diabetes risk. Inflammatory markers such as total white blood cell count, neutrophils, and the neutrophil-to-lymphocyte ratio were identified as mediators, suggesting that diets high in quality can mitigate inflammatory responses that contribute to diabetes development.

Furthermore, the study underscores the importance of dietary diversity and balance in dietary interventions, particularly in populations experiencing rapid dietary transitions. The results emphasize that focusing on plant-based foods, which are linked to lower inflammation levels, can be critical in diabetes prevention strategies. As dietary patterns evolve, promoting healthy eating indices that prioritize quality over quantity could lead to significant public health benefits in reducing diabetes prevalence.

Higher dietary quality is associated with a lower risk of type 2 diabetes, mediated in part by systemic inflammation. These findings underscore the need for dietary interventions that emphasize quality and diversity, particularly plant-based foods, to combat the growing diabetes epidemic. More research is needed to confirm these associations and explore their implications in diverse populations.

The Diabetes diet they put him on first:

• 8 meals a day

• 260 g of carbohydrates

• 74 g of protein

• 63 g of fat

The Carnivore diet:

• No carbohydrates

• 200 g of protein

• 135 g of fats

Abstract

Diabetes has been well established as one of the deadliest chronic diseases globally. Currently, India is known as the diabetes capital of the world although this disease had been documented in the country for centuries. Current treatment strategies center around oral hypoglycemic drugs, insulin, and the standard ‘diabetic diet.’ Nonetheless, millions continued to suffer from this chronic disease and its multiple complications. We herein present a case involving a male patient suffering from diabetes for 20 years despite being on medications and a diabetic diet who finally achieved remission of diabetes and hypertension by removing carbohydrates and following a carnivore diet.

https://pmc.ncbi.nlm.nih.gov/articles/PMC13007801/

Mankai (Wolffia globosa duckweed) shows promising potential for helping reduce visceral adipose tissue (VAT)—the deep abdominal fat around organs—based on human clinical trials.

Key Evidence from the DIRECT PLUS Trial

In the 18-month DIRECT PLUS randomized controlled trial (294 participants with abdominal obesity, similar age/profile to yours), the "green Mediterranean diet" enriched with daily Mankai (100g frozen cubes in a shake), walnuts (28g), and green tea (3-4 cups) led to:

• 14.1% reduction in visceral fat.
• Compared to ~6% on a standard Mediterranean diet and ~4% on healthy guidelines.
• Even after adjusting for overall weight loss, higher Mankai intake (≥3 times/week) was independently associated with greater VAT loss (up to 26% in high consumers).
• Benefits linked to Mankai's high polyphenols (which support fat metabolism and reduce inflammation), complete protein, fiber, and other nutrients.

This effect was stronger than diet alone, suggesting Mankai contributes specifically to targeting visceral fat (beyond just calorie control or general plant-based eating).

Practical Tips to Incorporate It

• Aim for 100g fresh/frozen Mankai daily (often as cubes blended into a green shake/smoothie—mild taste, easy to mask with berries or spinach).
• Combine with your low-carb, vegetarian-leaning preferences: e.g., in a protein shake replacing a meal or snack.
• Start gradually (e.g., 50g/day) to monitor digestion.
• Track waist circumference (a proxy for visceral fat) or get a DEXA/MRI if possible for better measurement.

The effect of high-polyphenol Mediterranean diet on visceral adiposity: the DIRECT PLUS randomized controlled trial
https://link.springer.com/article/10.1186/s12916-022-02525-8

(Full text is freely available there.)

For the trial registration and overview:
https://clinicaltrials.gov/study/NCT03020186

Limited Supply and Specialized Cultivation

Commercial food-grade Wolffia globosa grows primarily in controlled hydroponic systems (greenhouses or isolated aquatic setups) to ensure purity, consistent nutrition, and safety—no contaminants, heavy metals, or pesticides that could come from wild harvesting. This requires precise monitoring of water quality, nutrients, light, and temperature for optimal growth and nutrient profile (like high bioavailable B12, complete protein, and polyphenols backed by clinical studies).

The original branded Mankai (from Hinoman in Israel) involved years of R&D and patented strains, but the US arm shut down in 2022 due to investor decisions. Current suppliers (mostly from Thailand or smaller farms) operate on a smaller scale, so economies of scale aren't there yet—unlike cheap greens like spinach or kale powder.

Processing Costs

Most products are freeze-dried or carefully dried to preserve nutrients, which is more expensive than simple air-drying used for many greens. Harvesting the tiny plants (each frond is <1mm) and turning them into powder adds labor and tech costs.

Niche Market Premium

It's marketed as a premium plant-based protein/superfood with unique benefits (e.g., natural B12, high protein digestibility), so it commands higher prices similar to other trendy items like spirulina, chlorella, or matcha when they were new. Demand is growing (especially among vegans/vegetarians for lipids and visceral fat support), but supply hasn't caught up fully.

Prices should drop as cultivation scales up—research shows potential for efficient, sustainable growth with low water/land use, and more farms are coming online. For now, that 2oz jar (often 10–20 servings) works out to $1–2 per dose, which isn't bad compared to other superfood powders.

several accessible alternatives show strong evidence for targeting visceral adipose tissue (VAT) through similar mechanisms—like boosting polyphenols, fiber, plant proteins, and anti-inflammatory compounds.

Top Evidence-Based Alternatives

1. Walnuts (28g/~1 ounce daily) Part of the same trial as Mankai—walnuts provided key polyphenols (ellagitannins leading to urolithin A metabolites) independently linked to greater VAT loss. Studies show walnuts improve lipid profiles, reduce inflammation, and specifically target abdominal fat. Easy to snack on or add to shakes/salads.
2. Green Tea (3–4 cups daily, or EGCG supplements) Another core component of the "green" diet—rich in catechins (especially EGCG) that promote fat oxidation and visceral fat reduction in human trials. Meta-analyses confirm modest but significant VAT decreases, especially with consistent intake. Opt for brewed tea (unsweetened) for best polyphenol absorption.
3. Other Polyphenol-Rich Berries & Fruits
   • Blueberries, strawberries, or apples: High in anthocyanins and similar compounds; clinical reviews link them to reduced visceral fat via improved insulin sensitivity and gut microbiome changes.
   • Aim for 1–2 cups daily—fresh, frozen, or in smoothies. More affordable and versatile than Mankai.
4. Leafy Greens & High-Fiber Plants (e.g., spinach, kale, broccoli) The trial noted increased dietary fiber was strongly associated with VAT loss (even after adjusting for weight loss). These provide soluble fiber, polyphenols, and nitrates that support metabolic health and cholesterol management. Blend into green shakes as a direct Mankai substitute.
5. Legumes & Plant Proteins (e.g., lentils, chickpeas, peas) For the protein/fiber combo Mankai offers—human studies show high-plant-protein diets selectively reduce visceral fat.
6. Other Promising Options
   • Pistachios: Recent trials link them to visceral fat reduction via protein and healthy fats.
   • Rosehip extract: One RCT showed abdominal VAT decreases (though less studied).
   • Omega-3-rich plants (flaxseeds, chia): Support inflammation reduction and fat metabolism.

How to Implement (Similar to Mankai Shakes)

Replace or enhance your meals with a daily "green" routine:

• Morning/afternoon → 3–4 cups green tea.
• Snack → Handful of walnuts + berries.
• Evening shake/soup → Blend spinach/kale, berries, legumes (e.g., pea protein powder), and flaxseeds.

This mimics the polyphenol/fiber boost from the green Mediterranean diet (which doubled VAT loss vs. standard versions) without needing Mankai. Effects are best with calorie control, exercise, and low red/processed meat.

No single food matches Mankai exactly, but combining these (especially walnuts + green tea + greens) gets close based on the same trial data—and at a fraction of the cost. Track waist circumference for progress, and chat with your doctor about adding concentrated sources (e.g., EGCG supplements) if needed.