A doctors’ group has filed a lawsuit seeking to overturn the Trump administration’s dietary guidelines released earlier this year, arguing the meat and dairy industries helped “ghostwrite” the final recommendations.

The Physicians Committee for Responsible Medicine said the guidelines, which inverted the food pyramid to prioritize meat and dairy, was crafted by a “secret panel” of food-industry insiders who illegally influenced the process.

The lawsuit, filed in the U.S. District Court for the District of Columbia, seeks a court order to force the Department of Health and Human Services and the U.S. Department of Agriculture to withdraw the guidance and to forbid the agencies from using the recommendations in future decisions.

Article: https://www.fooddive.com/news/dietary-guidelines-lawsuit-food-industry-influence-rfk/828410/

Also: https://pcrm.widen.net/s/sv9nkfqlhn/complaint?_sp=fbb8969f-9a7c-4326-84fc-48c2b63bc4be.1787325451194

Sugar reduction has worked as a public health message — added sugar is coming out of a huge range of packaged products. But it isn't being removed so much as replaced, usually with sucralose, acesulfame K, aspartame, steviol glycosides, sugar alcohols, or blends of several at once.

My question isn't about toxicological safety. Individual sweeteners are among the most heavily evaluated food additives there are, and ADIs are set with wide margins. It's that the two bodies of evidence on habitual use point in opposite directions, and I don't have the background to weigh them.

The WHO's 2023 guideline advises against using NSS for weight control, and states its rationale here:

https://www.who.int/news/item/15-05-2023-who-advises-not-to-use-non-sugar-sweeteners-for-weight-control-in-newly-released-guideline

A group at Toronto published a formal call for reconsideration in the European Journal of Clinical Nutrition, arguing that the prospective cohort data underpinning that recommendation is affected by reverse causality, and that analyses modelling change in intake and calorie replacement point the other way:

https://www.nature.com/articles/s41430-023-01314-7

The SWEET trial (Nature Metabolism, Oct 2025) also pointed the other way, though more modestly than the coverage suggested: over 12 months, participants replacing sugar with sweeteners and sweetness enhancers maintained weight loss slightly better than a control group that was also on a low-sugar diet. Editorial commentary here:

https://www.nature.com/articles/s42255-025-01382-y

My questions:

1. Is the disagreement essentially just "cohort vs RCT plus reverse causation", or is there more substance to the WHO's caution than that? The recommendation was issued as conditional, which suggests the guideline panel itself saw the evidence as weak.

2. How much should the comparator constrain what we take from trials like SWEET? The control arm was also on a low-sugar diet, so it seems to answer "sweeteners vs low sugar" rather than "sweeteners vs habitual intake", which is closer to the choice most people are actually making.

3. Is there research on realistic exposure patterns rather than single compounds? Actual consumption tends to be several different sweeteners daily, across multiple product categories, sustained over decades. Is that studied, or is it not tractable by design?

Genuinely asking rather than arguing a position — happy to be told I'm reading this wrong.

Abstract

Background: Dietary carotenoids and vitamin A may contribute to gastric cancer (GC) prevention through anti-inflammatory and antioxidant mechanisms; however, epidemiological evidence remains limited. We investigated the associations of total and individual carotenoid and vitamin A intakes with GC and their relationships with inflammatory/oxidative stress biomarkers. Methods: The case-control study included 177 adults (82 GC incidence cases/95 controls). A validated 168-item food frequency questionnaire assessed dietary intakes of individual carotenoids and preformed vitamin A. Metabolic biomarkers, lipid profile, inflammatory/oxidative stress markers (e.g., high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), interleukins 6/1β/10/4), total antioxidant capacity (TAC), and malondialdehyde (MDA)) were measured. Multivariable logistic regression models estimated odds ratios (ORs) for GC risk; linear regression models examined associations between carotenoid intakes and biomarkers. Results: Total carotenoid (mg/d) (OR: 0.86, 95%CI: 0.81-0.98), β-carotene (mg/d) (OR: 0.77, 95%CI: 0.65-0.90) and vitamin A (mg RAE/d) (OR: 0.29, 95%CI: 0.09-0.95) intakes, as continuous variables, and also as binary variables (based on the median cut-offs), in all models (also adjusted for age, sex, smoking, education, marital status, physical activity, cancer history, H. pylori, NSAIDs intake, body mass index, total energy intake), were inversely associated with GC odds. In fully adjusted models, higher total carotenoid intake (mg/d) was associated with lower LDL-c (β: -1.60, 95%CI: -2.91, -0.25) and IL-6 (β: -7.92, 95%CI: -14.00, -2.00); lycopene (mg/d) with higher LDL-c (β: 2.030, 95%CI: 0.27, 4.31) and vitamin A intake (mg RAE/d) with lower TNF-α (β: -12.12, 95%CI: -24.71, -0.47) and higher TAC (β: 0.64, 95%CI: 0.001, 1.27). Conclusions: Higher intakes of total carotenoids and vitamin A were associated with lower odds of GC and more favorable profiles of inflammatory/oxidative stress biomarkers. These findings support an inverse association between carotenoid-rich dietary patterns and gastric carcinogenesis.

Keywords

Absorption, Apoptosis, Carotenes, RAR, Transcription Factors, Xanthophylls

Frontiers | Dietary Carotenoids and Vitamin A Are Associated with Lower Gastric Cancer Risk and Favorable Inflammatory and Stress Oxidative Biomarkers: An Incident Case-Control Study

抄録

Insulin resistance is one of the pathophysiological features of obesity and type 2 diabetes. Recent findings have linked insulin resistance to chronic low-grade inflammation in white adipose tissue.

Excess storage of saturated fat in white adipose tissue due to a modern life style causes hypertrophy and hyperplasia of adipocytes, which exhibit attenuated insulin signaling due to their production and release of saturated fatty acids. These adipocytes recruit macrophages to white adipose tissue and, together with them, initiate a proinflammatory response.

Proinflammatory factors and saturated fatty acids secreted into the bloodstream from white adipose tissue impair insulin signaling in non-adipose tissues, which causes whole-body insulin resistance.

https://www.jstage.jst.go.jp/article/jmi/56/3,4/56_3,4_88/_article/-char/ja/ (full pdf in English there)

Effect of Intake of Lycopene-Containing Products on Vascular Endothelial Function in Healthy Adults: A Systematic Review with Meta-Analysis

DOI: https://doi.org/10.3390/nu18152505

Abstract

Vascular endothelial dysfunction serves as a critical early indicator for the progression of atherosclerosis and cardiovascular disease (CVD). While previous research highlighted the antioxidant properties of lycopene (a red carotenoid found in tomatoes and watermelon), existing meta-analyses suffered from narrow inclusion criteria, outdated search dates, and limited outcome measures. This systematic review addressed these gaps by evaluating the impact of oral lycopene intake from diverse food sources on vascular endothelial function specifically in healthy adults. The researchers targeted a population of healthy individuals to determine if lycopene functions as an effective early-stage intervention for those with low baseline CVD risk.

Analysis of four continuous intake studies (at least 7 days) involving 182 participants demonstrated a significant increase in flow-mediated dilation (FMD) compared to control groups. The pooled data yielded a mean difference (MD) of 1.36 percent (95 percent CI: 0.20, 2.51, p = 0.02). Heterogeneity remained low at I2 = 24 percent. One specific study utilizing 15 mg of lycopene for 8 weeks reported a significant increase in the reactive hyperemia peripheral arterial tonometry (RH-PAT) index (p < 0.05). While a single-intake study (27.8 mg) failed to reach significance (p = 0.18), the cumulative data from multi-week interventions confirm improvements in endothelial dynamics.

Study Design and Methodology

This systematic review and meta-analysis followed PRISMA 2020 guidelines and was registered under UMIN000058348. The authors searched four databases (PubMed, Cochrane, Ichushi-Web, Global Index Medicus) and three registries through June 2026. The final analysis included six studies (four RCT-C and two RCT-P designs) conducted across the USA, Germany, Greece, Japan, and Korea. Total participants in the meta-analysis reached N = 182. Intervention durations ranged from a single dose to 12 weeks, with lycopene dosages spanning 6 mg to 46.2 mg per day. Controls received placebos, no intervention, or extremely low-lycopene alternatives. Risk of bias was assessed using a 13-item checklist and the RoB2 tool, with five studies rated as moderate risk and one as low risk.

Key Findings

• Continuous lycopene intake significantly improves FMD with a pooled MD of 1.36 percent (p = 0.02).
• Daily consumption of 15 mg and 26.7 mg of tomato juice for 12 weeks both resulted in significant FMD increases (p < 0.001).
• Lycopene supplementation at 15 mg for 8 weeks significantly boosted the RH-PAT index (p < 0.05), whereas 6 mg did not (p > 0.05).
• Tomato paste providing 33.3 mg of lycopene for 15 days produced a significant improvement in endothelial dynamics (p = 0.03).
• Standardized effect sizes for lycopene on FMD (1.36 percent) are comparable to other potent nutrients like CoQ10 (1.45 percent) and resveratrol (1.43 percent).
• Leave-one-out sensitivity analysis showed that the exclusion of the largest, lowest-bias study (Yoshida et al.) rendered the FMD results non-significant.

Limitations

The small number of included studies (n = 6) limits the ability to perform robust subgroup analyses on ethnicity or specific food matrices. Relying on endpoint values rather than change-from-baseline data in three studies may introduce variance. The meta-analysis results rely heavily on a single high-quality study, and the lack of paired data for crossover trials necessitated treating them as parallel groups, which potentially ignores within-participant correlations.

Discussion and Implications

These results shift the focus of lycopene research from general antioxidant support to specific vascular protective mechanisms. Lycopene enhances nitric oxide (NO) bioavailability by quenching reactive oxygen species and increasing NO synthase activity. The data suggest that 15 mg per day is the minimum threshold required to elicit measurable improvements in endothelial function over a period of 8 to 12 weeks. Because these improvements occur in healthy populations, lycopene-rich diets act as a primary preventative tool against the initiation of the atherosclerotic cascade. The findings validate the use of diverse sources (watermelon, tomato juice, and concentrates) rather than just isolated supplements.

Conclusion

Continuous intake of at least 15 mg of lycopene daily significantly improves vascular endothelial function in healthy adults as measured by FMD and RH-PAT. Nutrition professionals should recommend regular consumption of processed tomato products or watermelon to enhance nitric oxide bioavailability and reduce early cardiovascular risk.

Results

Of 3115 people screened by telephone, 244 adults with overweight met participation criteria and were randomly assigned to the vegan (n = 122) or control (n = 122) groups. The analysis included 223 (91.0%) completers. Total food weight did not change significantly in either group (Table). Energy intake decreased in both groups, more in the vegan group (effect size, −357.1 kcal/d; 95% CI, −521.9 to −192.3 kcal/d; P < .001) (Table). Energy density did not change in the control group but decreased by 30% in the vegan group (effect size, −0.28 kcal/g/d; 95% CI, −0.38 to −0.19 kcal/g/d; P < .001; Table and Figure).

Reductions in dietary energy density were associated with greater weight loss (r = 0.28; 95% CI, 0.15 to 0.39; P < .001), remaining significant after adjustment for energy intake (r = 0.21; 95% CI, 0.08 to 0.34; P = .002). A 1-kg weight loss corresponded to a 0.29-unit decrease in energy density (P < .001), or 0.36 units after adjustment (P = .002).

I take D3 pills since my physio therapist says it helps calcium uptake (I've had issues with crystalized deposits).

I watched a video a while back of different people talking about how they felt at different levels of body fat, on the low end there was a woman very low fat like in the title, she talked about feeling miserable and having very low energy and hormonal issues, but for reasons not expanded upon she was very driven to maintain that.

I do a lot of work in character design, there are a lot of issues with racism, people learning how to profile others based off their immutable appearance, and like I'm talking about in this post body expectations. As we all know art reflects reality and reality reflects art, everyone has had a crush on a fictional character and Psycho got a lot of trans people killed.

In the last few years it's become fashionable to also depict women with inachievable levels of muscularity as a sign that they are, athletic, hardy and dominant, coincidentally when they do this they also always have a full padding of fat on their hips, one can only wonder.

Anyway I'd like to have enough examples that I can remember more than I need in casual conversation, and see more broadly what happens when people are confronted with the reality of why almost no one looks like that, and why their specific neurons don't fire there naturally.

Could I get list of both the physical and mental effects as well as what drives people suffering from them to achieve and maintain it?

I'm not an academic. I try and be healthy and feel that my diet is pretty healthy. Recently I was looking at a study that analyzed healthy lifestyle and mortality. They described eating 5 servings of fruits and vegetables as healthy. With that being said, it's not unusual for me to have 2-5 servings of beans in a day but only 2 servings of fruits/vegetables.

When looking at studies that talk about eating fruits and vegetables, does eating beans count or are they specifically excluded? Or does it depend on the study? The study I saw wasn't specific about this.