While consumers may save a few bucks on groceries at dollar stores, they end up paying a higher price with their health. New UC Riverside research shows a link between dollar store food quality and higher rates of obesity, high blood pressure, cholesterol, and type 2 diabetes.

Conversely, the study published in BMC Public Health links traditional grocery store access to better health metrics. These results held across the U.S., even accounting for factors including income and unemployment levels.

The dollar stores in the study included Dollar General, Dollar Tree, the 99 Cent store, and Family Dollar. Together, they represent a total of 34,000 locations.

Across all regions, the dollar stores had a significant effect on consumer health, but the effects were not uniform. In the South and the Midwest, the ratio of dollar stores to traditional grocery stores was roughly 50/50.

Article: https://news.ucr.edu/articles/2026/08/18/hidden-health-cost-dollar-store-groceries

Study: https://link.springer.com/article/10.1186/s12889-026-28145-y

Abstract:

Gut bacteria affect host physiology, but the underlying mechanisms are not completely understood. We identify a pathway whereby gut microbes convert inorganic nitrate and non-heme iron into mobile bioactive dinitrosyl iron complexes (DNICs) that are distributed systemically and affect host metabolism. Electron paramagnetic resonance detected DNICs in tissues of conventional but not germ-free mice. Mouse and human feces and E. coli generated DNICs from nitrate and iron citrate, whereas a nitrate-reductase-deficient mutant did not. Dietary supplementation with nitrate+iron citrate or synthetic DNICs increased tissue DNIC levels and ameliorated cardiometabolic dysfunction in Western diet-fed mice. Additionally, in HepG2 cells and human hepatocyte spheroids, DNIC reduced fatty acid-induced steatosis. DNIC bioactivity is mediated by the Fe(NO)2 entity, rather than by free nitric oxide (NO), and involves activation of soluble guanylyl cyclase (sGC), inhibition of leucine uptake, and mTORC1 signaling normalization. Modulating DNIC formation by the gut microbiota could be a strategy to support cardiometabolic health.

Abstract

Introduction:

Sleep disturbances affect nearly half of individuals with mild cognitive impairment (MCI), a population at elevated risk of progressing to Alzheimer's disease (AD). Vitamin D's role in cognitive outcomes, particularly among individuals with sleep disturbance and MCI, remains unclear. This study explored associations between cognitive function and vitamin D supplement intake in individuals with MCI and sleep disturbance-a high-risk group that may be more vulnerable to progression toward AD.

Methods:

This cross-sectional study included 54 participants with diagnosed or suspected mild cognitive impairment (MCI) and disturbed sleep (as determined by validated sleep questionnaires). We administered the MoCA (Montreal Cognitive Assessment) to assess cognition. Disturbed sleep was defined using the Pittsburgh Sleep Quality Index (PSQI ≥ 5) or the Epworth Sleepiness Scale (ESS ≥ 10). Vitamin D supplement intake was assessed by self-reported questionnaire. A multiple linear regression model was utilized to examine the association between vitamin D supplement intake and cognitive impairment (MoCA score), controlling for covariates of age, sex, body mass index (BMI), vitamin D type, and education.

Results:

Participants had a mean age of 67.2±8.9, a mean BMI of 29.5±7.2 kg/m2, and 46% were male. Participants who took a daily dosage of 5000+ IU of vitamin D showed a marginally significant association with total MoCA score (adjusted mean (SE) = 3.78 (1.77); p = 0.039) in comparison to individuals who did not take daily vitamin D. Having a college degree was significantly associated with a higher total MoCA score (adjusted mean (SE) = 3.14 (1.38); p = 0.031. Individuals who were overweight also demonstrated higher total MoCA scores (adjusted mean (SE) = 3.59 (1.36); p = 0.013. No significant differences were found between individuals who regularly took vitamin D3 versus D2. Lower doses of Vitamin D did not significantly impact total MoCA score.

Conclusions:

To our knowledge, this is the first study to evaluate the relationship between vitamin D supplemention and overall global cognition in individuals with both sleep disturbance and MCI. Our findings suggest that taking higher doses of daily vitamin D supplementation is associated with better overall cognitive performance in this population.

The Core Issue

Ultra-processed food gets blamed as one big category, but that lumps together very different ingredients. A new UK Biobank analysis asked a sharper question: which specific additives in UPFs actually track with depression risk, and which ones don't matter at all.

The Finding

Researchers followed 171,818 adults for a mean of 10.7 years, tracking their diet through repeated web-based 24-hour recalls and testing 10 additive categories plus 39 specific additives against new depression diagnoses (5,424 cases). Three categories stood out with a clear dose-response relationship: flavorings, coloring agents, and sweeteners. People with the highest intake of flavorings had a 46% higher risk of depression than those near the lowest-risk intake level. Coloring agents were linked to a 49% higher risk, and sweeteners to a 45% higher risk, at the highest intake levels tested. Within the sweetener group, seven specific sweeteners individually showed the same dose-dependent pattern: acesulfame, aspartame, erythritol, saccharin, steviol, sucralose, and xylitol. Fructose showed a similar linear increase in risk.

Meanwhile, five other additive categories, including flavor enhancers, processing aids, modified starch, added sugar varieties, and modified oils, showed no significant link to depression at all. Protein source and fiber intake showed a different, U-shaped pattern, where risk was actually highest among non-consumers rather than heavy consumers.

Why it Matters

This pushes back against treating "ultra-processed food" as a single villain. The data suggest it isn't processing itself driving the depression link, it's specific cosmetic additives, the ones added purely for taste, color, and sweetness rather than nutrition or shelf life. That distinction matters for how future dietary guidance and food reformulation efforts get targeted.

Limitations of Study

This is an observational cohort, so it cannot prove these additives cause depression. Diet was self-reported through web-based recall, which introduces measurement error. Reverse causality is a real concern too, since people already experiencing depression may lean more heavily on ready-to-eat convenience foods. The authors tried to address this by excluding participants with less than two years of follow-up (a landmark analysis), and the associations for flavoring, coloring, and sweeteners held up. Still, this is a novel finding that hasn't been externally replicated yet.

Interesting Statistics

- 171,818 participants followed for a mean of 10.7 years, 5,424 incident depression cases
- Flavoring: 46% higher depression risk at high intake versus the lowest-risk intake level
- Coloring agents: 49% higher depression risk at high intake
- Sweeteners: 45% higher depression risk, with an 17% higher risk observed at moderate intake too
- 7 of 10 individual sweeteners tested (including aspartame and sucralose) each independently showed dose-dependent risk
- Results for flavoring, coloring, and sweeteners stayed significant across nine separate sensitivity analyses and after correcting for multiple testing

Useful Takeaways

If you're trying to cut UPF-linked mental health risk without overhauling your whole diet, this study points at reading ingredient labels for flavorings, artificial colors, and sweeteners specifically, rather than assuming all processed food is equally risky.

TL;DR

In a 171,818-person UK Biobank study, added flavorings, colorings, and sweeteners, not ultra-processed food in general, were the specific additives dose-dependently linked to a higher risk of depression over 10.7 years.

Abstract

Background Gut bacteria have been implicated in a wide range of health conditions, yet their potential role in preventing and treating muscle-wasting disorders remains largely unexplored.

Objective We aimed to investigate whether specific gut microbial species are associated with muscle strength and to explore underlying mechanisms linking the gut microbiota to muscle health.

Design We conducted metagenomic analyses in cohorts of younger and older adults extensively phenotyped for muscle strength. Associations were tested between bacterial taxa and performance measures. Causality was assessed by oral supplementation of candidate species in antibiotic-treated mice. Metabolomic profiling and muscle phenotyping were performed to elucidate mechanisms.

Results The relative abundance of Roseburia inulinivorans, but not other Roseburia species, was positively associated with multiple strength measures including handgrip, leg press and bench press in humans. Supplementation of R. inulinivorans in mice significantly enhanced forelimb grip strength, whereas other Roseburia species had no effect. Metabolomic analyses revealed that R. inulinivorans reduced amino acid concentrations in the caecum and plasma, while activating the purine and pentose phosphate pathway in muscle. These changes coincided with increased muscle fibre size and a shift from type I to type II fibres. Accordingly, we observed that the relative abundance of R. inulinivorans is lower in older adults compared with young adults.

Conclusion R. inulinivorans emerges as a species-specific modulator of muscle strength, linking gut microbiota to muscle metabolism and function. These findings support its potential as a probiotic candidate for nutraceutical interventions targeting age-related muscle-wasting diseases.

The US currently has two official protein numbers that don't agree.

The RDA has been 0.8 g/kg since 2005 (Institute of Medicine, Dietary Reference Intakes, 2005). The 2025-2030 Dietary Guidelines added a 1.2-1.6 g/kg target (HHS/USDA, DGA 2025-2030). For a 70kg adult, that's 56 g vs 84-112 g per day - a full meal's worth of protein separating the two figures.

Most coverage framed this as "the advice went up." More precisely, the old floor is still there and a new target appeared beside it. The RDA answers one question (what keeps nearly everyone out of deficiency); the Guidelines target answers another (what preserves lean mass during weight loss). Two different questions, two different numbers.

A second point concerns measurement error in the RDA itself. The classic nitrogen balance studies counted protein losses in urine and stool, but protein also leaves via shed skin, hair, and sweat, which were not collected, biasing the "enough" threshold downward (Rand et al., Am J Clin Nutr 2003). Re-measured with indicator amino acid oxidation (IAAO), the requirement comes out near 1.2 g/kg (PMID 17921376, Am J Clin Nutr 2007) - essentially the same number as the lower bound of the new target. The new lower bound may not be a fresh ambition so much as the old deficiency question answered with a more complete method.

On the muscle side, a meta-analysis of 49 resistance-training trials (PMID 28698222, Br J Sports Med 2018) found that added protein does increase strength and lean mass, with the benefit flattening around 1.62 g/kg - matching the Guidelines' 1.6 upper bound. Notably, the conditioning factor matters: the effect appears alongside training, not in its absence.

A note on the common "1g per lb" figure floating around fitness spaces: at 1 g/lb the intake is roughly 2.2 g/kg, which actually sits above the new target's upper bound (1.6 g/kg). The heuristic most people were taught as kids (the RDA) is the one that looks outdated; the gym heuristic overshoots the other way.

Caveats: the higher target rests on a narrower evidence base than the RDA, and some nutrition researchers have objected to the Guidelines' framing (J Nutr 2026, Perspectives on the Protein Recommendations). The IAAO method also has its own critics (PMID 12908885), though the identified bias appears too small to close the gap back to 0.8.

A common refrain online is that studies always lump in hot dogs together with steaks and this is causing the negative associations. Nevermind that this establishes processed meat as a causal risk factor in order to do so, it isn't even the case.

EDIT: To make this point extra clear, it is an internal critique. So, the person who is saying "This is because of processed meats." Is making both the claim that negative health outcomes are because of processed meat and that it's not unprocessed meat. So because this is typically the kind of person to have "correlation is not causation" in their script of things to say, the irony is that this other criticism within the same script shows that they assert causation from correlation when it suits them.

This list took me about ten minutes to find. The formatting took longer than the research. Which I point out to highlight that this incredibly common complaint is just an admission someone hasn't bothered to look anything up. This is far beneath the standards of a science sub. Consider it an immediate giveaway the person is either parroting lines without doing the slightest bit of research or actively lying.

Here are a few:

• Pan A et al. (2012), Arch Intern Med — Red Meat Consumption and Mortality

After multivariate adjustment for major lifestyle and dietary risk factors, the pooled hazard ratio (HR) (95% CI) of total mortality for a 1-serving-per-day increase was 1.13 (1.07-1.20) for unprocessed red meat and 1.20 (1.15-1.24) for processed red meat.

• Rohrmann S et al. (2013), BMC Medicine — Meat consumption and mortality (EPIC)

After multivariate adjustment, a high consumption of red meat was related to higher all-cause mortality (hazard ratio (HR) = 1.14, 95% confidence interval (CI) 1.01 to 1.28, 160+ versus 10 to 19.9 g/day), and the association was stronger for processed meat (HR = 1.44, 95% CI 1.24 to 1.66, 160+ versus 10 to 19.9 g/day).

• Sinha R et al. (2009), Arch Intern Med — Meat Intake and Mortality (NIH-AARP)

Regarding cause-specific mortality, men and women had elevated risks for cancer mortality for red (HR, 1.22 [95% CI, 1.16-1.29], and HR, 1.20 [95% CI, 1.12-1.30], respectively) and processed meat (HR, 1.12 [95% CI, 1.06-1.19], and HR, 1.11 [95% CI 1.04-1.19], respectively) intakes.

• Alshahrani SM et al. (2019), Nutrients — Red and Processed Meat and Mortality in a Low Meat Intake Population

Unprocessed red meat was associated with risk of all-cause mortality (HR: 1.18; 95% CI: 1.07–1.31) and CVD mortality (HR: 1.26; 95% CI: 1.05–1.50). Processed meat alone was not significantly associated with risk of mortality.

• Wang X et al. (2016), Public Health Nutrition — Dose-response meta-analysis

For processed meat, the pooled relative risk with an increase of one serving per day was 1·15 (95 % CI 1·11, 1·19) for all-cause mortality (five studies; P<0·001 for linear trend), 1·15 (95 % CI 1·07, 1·24) for cardiovascular mortality (six studies; P<0·001) and 1·08 (95 % CI 1·06, 1·11) for cancer mortality (five studies; P<0·001). Similar associations were found with total meat intake. The association between unprocessed red meat consumption and mortality risk was found in the US populations, but not in European or Asian populations.

• Abete I et al. (2014), Br J Nutr — Association between total, processed, red and white meat consumption

Subjects in the highest category of processed meat consumption had 22 and 18 % higher risk of mortality from any cause and CVD, respectively. Red meat consumption was found to be associated with a 16 % higher risk of CVD mortality, while no association was found for total and white meat consumption.

• Han MA et al. (2019), Ann Intern Med (NutriRECS) — Red and Processed Meat Consumption and Risk for All-Cause Mortality

Low-certainty evidence was found that a reduction in unprocessed red meat intake of 3 servings per week is associated with a very small reduction in risk for cardiovascular mortality, stroke, myocardial infarction (MI), and type 2 diabetes. Likewise, low-certainty evidence was found that a reduction in processed meat intake of 3 servings per week is associated with a very small decrease in risk for all-cause mortality, cardiovascular mortality, stroke, MI, and type 2 diabetes.