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

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 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.

Hi all, figured this would be a good place to ask. Maybe some of you might be working on this very thing?

I think this is one of the most exciting things to look forward to in the future. Not sure if we’ll really be able to cut down on how calorically dense these things are, but at the end of the day, I could easily live with just needing to worry about how to fit these things into my diet in terms of calories, and not how much they’re clogging my arteries and raising my cholesterol lol. If I could enjoy as much chocolate as fits in my daily calorie limit without needing to worry about my heart health, I think that’s an exciting future!! Same goes with butter and heavy cream when it comes to thinks like
pasta sauces, ice cream and other desserts, etc..

I always thought coffee was unhealthy, but all of the studies I've checked so far linked a few cups of a coffee per day to reduced risk of all-cause mortality. Is coffee actually healthy? If not, what factors are responsible for the correlation? I thought the correlation would be unfavourable for coffee since health-conscious people were more likely to avoid coffee and high consumption of coffee may be due to fatigue from poor sleep. Also, this study (https://doi.org/10.1186/s12889-024-18515-9) found coffee consumption reduced all-cause mortality risk in both sedentary and more active adults.

https://doi.org/10.1017/S1368980019000764

https://doi.org/10.1016/j.jand.2021.03.014

https://doi.org/10.1186/s13098-023-01222-7

https://doi.org/10.1186/s12916-022-02636-2

https://doi.org/10.1093/eurheartj/ehae871

https://doi.org/10.1016/j.tjnut.2025.05.004

https://doi.org/10.1186/s12889-024-18515-9

https://doi.org/10.1136/bmj.j5024

Significance

Plant-based diets are consistently associated with improved gut health, yet the mechanisms responsible remain incompletely understood. Here, we explore two aspects of plant-based foods: digestion-resistant carbohydrate (fiber) and digestion-resistant protein (which we term Prif). Because they resist mammalian digestion, both fiber and Prif pass through the host small intestine to feed the colonic microbiome. In this work, we show that these two components of a plant-based diet work together to rewire microbial metabolism to produce beneficial rather than noxious phenol metabolites.

I understand that there is enhanced nutritional value in sprouted grains such as higher nutrient absorption and increased vitamins and minerals. This is something well established in scientific literature.

I’ve recently come across a post on Instagram that I can’t find solid evidence for, but I’ve also been hearing this from someone I know in real life too, so I want to know if there’s any truth to it or if it’s just pseudoscience.

The claim is as follows:
“SPROUTING WHEAT determines if the wheat kernel is still alive, meaning can it grow and gives the body the nutrients needed. Recently we were given someone's very old bags of wheat so this post is how we determined if the wheat was still alive for maximum nutritional values. I must say sprouting and soaking wheat has been a part of cultures all over the world. Sprouting reduces phytic acid - an enzyme that inhibits our digestive system from absorbing nutrients.
Sprouting wheat also stabilizes natural oils in the wheat and reduces bitterness and enhances natural flavor.
Germinated grains contain 700 times more magnesium five times more calcium and 12 times more phosphorus. Storing wheat seeds (sometimes called wheat berries) is cheaper and also has a longer shelflife than storing just flour that's already ground. For us, we want maximum nutrition to go into our bodies so if the wheat cannot be sprouted and is dead, then it becomes chicken and animal food on our farm.”

However, I’m failing to understand why grains should be tested for their sprouting ability to determine their nutritional state. From what I understand, there are several factors that can influence a grains sprouting ability such as how old it is and whether it was subject to heat treatment. If a batch of grains do not sprout, is that really an indicator of “dead” grains and should they really just be thrown out as farm food?

If anyone can provide scientifically backed clarification, that will be great.

Thank you.

A new study from UC Davis found that "most mayonnaise samples and all avocado oil salad dressings fell outside the Codex standard ranges for C16:0, C16:1 and C18:0," meaning they contained oils other than 100% pure avocado oil, including seed oils. Both Chosen Foods brand and Primal Kitchens failed. Back to making it homemade (good thing it's easy). https://www.sciencedirect.com/science/article/pii/S2772502226007274

Effects of Ultra-Processed Meals with Differing Energy Density on Postprandial Glyco-Insulinemic and Appetite-Related Hormonal Responses: A Randomized Crossover Trial

https://preview.redd.it/0z9j2xcfkdjh1.png?width=643&format=png&auto=webp&s=c09b612198f036fd42975e798b7f85902dda0cea

DOI

Modern dietary environments favor metabolic disorders through the hyper-palatability of ultra-processed foods (UPF) and high energy density (ED). While previous trials identified weight gain associated with UPF, the independent role of energy density as a confounder or driver of metabolic impact remains poorly understood. This study aimed to disentangle these effects by evaluating 19 adults without obesity (mean age 22 years, mean BMI 23.5 kg/m2) using meals strictly matched for macronutrients, fiber, saturated fat, free sugar, and sodium.

The UPF condition resulted in statistically significant increases in postprandial circulating insulin concentrations throughout the day (p = 0.016). No significant interactions were found between UPF and meal timing (p = 0.09) or between UPF and ED for any outcome. Glucose (p = 0.080) and triglycerides (p = 0.199) did not show significant main effects from UPF exposure. Appetite-regulating hormones, specifically ghrelin (p = 0.235) and leptin (p = 0.795), remained stable across conditions. The data indicate that UPF consumption drives higher insulin demand or delayed clearance regardless of the meal's caloric concentration per gram.

Study Design and Methodology
This randomized, 2 x 2 crossover-controlled feeding trial involved 19 participants (9 females, 10 men) who completed four distinct conditions: UPF+/ED+, UPF+/ED-, UPF-/ED+, and UPF-/ED-. Each intervention lasted one day with a minimum three-day washout. Researchers determined total energy intake (TEI) via indirect calorimetry and triaxial accelerometry to ensure neutral energy balance. Standardized test meals (breakfast and lunch) were matched for energy, protein, carbohydrates, lipids, fiber (25g/day), saturated fat (10% TEI), and free sugar (10% TEI). Blood samples were collected at 12 hour fasting, 240 minutes post-breakfast, and 240 minutes post-lunch. Linear mixed models accounted for repeated measures and baseline covariates.

Key Findings

• Ultra-processed food consumption significantly elevated postprandial insulin ( p = 0.016 ) compared to unprocessed meals.
• Energy density (ED) showed no significant main effect on insulin ( p = 0.710 ) or glucose ( p = 0.650 ).
• Glucose concentrations remained statistically similar between UPF and non-UPF conditions ( p = 0.080 ).
• Triglyceride levels were not significantly altered by processing level ( p = 0.199 ) or energy density ( p = 0.141 ).
• Meal timing significantly influenced glucose ( p = 0.034 ), insulin ( p < 0.001 ), and leptin ( p = 0.003 ) concentrations.
• Ghrelin ( p = 0.515 ) and leptin ( p = 0.994 ) showed no response to changes in energy density.

Limitations
The small sample size (N=19) limits the power to detect subtle hormonal shifts. Financial constraints restricted ghrelin (n=13) and leptin (n=8) analyses to subsamples, with several leptin samples falling below the assay detection limit. The 240 minute post-meal sampling window missed early-phase insulin kinetics and dynamic peaks. The study population was restricted to healthy, non-obese young adults, which prevents generalization to populations with metabolic syndrome or obesity.

Discussion and Implications
These results shift the focus from caloric concentration to food matrix integrity. The fact that insulin rose significantly while glucose remained stable indicates that UPF intake forces a higher insulin demand or impairs hepatic insulin clearance to maintain euglycemia. Because the meals were matched for fiber and sugar, the metabolic disruption stems from the structural degradation of the food matrix or the presence of cosmetic additives rather than simple nutrient ratios. Energy density is often blamed for metabolic dysfunction, but this trial proves that the degree of processing is the primary driver of postprandial hyperinsulinemia.

Conclusion
Acute consumption of ultra-processed foods drives significant postprandial hyperinsulinemia in healthy adults even when calories, fiber, and sugar are perfectly matched. This metabolic strain occurs independently of energy density, proving that the industrial degradation of the food matrix is a standalone risk factor for increased insulin demand.

Edits: Added figures.

A prospective study followed 5,301 adults aged 55 and older to examine the relationship between low-carbohydrate and low-fat diets and dementia risk.

The researchers also looked at genetic susceptibility, including APOE genotype and Alzheimer’s disease polygenic risk score.

It looks beyond the diet itself and asks whether the same dietary pattern may be associated with dementia risk differently depending on a person’s genetic background.

Diet and healthy aging are probably not as straightforward as “low-carb vs. low-fat.”

Low-carbohydrate and low-fat diets, genetic susceptibility, and long-term risk of dementia: A prospective cohort study - The American Journal of Clinical Nutrition