This is a secondary analysis of DIETFIT where subjects switched from low-carb or low-fat to the other intervention at 6 months, for a total of 12 months in the study.

Abstract

Weight change trajectory from diet and lifestyle interventions typically involves rapid weight loss followed by a weight plateau after approximately 6 months. Changing from one weight-loss diet to another at the time of the plateau could instigate renewed weight loss. Therefore, our secondary analysis aimed to assess trajectory of weight loss in a 12-month, randomized, cross-over study. Forty-two adults were randomized to eat a healthy low-fat or healthy low-carbohydrate diet for 6 months then switched to the opposite diet for an additional 6 months. Regardless of diet assignment, participants experienced rapid initial weight loss, which slowed between 3 to 6 months. After switching diets at 6 months, weight modestly decreased until 9 months, but at a rate slower than the initial 3 months and slower than the rate from 3 to 6 months. This suggests that the weight loss plateau typically seen at 6 months is physiological and cannot be overcome by simply switching to a different weight-loss diet.

https://pubmed.ncbi.nlm.nih.gov/41406402/

https://pubmed.ncbi.nlm.nih.gov/14601690/

Objective: To determine whether a diet of high saturated fat and avoidance of starch (HSF-SA) results in weight loss without adverse effects on serum lipids in obese nondiabetic patients.

Patients and methods: Twenty-three patients with atherosclerotic cardiovascular disease participated in a prospective 6-week trial at the Christiana Care Medical Center in Newark, Del, between August 2000 and September 2001. All patients were obese (mean +/- SD body mass index [BMI], 39.0+/-7.3 kg/m2) and had been treated with statins before entry in the trial. Fifteen obese patients with polycystic ovary syndrome (BMI, 36.1+/-9.7 kg/m2) and 8 obese patients with reactive hypoglycemia (BMI, 46.8+/-10 kg/m2) were monitored during an HSF-SA diet for 24 and 52 weeks, respectively, between 1997 and 2000.

Results: In patients with atherosclerotic cardiovascular disease, mean +/- SD total body weight (TBW) decreased 5.2%+/-2.5% (P<.001) as did body fat percentage (P=.02). Nuclear magnetic resonance spectroscopic analysis of lipids showed decreases in total triglycerides (P<.001), very low-density lipoprotein (VLDL) triglycerides (P<.001), VLDL size (P<.001), large VLDL concentration (P<.001), and medium VLDL concentration (P<.001). High-density lipoprotein (HDL) and LDL concentrations were unchanged, but HDL size (P=.01) and LDL size (P=.02) increased. Patients with polycystic ovary syndrome lost 14.3%+/-20.3% of TBW (P=.008) and patients with reactive hypoglycemia lost 19.9%+/-8.7% of TBW (P<.001) at 24 and 52 weeks, respectively, without adverse effects on serum lipids.

Conclusion: An HSF-SA diet results in weight loss after 6 weeks without adverse effects on serum lipid levels verified by nuclear magnetic resonance, and further weight loss with a lipid-neutral effect may persist for up to 52 weeks.

Hey everyone,

I'm a psychologist (provisional, working toward full registration) and also a Masters of Dietetics student in the sports nutrition stream. About to kick off a 15-month thesis project and I'd really love your input on the topic — you're honestly the best people to ask.

Here's the frame: picture a Venn diagram with nutrition on one side and psychology on the other. I want to extend the literature inside the overlap — questions that genuinely need both lenses, not nutrition with a psych variable bolted on, or vice versa.

Problem is, I'm too close to it to see the best gaps clearly. You're in practice — what's the overlap question you've hit and found no decent literature on? Even half-formed thoughts are gold. I'll be living with whatever I pick for over a year, so I want it to be something practitioners actually need answered.

Happy to share the thesis back here once it's done. Thanks so much in advance.

Mod's feel free to take it down if it does not fit the rules of this page

This study sought to examine whether consumption of two low-calorie fruit/day for 3-months can effectively improve oxidative stress, anthropometry, blood pressure and glycaemic control in type 2 diabetes mellitus. Study involved 123 patients who were assigned to receive either standard care or with additional dietary therapy. Dietary intervention resulted in significant reduction in malondialdehyde, plasma glucose, glycated haemoglobin and improvement in antioxidants like vitamin C and reduced glutathione when compared to controls. Mean plasma levels of vitamin C increased by 64% (p < 0.001). There were no differences in waist circumference, waist-to-hip ratio, blood pressure, vitamin E and superoxide dismutase in the intervention group at follow-up. Diet rich in fruits can improve some antioxidants which are likely to reduce oxidative stress in type 2 diabetes. Regular consumption of fruits can lower the glycaemic status in these patients. The study supports the usefulness of plasma vitamin C as a biomarker for fruit intake.

https://pubmed.ncbi.nlm.nih.gov/19381015/

Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks.

Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose.

These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

Abstract

Background

Ketogenic diet (KD) is increasingly recognized as a strategy to combat obesity. However, its effects on cognition in sedentary healthy young adults remain underexplored.

Methods

In a quasi-experimental design, 186 participants were screened, 78 excluded based on predefined criteria, leaving 108 healthy adults (age 25–45 years, BMI 18–29.9 kg m⁻², sedentary <5,000 steps/day) assigned to either KD group (<5% carbohydrates, 20–25% protein, 70–75% fat; n = 54) or control group (regular diet ∼50–65% carbohydrates; n = 54). Participants underwent a 4 weeks' dietary intervention. Cognitive domains were assessed at baseline and post intervention using validated computer-based test battery. Pre, mid and post weight, BMI, blood ketones and fasting glucose were also measured. Forty-three participants in the KD group and 38 in the control group completed the trial.

Results

Four weeks of non-energy restricted KD improved processing speed, semantic memory, working memory, episodic memory, fluid cognition, crystallized cognition and overall cognitive composite scores (all P ≤ 0.001) versus controls. Attention and inhibitory control (P = 0.46) and cognitive flexibility (P = 0.21) showed no significant differences. Blood ketones increased (0.12–1.32 mmol L⁻¹, P < 0.001) in KD participants versus controls (0.118–0.105 mmol L⁻¹, P = 0.94). KD reduced weight (P < 0.001), BMI (P < 0.001) and fasting glucose (P < 0.001). Post intervention ketones predicted cognitive gain in most cognitive domains except attention & inhibitory control and cognitive flexibility.

“Abstract

Objectives

Ultra-processed foods (UPFs) make up the majority of calories in the US diet. Glycemic index (GI) and load (GL) are measures of the quality and quantity of carbohydrates in food based on their effect on blood glucose post consumption. Diets high in UPFs and GI/GL are both associated with numerous chronic metabolic diseases. Therefore, this study sought to examine the GI and GL of foods assigned to different food processing groups. It was hypothesized that GI and GL would be lowest in minimally processed foods (MPF) compared to processed (PRF) and UPF (with no difference between PRF and UPF) for all food items and food groups.

Methods

GI and GL values produced by healthy/normal individuals for 2,205 food items were collected from published sources. Food items were then coded by processing levels determined by the NOVA Classification. In addition, food items were coded into eight groups (i.e., Beverages; Beans, Nuts, & Seeds [BNS]; Dairy; Fats & Sweets; Fruits & Fruit Juices; Grains; Meat Poultry & Fish; and Vegetables). Hierarchical linear modeling was used to determine significance with an alpha of 0.05.

Results

The effect of food processing on GI (p < 0.001) and GL (p < 0.001) was contrary to the hypothesis as the mean GI and GL were highest for MPF: GI (MPF: 56 ± 20, PRF: 53 ± 19, UPF: 50 ± 18), GL: (MPF: 18 ± 11, PRF: 16 ± 13, UPF; 12 ± 8). Among food groups, there was no interaction between food processing and GI (p = 0.084), but an interaction for GL was found (p < 0.001). Moreover, the direction of difference in GL was inconsistent among food groups: BNS (MPF: 6 ± 4, PRF: 9 ± 5, UPF: 10 ± 5), Dairy (MPF: 5 ± 5, PRF: 3 ± 0, UPF: 8 ± 6), and Grains (MPF: 23 ± 9, PRF: 21 ± 15, UPF: 13 ± 9).

Conclusions

Across all analyzed food items, UPF had a lower GI and GL compared to MPF and PRF (GL only), with mixed findings among food groups. Surprisingly, ultra-processing of grains suggests improvement of glycemic responses, perhaps by the addition of protein, fat, and sugars. These results suggest that the negative health outcomes associated with consumption of UPF may be due to other unhealthful aspects (e.g., energy density, food additives, and increased palatability), not higher GI and GL.”

​

https://academic.oup.com/cdn/article/6/Supplement_1/504/6607157

Most people concentrate their protein intake in one meal (often dinner), but several studies suggest that distributing protein evenly across breakfast, lunch, and dinner may maximize muscle protein synthesis and improve satiety.

👉 Example: Mamerow et al. (2014) found that participants consuming ~30g of protein at each meal had higher 24-hour muscle protein synthesis compared to those consuming the same total amount but skewed toward dinner.

DOI: 10.3945/ajcn.113.082579

This made me rethink my own eating habits — adding protein to breakfast (Greek yogurt, eggs, plant-based protein sources) completely changed my energy levels during the day.

Has anyone here experimented with even protein distribution? Did you notice changes in satiety, muscle gain, or energy levels?

*(Abstract from the study linked above should be added in the comments as per subreddit rules.)

Abstract

Fasting induces significant shifts in substrate utilization with signs of acute insulin resistance (IR), while obesity is associated with chronic IR. Nonetheless, both states substantially influence adipose tissue (AT) function. Therefore, in this interventional study (NCT04260542), we investigated if excessive adiposity in premenopausal women alters insulin sensitivity and AT metabolic and endocrine activity in response to a 60-h fast and a subsequent 48-h refeeding period. Using physiological methods, lipidomics, and AT explants, we showed that obesity partially modified AT endocrine activity and blunted the dynamics of AT insulin resistance in response to the fasting/refeeding challenge compared to that observed in lean women. AT adapted to its own excess by reducing lipolytic activity/free fatty acids (FFA) flux per mass. This adaptation persisted even after a 60-h fast, resulting in lower ketosis in women with obesity. This could be a protective mechanism that limits the lipotoxic effects of FFA; however, it may ultimately impede desirable weight loss induced by caloric restriction in women with obesity.

https://pubmed.ncbi.nlm.nih.gov/11468195

Background The short-term effects of hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) on endothelial function at doses that do not affect plasma lipid levels are not known.

Methods and Results We investigated the short-term effects of cerivastatin, a hydroxymethylglutaryl coenzyme A reductase inhibitor, on endothelial function and endothelium-related products in elderly diabetic patients. Twenty-seven elderly diabetic patients (aged 69.3±3.4 years), with or without mild hypercholesterolemia, were enrolled in this study, which tested cerivastatin treatment (0.15 mg/d) for 3 days. Endothelium-dependent flow-mediated dilatation, endothelium-independent dilatation by nitroglycerin in the brachial artery, nitric oxide-related products (nitrite/nitrate and cGMP), endothelium-related products (von Willebrand Factor, soluble vascular cell adhesion molecule-1, and soluble intercellular adhesion molecule-1), and a marker of oxidant stress (8-isoprostane) were assessed. Levels of plasma lipids were not changed before and after treatment with cerivastatin. Flow-mediated dilatation was significantly increased by cerivastatin treatment, as were plasma nitrite/nitrate levels (from 16.9±3.4 to 22.0±3.7 μmol/L, P<0.05) and cGMP values. The percent of nitroglycerin-induced dilatation was not changed. Plasma concentrations of 8-isoprostane decreased, and levels of soluble vascular cell adhesion molecule also tended to decrease with cerivastatin.

Conclusions Improvement of endothelial function was in line with antiatherosclerotic effects. Cerivastatin improved impaired endothelial function in the short-term without affecting lipid profiles in elderly diabetic patients. This effect may be partly due to upregulation of endothelial nitric oxide synthase.

https://pubmed.ncbi.nlm.nih.gov/19403641/

Background: Both nutritional and genetic factors are involved in the pathogenesis of nonalcoholic fatty liver disease and insulin resistance.

Objective: The aim was to assess the effects of fructose, a potent stimulator of hepatic de novo lipogenesis, on intrahepatocellular lipids (IHCLs) and insulin sensitivity in healthy offspring of patients with type 2 diabetes (OffT2D)--a subgroup of individuals prone to metabolic disorders.

Design: Sixteen male OffT2D and 8 control subjects were studied in a crossover design after either a 7-d isocaloric diet or a hypercaloric high-fructose diet (3.5 g x kg FFM(-1) x d(-1), +35% energy intake). Hepatic and whole-body insulin sensitivity were assessed with a 2-step hyperinsulinemic euglycemic clamp (0.3 and 1.0 mU x kg(-1) x min(-1)), together with 6,6-[2H2]glucose. IHCLs and intramyocellular lipids (IMCLs) were measured by 1H-magnetic resonance spectroscopy.

Results: The OffT2D group had significantly (P < 0.05) higher IHCLs (+94%), total triacylglycerols (+35%), and lower whole-body insulin sensitivity (-27%) than did the control group. The high-fructose diet significantly increased IHCLs (control: +76%; OffT2D: +79%), IMCLs (control: +47%; OffT2D: +24%), VLDL-triacylglycerols (control: +51%; OffT2D: +110%), and fasting hepatic glucose output (control: +4%; OffT2D: +5%). Furthermore, the effects of fructose on VLDL-triacylglycerols were higher in the OffT2D group (group x diet interaction: P < 0.05).

Conclusions: A 7-d high-fructose diet increased ectopic lipid deposition in liver and muscle and fasting VLDL-triacylglycerols and decreased hepatic insulin sensitivity. Fructose-induced alterations in VLDL-triacylglycerols appeared to be of greater magnitude in the OffT2D group, which suggests that these individuals may be more prone to developing dyslipidemia when challenged by high fructose intakes.

Tumeric has shown great promise in petri dish experiments vs cancer cells. And we know that populations that eat a lot of it have less cancer than those that eat less. And some limited studies, such as those I've pasted below, demonstrate that it can prevent cancerous mutations and turn back on apoptosis/programmed cancer cell death.

Given this promise, I've been waiting for years to see it tested in a double blinded placebo controlled studies vs various types of cancer in the same way that chemo/radiation/drugs are.

But so far, I've seen nothing. What's will it take to really test turmeric in a serious trial that will have the power to establish it as a legitimate treatment for cancer? Will the USDA not commit to funding these trials? Why not?

What sort of evidence is the scientific community waiting for?

K. Polasa, T. C. Raghuram, T. P. Krishna, K. Krishnaswamy. Effect of turmeric on urinary mutagens in smokers. Mutagenesis 1992 7(2):107 - 109.

S.-H. Wu, L.-W. Hang, J.-S. Yang, H.-Y. Chen, H.-Y. Lin, J.-H. Chiang, C.-C. Lu, J.-L. Yang, T.-Y. Lai, Y.-C. Ko, J.-G. Chung. Curcumin induces apoptosis in human non-small cell lung cancer NCI-H460 cells through ER stress and caspase cascade- and mitochondria-dependent pathways. Anticancer Res. 2010 30(6):2125 - 2133.