Nutriciondannifitmx

29/04/2026

The assumption that fresh produce is nutritionally superior to frozen is one of the most durable beliefs in modern eating. It is also not what the data shows.

Bouzari and colleagues (2015, Journal of Agricultural and Food Chemistry) ran a controlled comparison at UC Davis, measuring four vitamins across eight commodities (corn, carrots, broccoli, spinach, peas, green beans, strawberries, blueberries) under both fresh and frozen storage conditions. The vitamins were ascorbic acid (vitamin C), α-tocopherol (vitamin E), riboflavin (B2), and β-carotene. Each commodity was sampled at three storage time points per condition.

For vitamin C, frozen samples were higher than fresh in 3 of 8 commodities and statistically equivalent in the remaining 5. Frozen lost in zero of eight comparisons.

For α-tocopherol, the pattern was identical. Frozen higher in 3 of 8, equivalent in the remaining 5, and never lower.

For riboflavin, 6 of 8 commodities showed no difference. Broccoli was higher in frozen, peas were higher in fresh. A wash.

For β-carotene, the pattern flipped. β-carotene was only present in measurable amounts in 5 of the 8 commodities (not in blueberries, strawberries, or corn). Of those 5, frozen was lower in 3 commodities (peas, carrots, and spinach showed measurable losses), with the remaining commodities showing no significant difference. β-carotene is the one vitamin where fresh tends to win.

The mechanism behind this pattern is straightforward. Frozen vegetables are blanched and frozen within hours of harvest, locking in the nutrient content at peak. The storage chain that follows ("the freezer aisle") is biochemically stable. Vitamin C, in particular, is held essentially indefinitely at standard freezer temperatures.

"Fresh" produce, by contrast, takes a different path. Commercial fresh vegetables are harvested days before they reach the supermarket. They sit in cold-chain transit for 3 to 7 days. They sit on display for 1 to 3 days. Then they sit in your refrigerator for another 3 to 7 days before you cook them. The full journey from field to plate is often 7 to 17 days, and vitamin C degrades meaningfully across that window.

By the time a head of broccoli has been in your fridge for a week, the frozen broccoli in the freezer aisle has retained more of its vitamin C than the "fresh" alternative on your plate. That is the finding.

What this does not mean. Frozen is not universally superior. β-carotene losses are real for some vegetables. Texture, taste, and certain phytochemicals not measured by Bouzari may differ between fresh and frozen. Garden-harvested produce eaten the day it is picked is a different category entirely and is not what this study measured. The relevant comparison is supermarket "fresh" vs. supermarket "frozen," which is what most people are actually choosing between.

What this does mean. The "fresh is better" assumption that drives produce purchasing decisions is not supported by the data on vitamin retention. For vitamin C and vitamin E, frozen vegetables are at least as good as fresh in every commodity tested, and better in nearly half of them. For most home cooks, the practical implication is that the frozen aisle deserves a serious look, especially for vegetables you will not get to within a couple of days of buying.

A note on the study itself. Bouzari 2015 measured 8 commodities and 4 vitamins. It is not a meta-analysis. It is a single well-designed study from UC Davis that has been broadly consistent with the wider food science literature. The findings would be stronger if replicated across more commodities and more nutrients, but the underlying biochemistry is well-understood and not in serious dispute.

Same vegetable. Different supply chain. Different vitamin retention.

Bouzari et al., Journal of Agricultural and Food Chemistry, 2015

29/04/2026

If you walk on a treadmill at low intensity, your muscles oxidize a higher percentage of fat as fuel during the workout. The cardio machine display picks up on this and labels the zone you're in as "fat-burning." The percentage is real. The label is correct about what it's measuring. The problem is that "% of fuel from fat right now" and "body fat lost over weeks" are different measurements operating on different timescales, and people treat them as the same.

This is a category error, not a marketing lie.

What the label is actually measuring. Romijn and colleagues (1993, American Journal of Physiology) used stable isotope tracers and indirect calorimetry to measure substrate utilization in trained subjects at exercise intensities of 25%, 65%, and 85% VO₂max. At low intensity, peripheral lipolysis was maximal and fat provided the largest share of energy. As intensity rose, plasma fatty acid release decreased and muscle glycogen oxidation increased. Achten and colleagues (2002, Medicine and Science in Sports and Exercise) refined this further. They found that the rate of fat oxidation peaks around 64% VO₂max, with a "Fatmax zone" between 55 and 72% VO₂max. This is the curve cardio machines are trying to summarize when they label a heart rate zone as "fat-burning."

What the label is not measuring. Body fat change is determined by total energy balance over time, integrated across all eating and movement, not by which fuel substrate the muscle preferred during a single 45-minute session. Melanson and colleagues (2009, Journal of Applied Physiology) demonstrated this directly. Lean sedentary, lean endurance-trained, and obese sedentary subjects performed one hour of cycling at 55% VO₂max. The exercise increased fat oxidation acutely. But when energy balance was maintained, 24-hour fat oxidation did not differ between the exercise and rest conditions. The exercise day's fat balance was actually slightly more positive than the control day. The acute substrate shift didn't translate into greater fat loss over 24 hours.

The reason is straightforward. Body fat is a storage pool. It changes when energy intake is below energy expenditure for long enough for the deficit to draw from stored fat. Whether your muscles oxidized fat or carbohydrate during a 45-minute window is a small input to that integrated calculation. Caloric balance over days and weeks is the dominant factor. Protein intake matters significantly because it determines how much of the lost mass is fat versus lean tissue. Exercise modality has a small effect. Substrate utilization within a single workout is essentially negligible for body fat change once caloric balance is accounted for.

A practical consequence. Walking is excellent exercise. It is sustainable, low-injury, accessible, and contributes to total daily energy expenditure in a way that most people can maintain for years. The "fat-burning zone" reading of why walking is good for fat loss is the wrong reading. The right reading is that walking adds to your daily energy expenditure, is consistent enough to compound across weeks and months, and pairs well with adequate protein and reasonable caloric intake. The fuel mix in any given session is not the variable.

Two honest caveats. First, exercise intensity does affect total caloric output per minute. Higher intensity work burns more calories in the same time window. So if time is constrained, intensity matters for the energy deficit equation, but the mechanism is total kcal, not fuel preference. Second, EPOC (excess post-exercise oxygen consumption) modestly favors higher-intensity work, but the magnitude is small (typically 6 to 15% of the workout's caloric cost) and doesn't change the basic conclusion. Third, individual fitness, training status, and feeding state all shift the substrate curves. The numbers in the post are representative averages, not exact values for any individual.

The label measures the wrong timescale.

Romijn et al., American Journal of Physiology, 1993 Achten et al., Medicine and Science in Sports and Exercise, 2002 Melanson et al., Journal of Applied Physiology, 2009

28/04/2026

Glycine is sold across the wellness internet as a sleep aid, a collagen builder, and an anti-aging amino acid for glutathione synthesis. The sleep evidence is real. The other two are mechanism-plausible but the isolated-glycine human RCTs that would prove them don't exist. The strongest non-sleep RCT on glycine is in a place most people don't expect: postprandial glucose.

The study. Gannon and colleagues (2002, American Journal of Clinical Nutrition) ran a randomized crossover trial in nine healthy adults. Each subject was tested on four separate occasions, ingesting either water alone, 25 g glucose alone, 1 mmol per kg lean body mass of glycine alone (about 4 to 5.5 g for most adults), or the same dose of glycine plus 25 g glucose. Plasma glucose, insulin, glucagon, and glycine were measured for two hours.

The result. When glycine was ingested with glucose, the plasma glucose response was attenuated by more than 50 percent compared with glucose alone. Half. Not a small effect. The glycine dose was modest and the glucose load was the standard 25 g used in oral glucose tolerance studies.

The mechanism. Gannon's data are compatible with the hypothesis that oral glycine stimulates the secretion of a gut hormone that potentiates the action of insulin on glucose removal from the circulation. The specific hormone wasn't identified in the paper, but glycine does stimulate glucagon release directly, and there is biological plausibility for L-cell mediated incretin involvement. The mechanism is hypothesis-level. The outcome is well-measured.

Why this matters for the marketing claims. The wellness internet sells glycine for collagen synthesis and for glutathione synthesis as an anti-aging strategy. Both have biological plausibility. Glycine is roughly 33 percent of collagen residues by amino acid count. Glycine is one of three amino acids that combine to form glutathione. But isolated-glycine human RCTs measuring collagen outcomes don't exist. The glutathione trials that show benefit, including the Sekhar group's GlyNAC studies, used glycine combined with N-acetylcysteine. Cysteine is the rate-limiting amino acid for glutathione synthesis in most adults. Isolated-glycine human RCTs demonstrating restored glutathione concentrations don't exist.

The other isolated-glycine RCT worth mentioning. High-dose glycine (0.8 g per kg per day) added to antipsychotic medication has been shown in randomized trials to reduce negative symptoms of schizophrenia by approximately 30 percent (Heresco-Levy et al., 1999, Archives of General Psychiatry). Mechanism: glycine is an obligatory co-agonist at NMDA receptors. The doses required are large and the application is specialized clinical use, not general supplementation.

The honest synthesis. Glycine has multiple plausible mechanisms in human biology. Outside of sleep, the strongest isolated-glycine RCT evidence is in postprandial glucose attenuation. The collagen and anti-aging glutathione claims that drive most consumer marketing have weak isolated-compound RCT support. If you're already taking glycine and want a measurable effect, the data suggests the dinner table is where to look. About 4 to 5.5 g of glycine consumed with a carbohydrate-containing meal is the dose Gannon's nine subjects took.

Two caveats. The study was small (n=9) and acute (single-dose, two-hour observation). Whether repeated dosing produces the same effect over weeks or months hasn't been tested at this dose. The participants were healthy adults, not people with diabetes or insulin resistance, so generalization to those populations is uncertain. The mechanism (gut hormone potentiation of insulin action) is hypothesis-level, not proven.

The label is honest. The study is good. The wellness internet is selling something the data doesn't support.

Gannon et al., American Journal of Clinical Nutrition, 2002 Heresco-Levy et al., Archives of General Psychiatry, 1999

27/04/2026

ZUMO DE CEREZA ÁCIDA Y RECUPERACIÓN MUSCULAR EN DEPORTE La suplementación con cereza ácida puede favorecer la recuperación tras ejercicio intenso, especialmente reduciendo dolor muscular y mejorando la preparación para sesiones posteriores. Sus efectos sobre fuerza y biomarcadores son variables, por lo que su uso debe contextualizarse y periodizarse estratégicamente. (lee el artículo completo en BLOG JL Chicharro en https://www.fisiologiadelejercicio.com) t.ly/YVIob

26/04/2026

🔬 Filtración Glomerular y ERC: lo que no puedes pasar por alto

La TFG (eGFR) es el pilar para evaluar función renal. La fórmula CKD-EPI 2021 (sin raza) permite una estimación más precisa basada en creatinina, edad y s**o.

📊 Diagnóstico de ERC:
✔ TFG < 60 ml/min/1.73 m² por ≥ 3 meses
✔ o evidencia de daño renal (albuminuria, alteraciones estructurales)

📌 Clasificación KDIGO:

- G (TFG): G1 a G5 según severidad
- A (Albuminuria): A1 (300 mg/g)

⚠ Clave clínica:
No basta la TFG---TFG + Albuminuria = Riesgo real
(renal + cardiovascular)

💡 Perlas:

- Creatinina “normal” ≠ función renal normal
- Pequeños cambios → gran impacto en TFG
- Ajuste farmacológico SIEMPRE según TFG

🧠 Medicina basada en evidencia = decisiones seguras

25/04/2026

Las grasas y el colesterol de la dieta pasan por un proceso digestivo y, al llegar al intestino delgado se ensamblan en quilomicrones, que son lipoproteínas encargadas de transportar a los lípidos por el sistema linfático hacia el torrente sanguíneo. Al circular por la sangre, la enzima lipoproteína lipasa degrada a los lípidos de los quilomicrones en glicerol y ácidos grasos; estos pueden ser utilizados por los músculos para obtener energía mediante la β-oxidación o bien almacenarse en el tejido adiposo en forma de triacilgliceroles (triglicéridos).

En la vía endógena, el hígado sintetiza triglicéridos y colesterol para empaquetarlos en partículas de VLDL (lipoproteínas de muy baja densidad). En el torrente sanguíneo, la VLDL va perdiendo triglicéridos por la hidrólisis de la lipoproteína lipasa y esto hace que se transforme secuencialmente en LDL (lipoproteína de baja densidad), una partícula que es captada por células de tejidos periféricos a través de la endocitosis mediada por receptores; al interior de la célula, las enzimas lisosomales degradan a la LDL liberando colesterol y aminoácidos para su uso celular.

Al final, si hay un exceso de colesterol en las células y los tejidos, las partículas HDL (lipoproteínas de alta densidad) actúan como recolectoras; recogen el exceso de colesterol, llevándolo de vuelta al hígado para su reciclaje o excreción a través de las sales biliares (bilis), un mecanismo fundamental para evitar la acumulación de colesterol/grasa en tejidos y vasos sanguíneos.

Excelente esquema para la colección.
*Transporte de grasas y metabolismo de las lipoproteínas.

25/04/2026

21/04/2026

Insulin and Glucose Blood Sugar Control

Ever wondered how your body keeps blood sugar levels stable after every meal?

Blood glucose is tightly regulated by the hormone insulin.

After eating, blood glucose levels rise
The pancreas releases insulin into the bloodstream
Insulin helps cells absorb glucose for energy or storage
Excess glucose is stored as glycogen in the liver and muscles

When blood glucose falls, insulin secretion decreases
Another hormone glucagon increases glucose release into the blood

This balance maintains a stable energy supply for the body

If this system fails, it can lead to conditions like diabetes

A precise hormonal control system… keeping your energy levels steady

Save this to quickly revise how blood sugar is regulated