New Leaf Functional Nutrition

09/03/2026

Crock Pot Picadillo (share this recipe!) 😋

Comment "RECIPE" to get the link DM'd

A flavorful Cuban ground beef dish made in a simmering sauce of veggies and spices. 🍛 A staple in my family for decades! Leftovers are so versatile for making tacos, empanadas, stuffed peppers, or quesadillas.

✨ WW Pts: 4 Cals: 207 Protein: 28 Carbs: 5 Fats: 8.5 Fiber: 1

09/01/2026

Chronic stress is not simply “high cortisol.” Repeated activation of stress-response systems can disrupt sleep, cardiovascular regulation, immune signaling and metabolism. Long-term psychological stress is also associated with higher cardiovascular risk, potentially in part through inflammatory pathways. Responses vary widely, and much of the long-term evidence is observational.

PMID 28932967; PMID 37007994.

08/28/2026

Omega-3s are often discussed as though they produce one broad “anti-inflammatory” effect. The biology is more specific than that.

The main long-chain omega-3 fatty acids, EPA and DHA, become part of the phospholipid membranes that surround cells throughout the body. DHA is especially concentrated in the brain and retina, where it contributes to membrane structure and function. ALA, the plant-derived omega-3 found in foods such as flax and walnuts, is essential too, but humans convert only small amounts of it into EPA and DHA.

The clearest clinical effect of EPA is on triglycerides. At prescription doses of about 4 g/day, omega-3 fatty acids typically lower elevated triglycerides by roughly 20–30%, with larger reductions possible when baseline triglycerides are very high. That is a pharmacologic dose and should not be confused with the amount in an ordinary fish-oil capsule or a serving of fish.

Blood pressure moves too, but much less dramatically. A dose-response meta-analysis of 71 randomized trials found that about 2–3 g/day of combined EPA and DHA reduced systolic pressure by roughly 2.6 mm Hg and diastolic pressure by about 1.6–1.8 mm Hg on average. The effect tended to be larger in people who already had hypertension or elevated blood lipids.

EPA and DHA also serve as raw material for signaling molecules involved in the regulation and resolution of inflammation. That does not mean taking fish oil simply “turns inflammation off.” The downstream response depends on dose, tissue, baseline status and the biological problem being studied.

This distinction matters because the strongest evidence for omega-3s is not equally strong across every claim attached to them. Their incorporation into cell membranes is established biology. DHA enrichment in brain and retinal tissue is well documented. Triglyceride lowering is a clear clinical effect, and blood-pressure lowering is modest but reproducible. Broader claims about cognition, mood, inflammation or cardiovascular protection depend much more heavily on the population, dose and specific EPA/DHA formulation being tested.

So omega-3s are better understood as structural and signaling fats with a few well-established measurable effects, rather than as a single-purpose supplement.

NIH Office of Dietary Supplements. Omega-3 Fatty Acids Fact Sheet.
PMID 31422671.
PMID 35647665.

08/24/2026

Your gut bacteria make B vitamins. That part is well established. The part nobody talks about is what some (or most, in some cases) of those vitamins do before they ever reach you.

Researchers assessed 256 common human gut bacteria for the genes to build all eight B vitamins: B1, B2, B3, B5, B6, B7, B9, and B12. Each vitamin could be made by roughly 40 to 65 percent of those microbes. Some bacteria carry every pathway. Others carry none and cannot make a single one on their own.

So the ones that cannot make their own get them from the ones that can. Inside the colon, B vitamins move between bacteria. Producers synthesize them, non-producers take them up through dedicated transporters, and the whole community stays fed. The vitamin is a shared currency that keeps the ecosystem running.

This is the part that reframes how you think about a B vitamin. It is not only a nutrient for you. It is a growth substrate for them. A bacterium that depends on outside B vitamins lives or dies by whether its neighbors are producing enough. Change the supply and you change which species can survive. In that sense a B vitamin behaves like a prebiotic, feeding specific members of the community rather than your own cells.

That also explains a strange finding: changing the composition of your gut bacteria can shift your B vitamin requirements. The microbes are both a source and a sink. They produce these vitamins and they consume them.

One honest limit. We can measure how many gut bacteria carry these pathways. We can show the vitamins moving between species. What we cannot yet cleanly measure in humans is how much of the bacterially made supply crosses your gut wall versus how much gets used up inside the community first. The colon does have transporters for several of these vitamins, so it is not nothing. The exact amount that reaches you is still being worked out.

The takeaway is not that you can skip B vitamins from food because your bacteria have you covered. It is that the vitamins inside your gut are doing a second job you never see, running an economy among the microbes that live there.

Magnusdottir et al., Front Genet, 2015
Yoshii et al., Front Nutr, 2019
Gholami et al., Cancers, 2023

08/24/2026

Vitamin D is taken for bones. In 498 Danish children, the dose their mothers took in pregnancy showed up in memory tests ten years later.

The trial was never designed to test the brain. In 2009 a Copenhagen team randomised 623 pregnancies at week 24 to an extra 2,400 IU of vitamin D3 daily on top of the standard 400, against the standard 400 alone, stopping a week after birth. The question was childhood wheeze. A near-identical American trial ran in parallel at 4,000 IU. Both groups received vitamin D throughout, which matters for reading anything that follows: the comparison is a high dose against an adequate one, not against nothing.

There was reason to look at the brain anyway. The developing cortex carries vitamin D receptors and matures fastest in the second half of pregnancy. Rodents deprived in the womb show learning deficits, and cohort studies have tied lower maternal levels to lower child test scores and higher rates of autism and attention disorders. That observational evidence has always been weak, because women with low vitamin D differ in income, diet, time outdoors and much else that shapes a child's scores independently. Randomising the dose removes all of it at once, which is why a decade-long follow-up of a randomised pregnancy trial carries more weight than any number of cohorts.

At age ten, 498 children completed an eleven-part battery. Three abilities favoured the high-dose group. Two survived correction for having run eleven tests: visual and verbal memory. Translated into something readable, pick one child from each group at random and the high-dose child scored higher on visual memory 57 times in 100, where a coin toss is 50. Verbal memory came out at 55. The third result, mental flexibility, disappeared once the correction was applied.

The reason for caution is that this is the third look at these children, and the first two found nothing. A prespecified analysis of their development from birth to age six reported no benefit on cognition, motor skills, general neurodevelopment or behaviour, and word production at age two was slightly lower in the high-dose group. A separate examination at age ten found no effect of the supplement on autism or attention disorder diagnoses. The current analysis was not the question this trial was built to answer, cognition was not its prespecified outcome, and running eleven comparisons is exactly the situation in which some cross the line by chance. Add that the cohort is one Danish sample which was 95.6 percent white, that women already taking more than 600 IU daily were excluded, and that families were unblinded when the children turned three, seven years before testing.

Size deserves as much attention as direction. A shift from 50 to 57 in 100 is real but faint, invisible in any individual child and detectable only across hundreds of them. It is smaller than the year-to-year swing in one child's own scores. Estimated intelligence, the measure most parents would ask about first, came out at 107.6 against 107.8, which is no difference at all.

The open question is whether any of this depends on starting deficient. The trial did not select women by vitamin D status. The age-ten autism analysis found that mothers' own levels before any supplement predicted lower risk in the child while the supplement itself did not, which points toward status rather than dose being the variable that matters.

A randomised increase in one prenatal supplement was followed, a decade later, by a small difference on two of eleven memory tests in the same children, in an analysis that was not planned in advance and that follows two planned analyses which found nothing. Standard advice already includes vitamin D in pregnancy. Nothing here establishes that seven times the usual dose should become routine, and both groups in this trial were taking it. The question was never whether, only how much.

Frederiksen et al., JAMA Netw Open 2026;9(5):e2611464 · PMID 42149595
Chawes et al., JAMA 2016;315(4):353-61 · PMID 26813208
Sass et al., JAMA Netw Open 2020;3(12):e2026018 · PMID 33289844
Aagaard et al., Am J Clin Nutr 2024;119(2):362-370 · PMID 38072183
Litonjua et al., JAMA 2016;315(4):362-70 · PMID 26813209

08/24/2026

Caffeinated coffee has repeatedly been shown to provide benefits for health and aging - though the exact amount to consume and the mechanisms it uses have been incompletely explained. A new study solves some of the mystery by showing compounds in coffee, particularly caffeic acid, activate a receptor that helps protect cells from stress, inflammation, and damage (NR4A1, also called Nur77). Some other great sources of caffeic acid include turmeric, thyme, sage, and olive oil. https://www.sciencedaily.com/releases/2026/07/260719035927.htm

08/23/2026

08/22/2026

Strive for healthy body composition not “weight loss”

A number on the scale is treated as the summary of a body. In 260,861 adults, the tape measure disagreed with it in more than a third of cases.

BMI is height and weight and nothing else. It cannot tell muscle from fat, and it cannot tell fat under the skin from fat packed around the organs. That second distinction is the one that matters, because visceral fat sits in the drainage of the portal vein and delivers free fatty acids and inflammatory signals straight to the liver. The idea that a tape measure captures what the scale misses is old. In 27,098 people across 52 countries, waist-to-hip ratio graded heart attack risk cleanly across every fifth of the distribution, while BMI's association collapsed to nothing once the ratio and other risk factors were accounted for.

Whether that translates into anything useful in a clinic has been genuinely contested. In 221,934 people across 58 cohorts, adding BMI, waist, or waist-to-hip ratio to a risk model that already contained blood pressure, lipids and diabetes history did not meaningfully improve discrimination, with C-index changes at the fourth decimal place. Waist also reproduces less reliably than BMI on repeat measurement. That analysis is the strongest argument against bothering. What has shifted the balance since is genetic evidence: a polygenic score for waist-to-hip ratio adjusted for BMI was associated with 1.77 times the odds of type 2 diabetes and 1.46 times the odds of coronary disease, alongside higher triglycerides, higher two-hour glucose and higher systolic pressure, which is what a causal relationship looks like rather than a marker travelling alongside one.

The new analysis pooled 15 cohorts followed a median of 20 years across nine cardiovascular outcomes. The reclassification was substantial in both directions. Among people whose BMI read normal, 18 percent had a high waist-to-hip ratio and 5 percent a high waist circumference. Among people with overweight, roughly 40 percent had one or the other. Among people whose BMI read obesity, 45 percent had a low waist-to-hip ratio and 9 percent a low waist. A high waist inside a normal or overweight BMI carried 15 to 50 percent greater risk across most outcomes.

Everything is observational, so nobody was assigned a body shape, and people who carry weight centrally differ in diet, alcohol, sleep and stress in ways no adjustment reaches. More particularly, this analysis reports how much better the tape classifies people, not whether measuring them changes what happens to them. No trial has randomised clinicians to measure waists. The thresholds used, 88 and 102 centimetres, were derived largely in European-ancestry populations and understate risk in South Asian and East Asian populations, where lower cut-points are recommended. And the reverse direction deserves as much attention as the forward one: among people with obesity, a low waist was not associated with different risk than normal weight for most outcomes, and was associated with lower all-cause mortality, though women with obesity and a low ratio kept elevated risk where men did not.

Among people with obesity, the share of cases attributable to a high waist circumference ran to 48.9 percent for heart failure and 46.2 percent for atrial fibrillation, against 28.8 percent for death from any cause. Nearly half the heart failure in that group tracked to where the fat sat rather than how much there was.

What is still missing is any demonstration that acting on the measurement helps. A consensus statement in 2020 argued waist circumference should be recorded as routinely as blood pressure, and it still generally is not.

A tape measure costs almost nothing and takes fifteen seconds, and in roughly one normal-weight adult in five it says something the scale did not. That is not a reason to discard BMI, which remains more reproducible and predicts perfectly well at a population level. It is a reason to record both, and to stop treating a normal BMI as an all-clear.

Dardari et al., J Am Coll Cardiol 2026;88(6):670-684 · PMID 42583989
Yusuf et al., Lancet 2005;366(9497):1640-9 · PMID 16271645
Wormser et al., Lancet 2011;377(9771):1085-95 · PMID 21397319
Emdin et al., JAMA 2017;317(6):626-634 · PMID 28196256
Ross et al., Nat Rev Endocrinol 2020;16(3):177-189 · PMID 32020062

08/19/2026

Let that hot drink cool down!

Heat injures the lining of your esophagus the same way it injures the lining of your mouth. The difference is what your nervous system tells you about it. The mouth has dense thermal pain receptors. The esophagus has visceral nerve endings that are tuned more to stretch than to temperature. You can swallow tea at temperatures that would burn your tongue without feeling pain. The damage is real but the warning signal isn't.

In 2016, the International Agency for Research on Cancer reviewed the evidence on hot beverages and esophageal cancer. They classified drinking beverages above 65°C as a Group 2A carcinogen, meaning a probable cause of cancer in humans. The mechanism is straightforward. Repeated thermal injury to the esophageal lining triggers chronic inflammation. Inflammation drives cell turnover. Faster cell turnover increases the rate at which mutations accumulate. Over years and decades, this combination raises the risk of esophageal squamous cell carcinoma.

The strongest data comes from the Golestan Cohort Study (Islami et al., 2019, International Journal of Cancer). Researchers prospectively followed 50,045 adults in northeastern Iran for a median of 10 years and recorded 317 new cases of esophageal squamous cell carcinoma. They measured tea drinking temperature objectively at baseline, not just by self-report.

The findings:

People who drank tea at 60°C or higher (objectively measured) had a 41% higher risk of esophageal squamous cell carcinoma than those who drank below 60°C. People who self-reported a preference for "very hot" tea (vs cold or lukewarm) had 141% higher risk. People who drank tea within 2 minutes of pouring had 51% higher risk than those who waited 6 minutes or more. People who drank 700 mL or more per day at 60°C or higher had about 90% higher risk than people who drank less at lower temperatures.

These findings are consistent across populations. Middleton and colleagues (2019, International Journal of Cancer) ran a separate case-control study in western Kenya, where esophageal squamous cell carcinoma incidence is also high. Drinkers of "very hot" beverages had 3.7 times the risk of warm-temperature drinkers. The association held after adjustment for alcohol and to***co use.

Two honest caveats. First, the IARC Group 2A classification means probable carcinogen, not confirmed carcinogen. Group 2A requires limited evidence in humans, sufficient evidence in animals, and a plausible mechanism. The temperature link is not as definitively established as Group 1 carcinogens like to***co. Second, the absolute risk for any one individual remains low. Esophageal squamous cell carcinoma is uncommon in most Western populations. The relative risk increases reported here are real but they apply to a baseline that's already small.

Practically: tea brewed at typical temperatures (85 to 95°C) cools below 65°C in roughly 4 to 5 minutes in a standard mug at room temperature. The exact time varies with cup material, volume, and ambient temperature. Letting tea cool for 4 to 6 minutes between pouring and drinking removes the temperature mechanism entirely. Coffee, hot chocolate, and any other hot beverage follow the same physics. The threshold is the temperature, not the drink.

The temperature is the variable. The drink isn't.

Islami et al., International Journal of Cancer, 2019 Middleton et al., International Journal of Cancer, 2019 IARC Monograph Volume 116, 2018