New Leaf Functional Nutrition

04/28/2026

This is fascinating! Why I love learning biochemistry 😍

Coffee's effect on your cholesterol depends on what catches the diterpenes before they reach your cup.

Coffee beans contain two natural compounds called diterpenes: cafestol and kahweol. They aren't oils themselves, but they ride along in coffee oil, the lipid fraction of the bean. When hot water passes through ground coffee, those diterpenes get carried into the brew on tiny lipid droplets. Once swallowed and absorbed, cafestol acts on your liver. It activates a receptor called FXR, which suppresses an enzyme called CYP7A1. CYP7A1 is the enzyme your liver uses to convert cholesterol into bile acids. With less of that conversion happening, your liver clears less LDL out of circulation, so blood LDL rises.

This is not a fringe finding. It has been replicated across decades of randomized controlled trials. Jee and colleagues (2001, American Journal of Epidemiology) pooled fourteen RCTs and found a clear pattern: unfiltered coffee raised total and LDL cholesterol in a dose-dependent way, while filtered coffee showed essentially no effect. Cai and colleagues (2012, European Journal of Clinical Nutrition) pooled twelve more RCTs in 1,017 subjects and found coffee raised LDL by an average of 5.4 mg/dL, with the largest effects in trials using unfiltered coffee.

The variable that determines whether you get a cup full of diterpenes or a cup that has had them stripped out is the filter material. Paper traps them. Metal mesh, the kind you'll find in a French press, an espresso basket, a percolator, or a moka pot, does not. A 2025 analysis of Swedish workplace coffee (Orrje et al., Nutrition, Metabolism and Cardiovascular Diseases) measured cafestol concentrations across brewing methods. Boiled coffee came in at 939 mg/L. Workplace brewing machines averaged 176 mg/L. French press and percolator landed around 90 mg/L. Some espresso samples reached 2,447 mg/L. Paper-filtered home drip averaged 12 mg/L. The same green coffee bean produces wildly different cardiovascular exposures depending on what comes between the grounds and your cup.

The downstream evidence comes from a 20-year prospective study of 508,747 Norwegian adults (Tverdal et al., 2020, European Journal of Preventive Cardiology). Adults who drank filtered coffee had about 15% lower all-cause mortality compared with non-drinkers. Unfiltered coffee drinkers showed a weaker, less consistent benefit. In adults drinking nine or more unfiltered cups per day, ischemic heart disease mortality was modestly elevated.

A few honest caveats. Cafestol's LDL-raising effect is real and reproducible, but the magnitude is moderate, not dramatic. A 5 mg/dL bump in LDL over years matters more for someone with elevated baseline cholesterol or established cardiovascular risk than for someone whose lipids are already excellent. Cloth filters, properly used, also remove a substantial fraction of diterpenes. And coffee carries other compounds: chlorogenic acids, polyphenols, caffeine, and trigonelline have their own metabolic effects, mostly favorable. These compounds are mostly water-soluble. Paper filters trap the lipid-soluble diterpenes while letting the water-soluble actors pass through.

Practically: if you have a family history of hypercholesterolemia, an existing LDL concern, or you're already managing cardiovascular risk, the brewing method is one of the easier levers. Switching from a French press to a pour-over with a paper filter changes nothing about caffeine, ritual, or flavor in any meaningful way. It just removes the diterpenes from the cup.
The bean isn't the variable. The filter is.

Jee et al., American Journal of Epidemiology, 2001
Cai et al., European Journal of Clinical Nutrition, 2012
Tverdal et al., European Journal of Preventive Cardiology, 2020
Orrje et al., Nutrition Metabolism and Cardiovascular Diseases, 2025

04/27/2026

Better off not using a microwave to rearrange the molecules in your food! I don’t even own one…

When you microwave food in a plastic container, three things move from the container into your food: plasticizers like phthalates, residual monomers like bisphenol A, and tiny particles of the plastic itself. This happens at temperatures most people use every day. The amount is measurable in laboratory studies. Whether it matters for your health at typical exposure levels is genuinely uncertain. The honest framing is the one that doesn't oversell either direction.

The "microwave-safe" label tells you something specific. It tells you the manufacturer has determined the container won't melt, warp, or deform under typical microwave use, and that any migrating substances stay below the FDA's specific migration limits for food contact materials. It does not tell you that nothing leaves the container. The FDA standard (21 CFR 177) is built around specific migration limits, not around zero migration. Compliance means migration stays below the legal threshold. It does not mean migration is absent.

What the studies show:
Lim and colleagues (2009, Journal of Toxicology and Environmental Health) tested polycarbonate bottles by microwaving them with steamed rice or cooked pork to 100°C for 9 minutes. Bisphenol A migration into the food rose from 6 to 18 parts per billion in the rice and 5 to 15 parts per billion in the pork. These levels were well below the regulatory limit of 600 parts per billion. The migration was real and measurable. The doses were not.
Hussain and colleagues (2023, Environmental Science and Technology) measured microplastic and nanoplastic release from polypropylene containers and reusable food pouches under different conditions. Microwave heating released the most particles per square centimeter compared to refrigeration or room-temperature storage. Some containers released up to 4.22 million microplastics and 2.11 billion nanoplastics per square centimeter of plastic surface within three minutes of microwave heating. The estimated daily intake came out to about 20 nanograms per kilogram of body weight for infants drinking microwaved water. Nanograms. The cytotoxicity demonstrated in the same study was at concentrations far higher than typical real-world exposure.

A second 2024 paper (Jin et al., Journal of Hazardous Materials) found hot water exposure released comparable or greater quantities of particles than microwave heating in their setup. Heat is the variable. The microwave is one source of heat among several.

Five things that scale migration from any plastic container into food:

First, heat. Higher temperature means more migration, full stop.
Second, fat content of the food. Phthalates and BHT are lipid-soluble. Fatty foods pull more out than aqueous foods.
Third, acidity. Tomato sauce, citrus, and vinegar accelerate migration relative to neutral foods.
Fourth, container age and condition. Microscratches from dishwashing and repeated heating cycles create more surface area and more particle release.
Fifth, duration of contact. Long storage allows continued migration even at room temperature.
What this does not mean: it does not mean microwaving food in plastic is poisoning you. The doses measured in real-world conditions are typically well below regulatory limits, and the daily intake estimates are in nanograms per kilogram per day. Phthalate exposure is associated with adverse outcomes in epidemiological studies, but the dominant exposure routes are personal care products, dust, and food packaging in general, not specifically microwave heating.

What this does mean: the label "microwave-safe" is not the assurance most people read it as. Migration into food is happening every time you microwave plastic. The magnitude depends on heat, fat content, acidity, container age, and time. Standard food-grade glass and ceramic are essentially inert under kitchen conditions and don't migrate meaningfully at any temperature with typical foods. The swap from plastic to glass for reheating removes the variable entirely.

The label is about whether the container survives. Whether anything leaves the container is a separate question.

Lim et al., Journal of Toxicology and Environmental Health, 2009
Hussain et al., Environmental Science and Technology, 2023
Jin et al., Journal of Hazardous Materials, 2024
21 CFR 177 (FDA food contact substances)

04/27/2026

I have been talking about the benefits of resistant starches on blood sugar for quite some time. This is an excellent science review of this concept!

You can create fiber inside food that didn't have it before. The trigger is temperature.

When you cook starchy food, water enters the starch granules and the long amylose and amylopectin chains unfold. This is gelatinization, and it's why hot rice, hot pasta, and hot mashed potato are so easy for your body to digest. The chains are loose, exposed, and your digestive enzymes break them down within minutes. Your blood sugar rises fast.

When you cool that same cooked starch, the chains do something interesting. They realign and partially recrystallize into a tightly ordered structure called retrograded starch. Your digestive enzymes can't break the crystals as efficiently. The starch reaches your colon largely intact, where your gut bacteria ferment it into short-chain fatty acids including butyrate. Resistant starch is especially butyrogenic compared to other fibers. The FDA and AOAC classify retrograded starch (resistant starch type 3) as dietary fiber for nutrition labeling purposes. Same molecule. Different physical structure. Different physiology.

The numbers across foods:

White rice (Sonia et al., 2015, Asia Pacific Journal of Clinical Nutrition). Researchers measured resistant starch in three preparations: freshly cooked, cooked and cooled at room temperature for 10 hours, and cooked and refrigerated at 4°C for 24 hours then reheated. Resistant starch went from 0.64 g per 100 g (fresh) to 1.30 g (room temp cooled) to 1.65 g (refrigerated and reheated). The clinical follow-up was a randomized crossover in 15 healthy adults. The cooled-and-reheated rice produced a meaningfully lower glucose response than the freshly cooked rice. Same calories, same ingredients.

Potato (Larder et al., 2018, Food Research International). Boiled potatoes cooled for 24 hours at 4°C had up to 114% more resistant starch than potatoes cooled for one hour at room temperature. The exact magnitude varies by cultivar.

Pasta (Hodges et al., 2019, Foods). Randomized crossover comparing freshly cooked pasta, cold pasta, and reheated pasta. Reheated pasta produced a smaller and faster-resolving glucose curve than freshly cooked pasta. The mechanism is the same starch retrogradation that happens in rice and potato.

A few honest caveats. First, "your enzymes can't break the crystals" is a simplification. Pancreatic amylase has reduced activity against retrograded starch but isn't blocked entirely. Some still gets digested. The functional shift is meaningful, not absolute. Second, the magnitude of the cooling effect varies by food, by cultivar, by cooking method, and by cooling time and temperature. Longer cooling at lower temperatures (24 hours at 4°C beats 10 hours at room temperature) produces more retrogradation. Third, repeated extreme reheating can partially reverse retrogradation, but normal microwave or stovetop reheating does not.

Practical implication. If you eat rice, pasta, or potatoes regularly, cooking a batch and refrigerating overnight before reheating roughly doubles the resistant starch content of the same food. Your post-meal glucose response is lower. Your colon gets more butyrate. The fiber on the nutrition label is what was in the raw ingredients. The fiber you actually consume depends on how you cooked and stored the food before eating it.
Same food. Different temperature history. Different physiology.

Sonia et al., Asia Pacific Journal of Clinical Nutrition, 2015 Hodges et al., Foods, 2019
Larder et al., Food Research International, 2018

04/26/2026

04/25/2026

You already know that candy is bad for brain health, but a new study will have you asking if that’s because of the sugar or the… arsenic. 28 popular candies, including Kit Kat, Snickers, and Swedish Fish, were found to have “toxic levels of arsenic” in a recent test. So please put down the sweets, they’re not worth the heavy metal detox you’ll need. https://www.southernliving.com/arsenic-in-candy-11900535

04/24/2026

Every thyroid hormone your body makes is built from iodine and an amino acid called tyrosine. A third nutrient, selenium, is what activates it.

Inside the thyroid, an enzyme called TPO takes iodine from your blood and attaches it to tyrosine residues on a storage protein. Pairs of these iodinated tyrosines then fuse together to form T4. That's the hormone your thyroid primarily releases. But T4 is inactive. It has to be converted to T3 before your body can use it.

That conversion happens mostly outside the thyroid, in the liver and kidneys, and it depends entirely on selenium. The enzymes that do this job (deiodinases) all require selenium at their active site.

Berry et al. identified this in Nature in 1991. Without adequate selenium, T4 gets made but doesn't get activated. Selenium-deficient patients show exactly this pattern: normal T4, low T3.
A few practical notes. Tyrosine is part of the structure, but it's made from dietary protein and is rarely the limiting factor unless someone is severely malnourished. Iodine and selenium are the ones most likely to actually matter. And while low selenium is one reason T4 might not convert to T3, it isn't the only one. Illness, caloric restriction, and chronic inflammation all suppress that same conversion step through different mechanisms.

The takeaway: if you're thinking about thyroid support, iodine alone doesn't cover it. The activation step is just as important as the building step, and that requires selenium.

Endotext Ch.2: Thyroid Hormone Synthesis, 2015.
Berry et al., Nature, 1991.
Di Jeso & Arvan, Endocrine Reviews, 2016.

04/21/2026

Brilliant!

04/21/2026

This is why I use CoQ10 (as ubiquinone not ubiquinol) & in softgel or chewable gel form ONLY.

The Q-SYMBIO trial, published in JACC: Heart Failure in 2014, is the most important study ever conducted on CoQ10 supplementation and cardiovascular outcomes. It is also a trial that most people promoting CoQ10 supplements seem to have selectively forgotten the details of.

Mortensen and colleagues enrolled 420 patients with moderate to severe chronic heart failure across 17 cardiology centers in nine countries. Half received 100mg of ubiquinone three times daily for two years as adjunct to standard heart failure therapy. The other half received matching placebo. The primary endpoint was a composite of unplanned heart failure hospitalization, cardiovascular death, urgent transplant, or need for mechanical support. Patients entered this trial already on guideline-directed medical therapy. The intervention was added on top of optimal care, not instead of it.

The results at two years: 15% of patients in the CoQ10 group hit the primary endpoint versus 26% in the placebo group. A 43% relative reduction in serious cardiac events. Cardiovascular mortality was 9% in the CoQ10 arm versus 16% in placebo, a 44% relative reduction. All-cause mortality was 10% versus 18%. Heart failure hospitalizations were 8% versus 14%. Every clinically meaningful endpoint moved in the same direction by similar magnitudes. This is the kind of effect size that earns a drug a breakthrough designation. It was achieved with a molecule that has been sold as a dietary supplement for decades.

The mechanism is not a mystery. CoQ10 is the electron shuttle that moves electrons from Complex I and Complex II to Complex III in the mitochondrial respiratory chain. That electron flow drives the proton gradient across the inner mitochondrial membrane, which powers ATP synthesis. No other molecule in human biology can perform this function. When myocardial CoQ10 is depleted, which occurs in heart failure and is worsened by statin use via the mevalonate pathway, cardiac mitochondrial efficiency drops. Myocardial CoQ10 levels correlate with heart failure severity. The CoQ10 deficit tracks with how sick the heart is.

The Q-SYMBIO finding was independently replicated by KiSel-10 (Alehagen et al., 2013), a Swedish trial in 443 elderly community-dwelling subjects given 200mg CoQ10 (ubiquinone) plus 200μg selenium daily for four years. Cardiovascular mortality dropped from 12.6% in the placebo arm to 5.9% in the treatment arm. The twelve-year follow-up published in 2018 showed the mortality benefit was sustained long after the intervention ended, which is an unusual and striking finding. Two independent trials. Two different patient populations. Both using ubiquinone. Both showing large reductions in cardiovascular death.

Here is the part the marketing departments would rather you not notice. Both trials used ubiquinone, the oxidized form of CoQ10, specifically the Bio-Quinone product sold under the Myoqinon brand name. Not ubiquinol. Every major clinical trial demonstrating hard cardiovascular outcomes from CoQ10 supplementation used the form that retails for a fraction of the price of "premium" ubiquinol products. Fladerer and Grollitsch published a systematic review in Current Cardiology Reports in 2023 that reviewed 28 clinical trials and found no ubiquinol trial has replicated these cardiovascular mortality findings. They explicitly recommend ubiquinone over ubiquinol for the prevention and treatment of cardiovascular disease in heart failure patients.

Why did it work? The formulation was not accidental. Bio-Quinone is crystal-dispersed ubiquinone delivered in a soft gel with a carrier oil. Crystal dispersion is the manufacturing step that breaks CoQ10 out of its native crystalline lattice so it can actually dissolve in gastrointestinal fluid. Without it, oral bioavailability drops by roughly 75% (Mantle and Dybring, Antioxidants, 2020). The soft gel with oil carrier ensures lipid-phase absorption. Three times daily dosing maintains serum levels above the approximately 3 μg/mL therapeutic threshold commonly cited in the CoQ10 cardiovascular literature. The trial worked because the formulation worked. Not because the form on the label was special.

The practical takeaways: if you or someone you care about has heart failure, CoQ10 has the strongest evidence base of any dietary intervention for reducing cardiovascular death. The dose is 100mg three times daily, ideally with meals, as ubiquinone in a crystal-dispersed soft gel. Cheaper forms without crystal dispersion do not produce the same bioavailability. Neither does ubiquinol at standard doses, despite the marketing. Talk to a cardiologist before starting. If you are on warfarin, CoQ10 can alter INR and requires monitoring. This is adjunct therapy, not a replacement for guideline-directed medical care.

The broader point for the dietary supplement industry is this. When the best-designed trial on a supplement outperforms most pharmaceutical interventions in its target population, the industry should probably be shouting about it from the rooftops. Instead, the field pivoted to selling a more expensive form that has not replicated the outcome data, while the cheaper form that generated the evidence base sits in the background. Formulation science beat redox chemistry. The market has the story backwards.

Mortensen, JACC HF, 2014
Alehagen, Int J Cardiol, 2013
Fladerer & Grollitsch, Curr Cardiol Rep, 2023
Mantle & Dybring, Antioxidants, 2020

04/15/2026

If you’ve ever cut your hand or rolled your ankle, you’ve experienced inflammation firsthand — the redness, the swelling, the pain. That’s your immune system doing exactly what it’s supposed to do.

But that same process can happen deep inside your body, in ways you can’t see. And when it doesn’t shut off, chronic inflammation can leave you bloated, foggy, tired, and achy — and increase your risk of major health issues over time.

The biggest driver of this is The Standard American Diet. High in refined grains, added sugars, unhealthy fats, and ultra-processed foods that are literally engineered to be impossible to stop eating.

Your body was never meant to handle this, and it’s fighting back.

In my free Inflammation Fix guide, I walk you through the exact 5 steps I use with my patients:

- Clear out the big offenders
- Build your plate around color
- Upgrade your fats
- Spice it up
- Hydrate like you mean it

Your body wants to heal. You just have to stop getting in its way.

Grab the FREE guide here: https://drhyman.com/pages/inflammation-fix-guide

04/15/2026