Jad Patrick Naturopathy Nutrition Counselling

16/06/2026

Exercise not only is good for our heart and diabetes risk but may also reduce cancer risk via our microbiome

27/05/2026

Yum

23/04/2026

I love learning new info. Omega 3 levels may take a while longer than many might think !

An 8-week omega-3 trial catches your plasma. It misses the compartment most associated with long-term outcomes.

That compartment is the red blood cell membrane. The percentage of EPA and DHA it contains is the Omega-3 Index, proposed by Harris and Von Schacky in 2004 as a biomarker of long-term omega-3 status. In their 2006 follow-up review of epidemiologic data, individuals with an O3I above 8% had roughly 90% lower risk of sudden cardiac death compared to those below 4%. This is an observational association derived from modeling cohort data, not an interventional finding. No RCT has used achieving a specific O3I threshold as the primary endpoint for a hard cardiovascular outcome.

The loading kinetics of the membrane matter because it doesn't fill fast.

Katan and colleagues (1997, J Lipid Res) ran the definitive kinetic study. 58 men took 0, 3, 6, or 9 grams of fish oil daily for 12 months, with follow-up extending to 18. They tracked EPA and DHA in plasma cholesteryl esters, erythrocyte membranes, and subcutaneous fat.

The compartments moved at different speeds. EPA in plasma cholesteryl esters plateaued at 4 to 8 weeks, with an incorporation half-life of 4.8 days. EPA in RBC membranes took 180 days to reach steady state, with a half-life of 28 days. Adipose tissue was still changing at 12 months. Katan's own summary line: "EPA levels in cholesteryl esters reflect intake over the past week or two, erythrocytes over the past month or two, and adipose tissue over a period of years."
This creates an interpretation problem for shorter studies.

Mechanistic omega-3 studies often report outcomes at 8 to 12 weeks, especially for inflammatory markers, lipid changes, or blood pressure. Plasma fractions are near steady state by that window. The RBC membrane is not. If a clinical effect depends on membrane composition, a trial reading its biomarker at 8 weeks is reading a compartment that hasn't finished loading. This isn't a reason to dismiss null results outright. It's a reason to be cautious about how they get extrapolated.

The large cardiovascular outcome trials, VITAL, ASCEND, REDUCE-IT, STRENGTH, all ran for years, with median follow-up of roughly 3.5 to 7.4 years. Trial duration isn't their main issue. Those trials have their own well-documented criticisms: dose differences (REDUCE-IT used 4 g icosapent ethyl versus 1 g in VITAL), background dietary omega-3 intake, placebo choice (mineral oil in REDUCE-IT has been argued to raise cardiovascular risk markers relative to olive oil), and differing entry criteria. The compartment-loading argument applies mainly to shorter mechanistic studies.

For personal testing: if you start supplementation and retest your Omega-3 Index at 8 weeks, you're seeing an incomplete picture. Retest at 4 to 6 months for a value that reflects steady state. Body weight also matters. Flock and colleagues (2013, J Am Heart Assoc) found that adjusting dose per kilogram of body weight slightly improved prediction of O3I response over absolute dose, and larger participants showed smaller O3I changes at a given absolute dose. Dose alone explained 68% of response variability. Dose per kilogram explained 70%. When combined with baseline O3I, age, s*x, and physical activity, the model explained 78%.
None of this establishes that omega-3 supplementation reduces hard cardiovascular outcomes. The RCT evidence on that question remains mixed. What it does establish is that the biomarker most strongly associated with long-term status takes about six months to reflect a change in intake. Trial design, and personal tracking, should be calibrated to that timeline.

Harris & Von Schacky, Prev Med, 2004
von Schacky & Harris, Cardiovasc Res, 2006
Katan et al., J Lipid Res, 1997
Flock et al., J Am Heart Assoc, 2013

14/04/2026

A cup of cooked spinach has about 6mg of iron. A 3oz serving of beef has about 2.5mg. Most people look at those numbers and assume spinach is the better iron source. It is not that simple. The number on the label measures what is in the food. Not what makes it into your blood.

Iron exists in two forms in the diet. Heme iron is the iron embedded inside a porphyrin ring structure, the same structure found in hemoglobin and myoglobin. It comes exclusively from animal tissue: red meat, poultry, fish, organ meats. Non-heme iron is ionic iron found in plants, eggs, dairy, fortified foods, and iron supplements. The two forms enter your body through completely different pathways, and the difference in absorption is not small.

Heme iron is absorbed intact as a complete metalloporphyrin molecule through a dedicated transporter (HCP1) on the surface of intestinal cells. Once inside the enterocyte, the enzyme heme oxygenase cracks open the porphyrin ring and releases the iron. Because the iron is shielded inside that ring structure during transit through the gut, it is protected from the dietary factors that block non-heme absorption. Phytates, polyphenols, calcium, tannins from tea and coffee: none of them significantly impair heme iron absorption. The absorption rate ranges from 15 to 35% depending on your iron status.

Non-heme iron takes a harder path. It arrives in the gut primarily as ferric iron (Fe³⁺), but the transporter that moves iron into intestinal cells (DMT1) only accepts ferrous iron (Fe²⁺). The iron must first be reduced by an enzyme called duodenal cytochrome b (DcytB), an ascorbate-dependent ferrireductase on the brush border. This is why vitamin C increases non-heme iron absorption so dramatically: it directly reduces Fe³⁺ to Fe²⁺ and chelates the iron into a soluble complex that resists precipitation in the alkaline small intestine. Hallberg and Hulthen (2000, Am J Clin Nutr) quantified this across hundreds of meal compositions. Adding 50mg of vitamin C to a meal with significant inhibitors increased non-heme iron absorption by 3 to 6 times. That is half a bell pepper or one orange.

The inhibitors are equally dramatic. A single serving of a high-phytate food (whole grains, legumes, nuts) can reduce non-heme iron absorption from the same meal by 50-80%. Polyphenols in tea and coffee reduce it by 60-70%. Calcium competes with iron for DMT1 transport and reduces absorption by 50-60% in single-meal studies. The result is that non-heme iron absorption ranges from 2% to 20% depending almost entirely on what else you ate at the same meal.

The practical impact: heme iron makes up only about 10-15% of total dietary iron intake in a typical omnivore diet. But because of its dramatically higher absorption rate, it accounts for over 40% of total iron actually absorbed. The form matters more than the amount on the label.

Absorption rates by food source illustrate this clearly. Organ meats: 25-30% absorbed. Red meat: 15-25%. Leafy greens: 7-9%. Grains: approximately 4%. Dried legumes: approximately 2%.

This does not mean plant-based iron is useless. It means the delivery context matters. Pairing iron-rich plant foods with vitamin C at the same meal meaningfully changes how much iron you absorb. Tomatoes with lentils. Bell pepper with beans. Orange juice with fortified cereal. Soaking and fermenting legumes reduces phytate content by 50-90% and improves bioavailability. Drinking tea and coffee between meals rather than with them avoids the polyphenol competition. And taking iron supplements with dairy or calcium at the same time is working against yourself.

For anyone managing iron status, whether that is an athlete, a menstruating woman, a vegetarian, or someone with diagnosed deficiency, understanding the difference between label iron and absorbed iron changes how you plan meals. Spinach has about 6mg of iron per cup. You absorb roughly 8% of it. Beef has less total iron per serving, but its heme portion absorbs at 25%. The total absorbed amount can end up similar between the two, but the absorption rate difference is real and it compounds across every meal. The nutrition label is a starting point. What you eat it with is the rest of the equation.

Hallberg & Hulthen, Am J Clin Nutr, 2000
Hurrell & Egli, Am J Clin Nutr, 2010
Monsen, J Nutr, 1988

09/04/2026

Most people take their full magnesium dose in one sitting. The absorption data says that strategy may not “maximize efficiency.”

Fine et al. gave healthy subjects a standard meal supplemented with increasing amounts of magnesium. At the lowest dose (36 mg), 65% was absorbed. At the highest dose (1,009 mg), only 11%. The curve was not linear. It dropped steeply at first, then flattened. Their model explained it as two simultaneous processes: an active transport channel that saturates, plus a passive route that absorbs a fixed ~7% of whatever is present.

The active channel is TRPM6. It sits in the intestinal epithelium and actively pulls magnesium ions across the membrane. It works well at low concentrations but has a ceiling. Once it is saturated, additional magnesium can only cross passively between cells (paracellular transport), driven by the concentration gradient. That passive route never saturates, but it only captures about 7% of the dose regardless of how much is present.

This is why splitting a 400 mg dose into two 200 mg doses absorbs more total magnesium. Each dose stays closer to the steep part of the curve where TRPM6 is still contributing. One large dose overwhelms the active channel, and most of the magnesium passes through unabsorbed. The unabsorbed fraction is osmotically active, pulls water into the colon, and causes the loose stools people commonly experience.

A question that comes up: does the form of magnesium change this? The absorption curve from Fine et al. used magnesium acetate, which is highly soluble. The form determines how completely and quickly the magnesium salt dissolves and releases free Mg2+ ions in the gut. Oxide dissolves poorly at intestinal pH, so much of it never becomes available. Citrate, glycinate, and acetate dissolve more readily. But once the ion is free, it faces the same TRPM6 and paracellular bottleneck regardless of what delivered it. Form determines how much Mg2+ reaches the membrane. The curve determines how much of that gets through. A poorly soluble form at a high dose is the worst combination. A highly soluble form split across meals is the best.

The RDA for magnesium is 310-420 mg per day. NHANES data consistently shows about half of US adults fall short. Splitting the dose is free, requires no product change, and the physiology is clear.

Fine et al., J Clin Invest, 1991.

Schuchardt & Hahn, Curr Nutr Food Sci, 2017.