Jad Patrick Naturopathy Nutrition Counselling

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.

20/03/2026

20/02/2026

I love theanine and have had great clinical and personal results with it. I appreciate this post as it shares that we can’t be too quick to over identify with some of mechanistic claims made about it however

"L-theanine boosts alpha waves" is probably the most-repeated claim about theanine. It shows up on product pages, in influencer posts, in brand infographics, etc. The EEG research behind it tells a more complicated story.

Firstly, I like L-theanine quite a bit. Anecdotally, it "works" for me. I would like to provide nuance to things without it being perceived as an "attack on that thing." So, here is an attempt at that.

At rest with eyes closed, two studies found alpha increases after theanine. One was funded by Unilever (Nobre 2008, 50mg). The other found the effect only in participants with high trait anxiety, and used a multi-ingredient drink, not pure theanine (White 2016). That same paper noted that resting-state alpha is "at best a crude indicator" of relaxation.

During cognitive tasks, the pattern reverses. Two studies from the same lab found that theanine significantly decreased background alpha activity during attention tasks (Gomez-Ramirez 2007, 2009). A third found no effect from theanine alone. Caffeine improved performance by itself, and adding theanine to it didn't add anything. (Foxe 2012).

The direction alpha moves appears to depend on what the brain is doing when you measure it, the dose, and the anxiety level of the person taking it. The resting-state result is the one that made it onto labels. The task-based research didn't travel with it.

This matters because the alpha-wave claim is the most accessible part of theanine's story. It's the thing people point to when they say "we know how it works." Underneath it, the four proposed biological mechanisms have not been confirmed in humans at the mechanistic level. The most-cited receptor binding study is a single 2002 in vitro experiment. It has never been independently replicated (to my knowledge). The strongest new mechanistic evidence, imaging mass spectrometry showing a GABA increase across multiple brain regions, was published last year. In mice.

None of this means theanine doesn't do anything. Human trials have shown subjective relaxation and stress reduction effects. The science just hasn't caught up to the confidence level of the claims yet, and that's worth knowing.

References:

Nobre et al., Asia Pac J Clin Nutr 2008
Gomez-Ramirez et al., Clin Neuropharmacol 2007
Gomez-Ramirez et al., Brain Topogr 2009
Foxe et al., Neuropharmacology 2012
White et al., Nutrients 2016
Kakuda et al., Biosci Biotechnol Biochem 2002
Taira et al., Sci Rep 2025
Ibrahim et al., Biosci Biotechnol Biochem 2025

12/02/2026

2–3 structured resistance sessions per week using progressive, moderate to heavy loads significantly lowers brain age.

In a randomized controlled trial published in GeroScience, researchers used fMRI-derived brain clocks to estimate biological brain age over time.

Participants assigned to moderate- and high-intensity resistance training showed significant reductions in accelerated brain aging compared to non-exercise controls.
This wasn’t subtle.

• Brain Age Gaps (BAGs) decreased over 1–2 years
• Effects were distributed across networks — not isolated to one hub
• Functional connectivity shifted toward a “younger” pattern
• Non-exercise participants showed no significant change
These findings suggest brain aging trajectories are modifiable and mechanical loading of skeletal muscle may influence neural network integrity.

Mechanistically, resistance training is associated with:
• Increased cerebral perfusion
• Upregulation of neurotrophic signaling
• Improved insulin sensitivity
• Reduced systemic inflammation
• Enhanced mitochondrial efficiency
The implication is practical:

You don’t need exotic protocols.

2–3 structured resistance sessions per week — progressive, moderate to heavy loads may help preserve not just muscle, but the biological age of the brain.

Train the muscle.
Influence the network.
Slow the clock.

doi:10.1007/s11357-026-02141-x

07/02/2026

Bones aren’t just structural. They’re metabolic.

Mechanical loading on bone doesn’t stop at strength or density. It triggers endocrine signaling that directly influences glucose regulation.

When bone experiences load:
• Osteoblast and osteoclast activity increases
• Osteocalcin is released into circulation
• Insulin sensitivity improves
• Skeletal muscle glucose uptake increases

This creates a bone–pancreas–muscle feedback loop that links movement, bone health, and blood sugar control.

In simple terms:
Load the skeleton → signal the pancreas → improve glucose handling.

The B.O.N.E.S. framework captures how this works in practice:
• Bear weight regularly – resistance and impact matter
• Oppose gravity often – prolonged sitting blunts signaling
• Nourish bone function – vitamin D, K, protein, and minerals
• Every session matters – consistency beats intensity
• Strength training first – skeletal loading outperforms cardio alone for this pathway

This pathway is well-established in animal models, with growing human data showing strong correlations between bone loading, insulin sensitivity, and metabolic health.

Bone is not passive tissue.
It’s an active organ participating in energy regulation.

Movement doesn’t just burn glucose.
It teaches your body how to handle it.

03/02/2026

09/01/2026

Ketogenic (very low carb diets) appear to have some potential to treat symptoms of psychiatric illness. There are many benefits to low carb diets but also risks - especially if attention is not paid to the health of our gut microbes. It’s important to seek professional guidance when implementing these diets - especially for psychiatric conditions such as bipolar, depression and psychotic disorders.

Ketogenic diets (KDs) have been hypothesized to influence mental health through pathways involving mitochondrial function, inflammation, and neurotransmitters, but their therapeutic value in psychiatric populations remains uncertain.

This systematic review and meta-analysis evaluates associations of KD with mental health outcomes in psychiatric and other medical populations.

https://ja.ma/4qPdoqK

24/12/2025

Merry Christmas ! I hope 2026 is a year of hope and happiness and health ❤️🌈🎅🏻☮️🕊️✌️may all beings find peace and freedom from unecessary suffering 🙏🏻