Jad Patrick Naturopathy Nutrition Counselling

20/07/2026

Herbal Medicine is older than humanity

In 2024, biologists reported that a wild Sumatran orangutan named Raku treated his own facial wound with a poultice of chewed-up leaves. They weren’t just any leaves either—Raku selected leaves from a plant vine, Fibraurea tinctoria, known to have medicinal properties, from analgesic pain relief to antibacterial and anti-inflammatory effects.

Now, a recent study in Scientific Reports has found that Raku’s self-medicating moment wasn’t a one-off event, but rather part of a broader suite of orangutan behaviors. Researchers from the United Kingdom and Indonesia collected behavioral data for more than 20 years on a population of about 100 wild Bornean orangutans living in a peat-swamp forest. Observations of feeding included the species of plant as well as the parts eaten, whether fruit, seed, skin, pulp, pith, or bark. Two coauthors local to the study site offered ethnobotanical knowledge about medicinal properties and uses of the plants by humans.

A total of 12,236 feeding events were recorded, yielding 202 distinct plant species. Of those, about 30 percent were recognized as medicinal plants by the Indigenous Dayak communities of the region. Furthermore, orangutan consumption of the medicinal plants was found to be non-random.

“What makes the findings interesting is that some plant species appeared together in the orangutan diet far more often than we would expect by chance,” explained study author Georgia Allen, then a master’s student at the University of Exeter, in a press release. “Importantly, many of these plants aren’t major parts of the orangutan diet overall, suggesting they may be eaten for specific benefits rather than as everyday food sources.”

The orangutans appeared to select combinations of plants in sequences that confer a full complement of pharmacological benefits. Since orangutans don’t have a “medicine man” to prescribe the right concoctions of plant remedies, they’re likely using chemical cues and memory to favor healing species. The study authors hypothesized that botanical knowledge may even be passed down over generations.

Regardless, Allen added, “our findings suggest they selectively consume certain plants with medicinal properties in ways that go beyond simple nutrition.”

Study link -> https://www.nature.com/articles/s41598-026-52614-4

04/07/2026

Movement helps your brain keep pumping !

𝗧𝗵𝗲 𝗚𝘂𝘁-𝗕𝗿𝗮𝗶𝗻 𝗖𝗼𝗻𝗻𝗲𝗰𝘁𝗶𝗼𝗻 𝗶𝘀 𝗠𝗼𝗿𝗲 𝗣𝗵𝘆𝘀𝗶𝗰𝗮𝗹 𝗧𝗵𝗮𝗻 𝗪𝗲 𝗧𝗵𝗼𝘂𝗴𝗵𝘁: 𝗛𝗼𝘄 𝗬𝗼𝘂𝗿 𝗖𝗼𝗿𝗲 𝗠𝘂𝘀𝗰𝗹𝗲𝘀 𝗦𝗾𝘂𝗲𝗲𝘇𝗲 𝗬𝗼𝘂𝗿 𝗕𝗿𝗮𝗶𝗻

◼️ For a long time, the central nervous system was thought to be mechanically isolated from the rest of the body, protected by the rigid skull and vertebrae.

◼️ But groundbreaking new research has revealed that the brain is intimately linked to the physical dynamics of our core.

◼️ In fact, every time you brace your abdominal muscles, you are physically moving your brain.

◼️ Here is a deep dive into how researchers uncovered this fascinating hydraulic connection, and what it means for brain health, waste clearance, and conditions like obesity.

𝗪𝗮𝘁𝗰𝗵𝗶𝗻𝗴 𝘁𝗵𝗲 𝗕𝗿𝗮𝗶𝗻 𝗠𝗼𝘃𝗲 𝗶𝗻 𝗥𝗲𝗮𝗹-𝗧𝗶𝗺𝗲

◼️ To figure out what drives brain motion, researchers used high-speed, multiplane two-photon microscopy on awake, head-fixed mice.

◼️ By integrating an electrically tunable lens, they were able to rapidly switch focus between the skull and the brain tissue beneath it, allowing them to track relative movement.

◼️ They found that during wakefulness, brain movement is primarily driven by locomotion, not heartbeat or respiration.

◼️ When mice moved, their brains shifted forward (rostrally) and outward (laterally).

◼️ Strangely, this brain motion often preceded the actual physical movement of the mouse's body.

◼️ To find out what was causing this pre-movement shift, researchers implanted EMG electrodes in the mice's abdominal muscles.

◼️ They discovered a perfect correlation: before the mice moved, they tensed their core, and this abdominal muscle activation perfectly predicted the brain's movement.

◼️ To confirm this wasn't a coincidence, researchers placed a tiny pneumatic pressure cuff on the abdomens of lightly anesthetized mice.

◼️ Simply squeezing the abdomen immediately caused the brain to shift forward.

𝗧𝗵𝗲 𝗦𝗲𝗰𝗿𝗲𝘁 𝗛𝘆𝗱𝗿𝗮𝘂𝗹𝗶𝗰 𝗣𝗮𝘁𝗵𝘄𝗮𝘆: 𝗧𝗵𝗲 𝗩𝗩𝗣

◼️ How does a squeeze in the belly reach the brain?

◼️ The answer lies in the Vertebral Venous Plexus (VVP), a network of valveless veins.

◼️ Using microCT scans to reconstruct the vascular system, researchers found small holes in the lumbar and sacral vertebrae of mice.

◼️ Blood vessels run from the abdominal cavity through these holes, connecting directly to the vascular network lining the spinal canal.

◼️ When abdominal muscles contract, intra-abdominal pressure spikes drastically.

◼️ This forces blood out of the abdomen and into the spinal canal.

◼️ This rush of blood acts like a hydraulic pump—it narrows the dural sac, pushes cerebrospinal fluid (CSF) upward, and physically squeezes the brain against the skull.

𝗪𝗵𝘆 𝗗𝗼𝗲𝘀 𝗧𝗵𝗶𝘀 𝗦𝗾𝘂𝗲𝗲𝘇𝗶𝗻𝗴 𝗠𝗮𝘁𝘁𝗲𝗿?

◼️ The brain lacks a traditional lymphatic system to clear out waste, relying instead on the movement of interstitial fluid (ISF) and cerebrospinal fluid (CSF).

◼️ Because observing fluid flow inside an awake brain is incredibly difficult, researchers used poroelastic computer modeling to simulate the effects of this abdominal squeezing.

◼️ The simulations showed that this mechanical brain motion drives fluid out of the brain and into the subarachnoid space at rates several times higher than normal CSF production.

◼️ Crucially, this waking fluid flow goes in the exact opposite direction of the "glymphatic" fluid flow that occurs during sleep, which brings fluid into the brain.

◼️ This mechanical pushing during wakeful movement might explain why deep sleep is physiologically required to properly clear metabolic waste from the brain.

𝗕𝗿𝗼𝗮𝗱𝗲𝗿 𝗜𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀 𝗳𝗼𝗿 𝗛𝘂𝗺𝗮𝗻 𝗛𝗲𝗮𝗹𝘁𝗵

👇 𝗢𝗯𝗲𝘀𝗶𝘁𝘆 𝗮𝗻𝗱 𝗖𝗼𝗴𝗻𝗶𝘁𝗶𝗼𝗻

◼️ Obesity chronically elevates intra-abdominal pressure.

◼️ This constant pressure could disrupt the normal hydraulic flow between the abdomen and the spine, potentially impairing brain fluid circulation and contributing to the cognitive decline sometimes associated with obesity.

👉 𝗔 𝗗𝗶𝗿𝗲𝗰𝘁 𝗣𝗵𝘆𝘀𝗶𝗰𝗮𝗹 𝗦𝗶𝗴𝗻𝗮𝗹

◼️ The brain contains mechanosensitive channels that respond to physical forces.

◼️ The physical squeezing of the brain caused by our core muscles might serve as a direct, mechanical way for the body to communicate its internal visceral state to the brain.

𝗧𝗮𝗸𝗲𝗮𝘄𝗮𝘆

◼️ Ultimately, this research proves that our central nervous system isn't resting quietly in a static vault.

◼️ Instead, it is continuously massaged and manipulated by the movements of our core.

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.

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