Deirdre Parkinson, Clinical Naturopath, Herbalist, Nutritionist.

30/04/2026

A cup of tea brewed for 1 minute and a cup brewed for 5 minutes are not the same beverage. The dry leaf is identical. The water is identical. The amount of caffeine, catechins, and tannins extracted into your cup is dramatically different.

Astill and colleagues (2001, Journal of Agricultural and Food Chemistry) ran a comprehensive study at Unilever Research, mapping how each compound class extracts from black and green tea leaves over time. The kinetics they documented are consistent with established tea extraction chemistry.

Caffeine extracts fast. Most of the caffeine in the leaf is in your cup within the first 1-2 minutes of steeping. By 3 minutes, caffeine extraction is essentially complete and additional brew time adds little.

Catechins extract slower. EGCG, EGC, ECG, and EC, the polyphenols that drive most of the health-related research on green tea, are larger molecules with more complex extraction kinetics. They continue extracting meaningfully through 3-5 minutes. A 1-minute brew captures only a fraction of the catechin content the same leaf could deliver.

Tannins extract last. The high-molecular-weight polymeric polyphenols that produce astringency and harsh bitterness become prominent later in the brew. After roughly 4-5 minutes of steeping, the tannin fraction rises notably and the cup turns from bright to harsh.

A separate effect that applies regardless of brew time: tea polyphenols as a class bind non-heme iron. Hurrell and colleagues (1999, British Journal of Nutrition) reported that drinking tea with a meal reduced non-heme iron absorption by approximately 60 percent in healthy subjects. This effect is not specific to over-steeped tea. Even normally brewed tea consumed with iron-containing food has the same effect, because all the major tea polyphenols (catechins included) participate in iron binding.

What this means in practice. The tea bag dipped for 30 seconds and pulled out is mostly a caffeine delivery vehicle with minimal catechin content. The tea steeped for 8 minutes is a tannin-heavy infusion that tastes harsh. The 3 to 5 minute window captures the catechin peak before the astringent tannin fraction builds substantially.

Two caveats worth noting. The exact extraction kinetics depend on water temperature, leaf grade, and whether the tea is loose-leaf or in a bag. Higher temperatures accelerate all extraction. Smaller particle sizes (commercial tea bag dust) extract faster than whole leaves. The 3 to 5 minute window applies to typical brewing conditions: roughly 95 degrees Celsius water, standard tea bag, one cup volume. Green tea is often brewed at lower temperatures (75-85 degrees Celsius) which slows catechin extraction and extends the optimal window. The Astill 2001 study was conducted at Unilever, the parent company of Lipton, which is relevant context. The underlying kinetics are not industry-disputed and align with established food chemistry.

A practical implication. If you are drinking tea for the catechin and EGCG content that drives most of its associated health research, the 30-second tea bag dunk delivers roughly the same caffeine as a longer brew but only a fraction of the catechins. If you are drinking tea purely for caffeine, a short brew is fine. If you have iron status concerns and consume tea with meals, the binding effect happens regardless of brew time. Drinking tea between meals rather than with them is the relevant lever for iron absorption, not brew time.

Same leaf. Same water. Three minutes of difference changes the chemistry of what you are drinking.

Astill et al., Journal of Agricultural and Food Chemistry, 2001 Hurrell et al., British Journal of Nutrition, 1999

03/04/2026

The magical healing powers of herbal medicine is that it works with the body, rather than against it.

23/03/2026

The benefits of this age old herbal medicine is now being studied and proven in clinical trials. But before you take it, see a naturopathic practitioner if you are already in pharmaceuticals.

Ginkgo biloba is one of the most extensively studied herbal medicines in modern clinical research, with hundreds of randomised controlled trials (RCTs) across conditions such as cognitive decline, stroke recovery, tinnitus, peripheral arterial disease, anxiety and age-related vascular complaints. A common thread through much of this literature is circulatory physiology, particularly effects on endothelial function, blood flow regulation and microvascular perfusion. Rather than acting as a simple symptomatic agent, Ginkgo extract can be framed as a modulator of microcirculatory dynamics. Dizziness and vertigo, especially when aetiology is mixed or unclear, frequently have a vascular or microvascular component, which makes the therapeutic use of Ginkgo biologically plausible.

A 2026 trial directly compared standardised Ginkgo extract (120 mg/day) with betahistine (36 mg/day, best known under the proprietary name Serc) in 86 adults with dizziness or vertigo of unclear cause. It was randomised, double blind and placebo-matched, a methodologically sound design for a largely subjective symptom complex. Over 12 weeks, both groups improved significantly on validated measures (the 11-Point Box Scale and the Dizziness Handicap Inventory).

Betahistine showed a faster early response at week 2, with a large short-term effect size, but by week 12 there was no meaningful difference between the two treatments. In practical terms, both interventions were effective, and neither demonstrated clear superiority at the study endpoint. That said, with only 43 participants per arm, the study was likely underpowered to identify more modest, yet still clinically meaningful, between-treatment effects, and it was not designed as a formal non-inferiority trial.

This finding aligns with earlier research. A larger European multicentre RCT (n=160) in 2014 using 240 mg/day of Ginkgo extract also found it comparable to betahistine over 12 weeks. With 27 adverse events in 19 patients, Ginkgo showed better tolerability than betahistine with 39 adverse events in 31 patients.

Across multiple trials and pooled analyses, Ginkgo extract has shown consistent benefit in vertigo syndromes, particularly where vascular regulation may be relevant. The newer study is notable for demonstrating similar long-term outcomes at a lower Ginkgo dose, suggesting clinical activity even at 120 mg/day (about 6 g of the starting dried leaf).

Taken together, the evidence does not suggest that Ginkgo outperforms betahistine, but it does support the view that it performs similarly within standard dosing ranges. Betahistine may act more quickly, but Ginkgo appears to exert equal benefit over time. For clinicians, this positions Ginkgo extract as a legitimate therapeutic option in dizziness and vertigo, particularly where an altered microcirculatory rationale is compelling.

For more information see: https://pubmed.ncbi.nlm.nih.gov/41487075/

18/03/2026

Muscle loss, as Dr Berg explains, is an unfortunate effect that leads to a domino effect of health issues in the long term. Careful nutritional advice and exercise is imperative when talking this drug.

04/03/2026

This is why it is so important to include a test for homocysteine in the basic blood test panel.

To what extent can diet, lifestyle, supplements and herbal therapy modulate the biological vulnerability associated with APOE variants? At present, most research attention has centered on APOE4, and the evidence base is still evolving.

In humans, the strongest APOE4-specific mitigation signals come from large prospective cohort data examining dietary patterns. Higher adherence to a Mediterranean dietary pattern, characterised by extra-virgin olive oil, fish, legumes, vegetables, fruit, nuts, and relatively low saturated fat, has been associated with lower dementia incidence and slower cognitive decline even among APOE4 carriers, including homozygotes. Moreover, adherence to the Mediterranean diet more effectively modulated dementia-related metabolites in APOE4 homozygotes. Importantly, these analyses suggest that genetic risk does not nullify dietary benefit; rather, diet quality appears capable of attenuating at least part of the elevated baseline risk. While observational in nature, these studies are strengthened by large sample sizes, biomarker integration, and gene-diet interaction analyses.

In the FINGER multidomain intervention trial (dietary counselling, physical exercise, cognitive training and vascular risk monitoring), cognitive outcomes improved over two years, and subgroup analyses demonstrated that APOE4 carriers derived comparable benefit to non-carriers. In other words, APOE4 did not blunt responsiveness to lifestyle optimisation. This is clinically important because it shifts the narrative from genetic determinism to modifiable network biology: vascular integrity, metabolic control, neurotrophic signalling, and inflammatory tone remain therapeutically responsive even in genetically higher-risk individuals.

More targeted evidence comes from the PENSA prevention trial in cognitively normal APOE-ε4 carriers with subjective cognitive decline. This study combined an intensive multimodal lifestyle program with epigallocatechin gallate (EGCG) from green tea. Although the primary endpoint narrowly missed statistical significance, secondary and post-washout analyses showed signals of cognitive improvement in the intervention group. While more confirmatory trials are needed, PENSA represents one of the few genotype-specific, prospective attempts to biologically modulate APOE4-associated vulnerability, suggesting that polyphenol-based strategies may complement lifestyle optimisation in this population.

Omega-3 fatty acids, particularly DHA (docosahexaenoic acid), are one of the most biologically plausible strategies for mitigating APOE4-associated dementia risk, but the human data are nuanced.

First, mechanistically, APOE4 is associated with impaired cerebral lipid transport, reduced DHA delivery to the brain, greater oxidative stress, and heightened neuroinflammation. DHA, as a structural component of neuronal membranes, supports synaptic plasticity, modulates inflammation (via resolvins/protectins), and may influence amyloid processing. Imaging and tracer studies suggest that APOE4 carriers may have reduced brain DHA uptake or retention, which provides a rationale for higher or more sustained dosing strategies in this subgroup.

Second, clinical trial evidence is mixed, but suggestive when interpreted carefully. Large prevention trials in unselected older adults have often shown null results; however, several secondary analyses indicate that benefits are more likely in earlier disease stages (mild cognitive impairment or subjective cognitive decline), in those with low baseline omega-3 status, and sometimes in APOE4 non-carriers more than carriers. This contrast may reflect altered DHA trafficking in APOE4 brains, implying that standard dosing may be insufficient. Some smaller trials and biomarker studies suggest that higher DHA doses (≥ 1 to 2 g/day DHA specifically) can increase CSF DHA and may slow hippocampal atrophy in early impairment, though APOE4-stratified findings remain inconsistent.

Third, epidemiological data are generally more favourable. Higher dietary fish intake and higher plasma DHA levels have been associated with lower dementia risk, and some cohort analyses suggest that maintaining adequate omega-3 status may partially offset APOE4 risk. Importantly, omega-3 status appears to interact with homocysteine levels and B-vitamin status, suggesting a nutrient-network effect rather than a single-agent solution.

However, DHA cannot currently be framed as a proven APOE4-specific risk “antidote”; rather, it is a biologically coherent component of a systems-level preventative approach.

A 2024 randomised clinical trial reported that omega-3 PUFA supplementation did not reduce white matter lesion progression overall, but APOE4 carriers receiving omega-3s showed reduced breakdown of neuronal integrity over 3 years, implying genotype-specific neuroprotective effects.

Recent epidemiological and mechanistic syntheses continue to reaffirm that higher omega-3 status (dietary or blood levels) correlates with slower cognitive decline and lower dementia risk, and suggest APOE4 carriers may be particularly sensitive to DHA brain availability due to altered lipid transport. The authors of that review study suggested that increasing omega 3 intake provides APOE4 carriers with the highest potential for protection against AD when implemented early in life, many years before the onset of cognitive decline.

Finally, lowering elevated plasma homocysteine appears to attenuate the cognitive and neurodegenerative risk associated with APOE-ε4 in observational and biomarker-driven intervention studies, although definitive APOE4-stratified dementia-prevention trials are still lacking.

In practical terms, the most defensible conclusion is that maintaining homocysteine in an optimal range is a rational and low-risk strategy, especially in APOE4 carriers, because it targets a mechanistic pathway that converges with APOE4-related vascular and inflammatory vulnerability, even if definitive genotype-stratified prevention data are still emerging.

For more information:
https://pubmed.ncbi.nlm.nih.gov/40855194/
https://pubmed.ncbi.nlm.nih.gov/29356827/
https://pubmed.ncbi.nlm.nih.gov/40664536/
https://pubmed.ncbi.nlm.nih.gov/25333200/
https://pubmed.ncbi.nlm.nih.gov/27532692/
https://pubmed.ncbi.nlm.nih.gov/39088212/
https://pubmed.ncbi.nlm.nih.gov/38609814/
https://pubmed.ncbi.nlm.nih.gov/27431367/

26/01/2026

Ginkgo biloba, B12, folate, and vitamin D are just some of the nutrients that can help reduce the incidence of dementia. Of course, nothing will help if the diet is full of highly processed, refined carbohydrate, inflammatory foods.

Even with unprecedented investment, the dementia drug pipeline continues to deliver modest and uncertain gains at best. Despite the media fanfare, recent agents largely target late-stage amyloid pathology, offering small statistical benefits that translate into limited real-world clinical impact, while carrying substantial costs and safety concerns. There is little in the current pipeline that convincingly alters disease trajectory once neurodegeneration is established. This sobering reality underlines a critical truth: dementia is unlikely to be “cured” pharmacologically after onset. The greatest opportunity lies earlier—shifting focus toward prevention and delay through vascular health, metabolic resilience, inflammation control, and lifelong neuroprotection—where the biological leverage, population impact, and cost-effectiveness are far greater.

A recent umbrella review underlines that we already know a good deal about what to do. A total of 45 reviews covering 212 meta-analyses (including around 10,000 individual studies in total) were synthesised. From this the authors identified 14 broadly defined modifiable risk factors that were significantly associated with dementia disorders.

They were: alcohol consumption, body weight, depression, diabetes mellitus, diet, hypertension, less education, physical inactivity, sensory loss, sleep disturbance, smoking, social isolation, traumatic brain injury and vitamin D deficiency. All 14 factors were associated with the risk of major neurocognitive disorders (NCD), and five were associated with mild NCD. Of note, the scientists found considerably less research for vascular dementia and mild NCD.

The study highlighted the role of a key nutrient in prevention, namely vitamin D. Beyond vitamin D, several B vitamins and selected herbs may contribute meaningfully to dementia prevention. Folate and vitamin B12 are central to homocysteine metabolism; elevated homocysteine is strongly linked to brain atrophy, white-matter damage and faster cognitive decline, with trials suggesting benefit when deficiencies or low-normal levels are corrected. Among herbs, Ginkgo biloba has the most consistent human evidence, supporting cerebral microcirculation and endothelial function and mitochondrial activity. Turmeric (particularly bioavailable curcumin) targets neuroinflammation, oxidative stress and amyloid pathology. Low-dose lithium, even at trace nutritional levels, has emerging epidemiological and clinical support for neuroprotection, possibly reduced tau phosphorylation and enhanced neuronal resilience.

For more information see: https://pubmed.ncbi.nlm.nih.gov/38346414/

20/01/2026

Gotu kola herb excellent for wound healing of leg ulcers.

A pilot registry study found that treatment with an oral gotu kola extract (Centella asiatica) significantly improved the closure and healing rates of chronic venous leg ulcers when used in addition to best management treatment.

The study included 160 patients with venous ulcers and chronic venous insufficiency (CVI). One group received 675 mg/day of oral gotu kola extract (standardised to 35% total triterpenes) along with best management (BM) practices (compression, elevation, wound cleaning), while a control group received only BM.

The results demonstrated a significant improvement in the herbal group:
• Ulcer Closure Rate: 96.2% of ulcers in the gotu kola group achieved complete closure after 90 days, compared to 83.7% in the control group.
• Faster Healing: after just one month, 65% of ulcers in the gotu kola group were completely healed, versus only 18.75% in the control group.
• Reduced Ulcer Area: the average ulcer area in the gotu kola group decreased dramatically (from 2.34 cm² to 0.33 cm²), a significantly greater reduction than that observed in the control group (from 2.4 cm² to 1.61 cm²).
• Improved Microcirculation: the herbal group showed enhanced microcirculatory parameters, including improved skin resting flux and transcutaneous oxygen/carbon dioxide partial pressures, indicating better blood flow and tissue oxygenation.

Gotu kola remains our leading herb for tissue repair and microvascular support, and this trial further vindicates its clinical value. Notably, the dose used was high, but still realistic and achievable in practice. The benefits observed in this venous ulcer study are well explained by its established pharmacology. The triterpenes asiaticoside and madecassoside improve microcirculation and venous tone, helping reduce venous hypertension and local tissue hypoxia—central drivers of ulcer chronicity. At the same time, the herb promotes healing through enhanced fibroblast activity, collagen synthesis, and extracellular matrix repair, accelerating granulation and re-epithelialisation. Its anti-inflammatory effects temper chronic wound inflammation, while modulation of transforming growth factor beta (TGF-β) and vascular endothelial growth factor (VEGF) signalling supports angiogenesis and tissue remodelling.

For more information see: https://pubmed.ncbi.nlm.nih.gov/40719428/

02/01/2026

Psyllium husk can work wonderfully for some people, but for others, it can actually make constipation worse. Psyllium requires a lot of water, so if you aren't drinking big glasses of water every time you take a dose of psyllium, it can significantly slow gut motility.

My go-to is ground flaxseeds for all the reasons mentioned above. And I think chia seeds can be helpful too, especially if they are ground. Grinding chia ensures you get all the protein and omega-3 fats.

Ideally, use certified organic flax, and grind it yourself to ensure it's fresh and not rancid at the point of consumption.

If you prefer psyllium, please take it with a large glass of water. The dose that seems to work best for psyllium is 10-20 grams daily for at least 8 weeks.

02/01/2026

Great information about choosing the best salmon.

12/12/2025

https://youtu.be/10enqcw2Qiw

MTHFR, methylation, COMT, homocystene, CYP1A2, HbA1c, Insulin, are or test to establish a persons ability to maintain optimal health. Unfortunately, they’re not all available on Medicare and so people are not aware of them. But these are the tests I do in Clinic for my clients who want them.
This video interview explains why these tests are so valuable.

Gary Brecka is the co-founder of 10X Health System and is one of the world’s leading experts in human biology and biohacking. He has worked with CEOs, models...

29/10/2025

Simple self foot massage is to press your thumbs over each area of the sole of your foot. Massage gently over any sore spots until the tension is released.

02/09/2025