Revive Your Health Naturopathic

15/06/2026

I regularly hear people saying they are putting magnesium oil on their feet, and they think this is enough to supply their magnesium needs. The science in this article should burst that bubble.. You cannot measure accurately how much mg is in the body through blood, as 98% of mg is in muscle and bone. So the only method to gauge levels is symptoms and reviewing dietary intake. Most diet gives us around 100mg. The RDI says we need 330mg/day. That’s to just function. To feel GOOD, you need around 500mg..
So just spraying a bit of magnesium oil on your feet is not enough. It’s the tip of the iceberg. You need to supplement, morning and night, and if you exercise heavily, maybe ore then as well. And I use magnesium cream sometimes, but not to up intake, but to target specific areas on the body which are resolutely tight or cramping, such as calves.
For help with getting good quality and quantity of magnesium every day, please see me in clinic. www.reviveyourhealth.com.au to book an appointment.

Walk into any wellness shop and you'll find magnesium sprays, oils, and bath flakes promising to fix a deficiency through your skin. The pitch is that you skip the gut entirely and absorb magnesium straight into the body. The biophysics says otherwise, and the reason is one of the most basic facts about how this particular ion behaves in water.

Magnesium in solution doesn't travel as a bare atom. It carries a tightly held shell of water molecules, and the hydrated ion is roughly 400 times wider than its dehydrated core. That is the largest hydration ratio of any common biological cation, far beyond sodium, potassium, or calcium. The reason is charge density: magnesium packs a double positive charge onto a small ionic radius, so it grips water harder than almost anything else moving through your tissues. To cross a fatty membrane, it would have to strip that shell off at a steep energy cost, which is why no cell in the body moves magnesium by simple diffusion. Every bit of it is shuttled through dedicated protein transporters built for the job.

Now look at what the spray has to get through. The outermost layer of skin, the stratum corneum, is 15 to 20 layers of dead, flattened cells with no nuclei and no functioning transporters, packed into a water-repellent matrix of ceramides, cholesterol, and fatty acids. This layer is engineered to keep the outside world out, and only fat-soluble molecules cross it in meaningful amounts. A hydrated divalent ion is the chemical opposite of fat-soluble. The only real openings are hair follicles and sweat glands, and those account for somewhere between 0.1 and 1 percent of your skin's surface area. A pore here and there is not a delivery system.

A 2017 review in Nutrients concluded that transdermal magnesium is scientifically unsupported. A 2009 Israeli double-blind trial of a magnesium lotion in 34 volunteers, designed in part to rule out dangerous absorption, found no significant change in serum magnesium. The follicle route has been imaged directly, but it moves only trace amounts through that tiny fraction of skin. The one cream pilot people cite was null for the group as a whole, reaching significance only in a small non-athlete subgroup.

None of this means magnesium is useless. It means the route matters. Oral magnesium is one of the best-documented mineral interventions there is. The skin is doing exactly what it evolved to do: keeping a large, highly charged, water-cloaked ion on the outside. If your magnesium is low, the fix goes through your mouth, not your pores.

Gröber et al., Nutrients, 2017. Eisenkraft et al., Magnes Res, 2009. Chandrasekaran et al., Magnes Res, 2016. Kass et al., PLOS One, 2017.

12/06/2026

So excited to be attending this full day Metabolic Health Summit today in Sydney! Brushing up on metabolic disease, weight loss, heart disease and longevity. More later as the flood of information grows.. Biomedica Nutraceuticals

12/06/2026

Frozen shoulder is a distressingly common issue, particularly in women post menopause. If your shoulders are tight, painful, you are having trouble reaching up, or putting on a tshirt, investigate this. Learning to manage this earlier will help to resolve it sooner. Please see me in clinic for a remedial massage, as well as discussion about anti inflammatory diet and supplements which may help. I will also help to find other therapists, such as myotherapists or osteopaths who may be able to further support this. Book with me at www.reviveyourhealth.com.au

https://www.huffingtonpost.co.uk/entry/frozen-shoulder-common-women_uk_6a2ad826e4b01046d71745e4?ncid_tag=fcbklnkukhpmg00000001&utm_medium=Social&utm_source=Facebook&utm_campaign=uk_main&d_id=12044091&fb_comment=1&fbclid=IwZnRzaASZXBtleHRuA2FlbQIxMQBzcnRjBmFwcF9pZAo2NjI4NTY4Mzc5AAEePaxmI2H1flsfGAsMNfBsO1hDADrr9c6UDNpYz92YPiqfdb-TizqY7Dq34oo_aem_eJ7wa3jqYG0E6U7SMHORJw

The condition is painful, limiting and often mistaken for normal wear and tear. Here's what you need to know.

10/06/2026

Creatine was always touted for its benefits to muscle building, but what is realised now is just how valuable it is for brain health. Taking creatine daily is a step to maintaining body and mind, and can be used to support cognitive stress, such as sleep deficit, by Dr Rhonda Patrick in this video. For good quality creatine, other supplements, and robust discussion on what you may need at your stage of health, please see me in clinic. www.reviveyourhealth.com.au to book an appointment.

06/06/2026

Love this guy’s research. This is a great piece on the benefit of eggs on our health. I still get people thinking eggs cause cholesterol so are scared to eat them. This urban myth is stopping people from enjoying the health benefits of eggs. If you can’t (or won’t) eat eggs (around 5 per week), I do stock choline in capsule form, which helps. But honestly, it’s easier, better and tastier to just eat eggs!

For 50 years, eggs were treated like a cardiovascular threat. The 1960s dietary guidelines capped cholesterol intake at 300mg per day. Two eggs put you at the limit. The advice moved millions away from the food, and away from a nutrient profile we didn't fully appreciate at the time.

A new study from Loma Linda University followed 39,498 adults age 65 and older for 15.3 years. The team linked Adventist Health Study-2 dietary records with Medicare diagnoses. Over that window, 2,858 participants developed Alzheimer's disease.

The dose-response was clean.
Eating eggs 1 to 3 times a month: 17% lower incidence vs never-eaters.
2 to 4 per week: 20% lower.

5 or more per week, roughly one a day: 27% lower.
The mechanism story isn't new, but the cohort scale and 15-year follow-up are. Eggs are the densest natural source of choline in the American diet. One large egg supplies roughly 33% of the daily choline requirement. Choline is the substrate for acetylcholine, the neurotransmitter that drops in Alzheimer's. Donepezil, the most prescribed Alzheimer's drug, works by blocking acetylcholine breakdown. The disease is partly defined by cholinergic neuron loss.

Egg yolk also delivers lutein and zeaxanthin. These are the only two carotenoids that cross the blood-brain barrier and accumulate in cortical tissue. Higher tissue levels track with better processing speed and memory across multiple older-adult cohorts. Yolk also contains DHA, primarily in phospholipid form. Phospholipid DHA enters the brain more efficiently than DHA in triglyceride form, which is the dominant form in fish oil capsules.

Now the caveats, because they matter.
This is observational. Causation cannot be drawn from a cohort study. The Adventist Health Study-2 cohort skews heavily vegetarian and health-conscious, so people who eat eggs in this cohort do not look like the average American egg-eater. The "never eats eggs" comparison group is largely vegan, which is its own dietary pattern with its own complications. Reverse causation also has to be considered. People in early Alzheimer's often change eating patterns before diagnosis. Some of the apparent protection could be that healthier brains keep eating eggs, not the other way around.

The mechanism story I outlined above is supported by adjacent literature, not by this paper. The study did not measure choline status, lutein levels, or DHA in tissue. It measured eggs in, dementia out.

What we can say honestly: in a 40,000-person cohort followed for 15 years, egg intake tracked with substantially lower Alzheimer's incidence in a dose-response pattern. The mechanism is biochemically plausible, supported by other lines of evidence, and consistent with what we know about acetylcholine and brain carotenoid status. The randomized trial that would prove causation has not been run.

The practical version: if you are over 50 and not allergic, eating an egg most days has stronger evidence behind it for brain health than most products marketed for the same goal. Five days a week was the dose with the lowest risk in this cohort. Even 1 to 3 per month showed measurable benefit.

For 50 years the question was whether eggs were dangerous to your heart. The data behind that fear was always weaker than the guidelines made it sound, which is why the 2015 Dietary Guidelines for Americans quietly removed the 300mg cap. The brain question got asked too late.

Oh et al., J Nutr, 2026 (DOI: 10.1016/j.tjnut.2026.101541)

31/05/2026

My website appears to be offline - I'll try to get it fixed soonest, but if you need to book in for an appointment with me, and can't do it via my website, please send me a text via your last confirmation text, or reach out here via Messenger, and I will get back to you! Eve x

14/05/2026

Fish oils are in the top three of supplements you should take every day. The problem is that most people buy a cheap form, which is low amounts of EPA / DHA, not ethically sourced, and poorly absorbed, for the reasons outlined in this fabulous article. The fish oils which I stock are 3.5 times more potent than most over the counter varieties, tested for heavy metals, and in the triglyceride form to allow for better absorption. All you have to do is take them with a little fat in your diet, and your essential fatty acids will improve significantly. Please see me in clinic for more.

Fish oil absorption ranges from 20% to 90% depending on two variables most people never check: the chemical form of the supplement and how much fat is in the meal you take it with.

Lawson and Hughes published two studies in 1988 (Biochemical and Biophysical Research Communications) that measured EPA and DHA absorption from fish oil in different forms and with different meals. The data is straightforward but almost nobody in the supplement industry talks about it clearly.

With a low-fat meal (8g of fat), EPA from ethyl ester fish oil was absorbed at roughly 20% relative to free fatty acid absorption. With a high-fat meal (44g of fat), absorption of both EPA and DHA from ethyl esters tripled to approximately 60%. Same capsule. Same dose. The only variable was the meal.

For triglyceride-form fish oil, the picture is different. EPA absorption was already 69% with a low-fat meal and improved to 90% with a high-fat meal. DHA absorption from triglycerides was not significantly affected by meal fat content. The triglyceride form works reasonably well regardless of what you eat with it.

The reason is biochemical. Ethyl esters lack a glycerol backbone. To be absorbed, they must be hydrolyzed by pancreatic lipase and then reassembled into triglycerides inside the enterocyte using a glycerol backbone from another dietary fat source. Without enough fat in the meal, there is not enough glycerol available and the process stalls. Triglycerides already have the backbone. They are hydrolyzed and reassembled more efficiently because the structure the body needs is already partially present.

This is not an obscure distinction. Most inexpensive fish oil supplements are ethyl esters. The concentration process that produces high-potency capsules (1,000mg EPA/DHA per softgel) typically converts the natural triglyceride form into ethyl esters. Unless the label specifically says "triglyceride," "TG," or "rTG" (re-esterified triglyceride), you are likely taking ethyl esters.

The Dyerberg et al. study (2010, Prostaglandins Leukotrienes and Essential Fatty Acids) confirmed the form hierarchy in 72 volunteers over two weeks: re-esterified triglycerides showed 124% bioavailability relative to natural fish oil. Ethyl esters showed 73%. Free fatty acids were roughly equivalent to natural triglycerides at 91%.

Two practical points.

First, check the form. If your label says triglyceride or rTG, you are getting better absorption and the meal matters less. If it says ethyl ester or does not specify the form at all, take it with a meal that contains meaningful fat. A few eggs, avocado, olive oil, nuts. Not a piece of toast.

Second, understand that many fish oil trials that reported no clinical benefit did not control for chemical form or meal fat content. Schuchardt and Hahn (2013, Prostaglandins Leukotrienes and Essential Fatty Acids) noted that bioavailability has been largely disregarded in omega-3 research, which may have contributed to neutral or negative trial results. It is difficult to demonstrate a clinical effect from a nutrient that was never adequately absorbed.

Lawson & Hughes, Biochem Biophys Res Commun, 1988
Dyerberg et al., Prostaglandins Leukot Essent Fatty Acids, 2010
Schuchardt & Hahn, Prostaglandins Leukot Essent Fatty Acids, 2013

13/05/2026

This story is a great example of why I always recommend getting a bone density scan earlier than the free one, offered far too late, at 70. Get a referral from your GP, pay the money and be aware of any potential risk when you are still able to make changes. I usually recommend a scan in your late 50’s. For help with bone health and other issues please see me in clinic.

Jane Alexander thought she was doing everything right.
The 62-year-old health writer had been attending Pilates classes regularly, the kind of low-impact exercise widely recommended for women her age. Then during one routine session, she felt it — a sudden, excruciating snap in her back.
She assumed it was a muscle strain.
It was not.
Medical examinations revealed Jane had suffered multiple spinal fractures. And the diagnosis behind those fractures stopped her cold: severe osteoporosis, so advanced that a standard Pilates movement had been enough to break her spine.
What made it worse was what came next.
Looking back at her medical history, Jane believes the warning signs had been there for years. Persistent back pain. Minor injuries that never quite made sense. Small things that were dismissed or overlooked during routine appointments.
She calls osteoporosis a silent disease — and she is right. It causes no symptoms until something breaks. By the time most people find out they have it, serious damage has already been done.
Jane is now speaking publicly about her experience because she does not want other women to go through what she went through. She wants them to ask the questions she wishes she had asked sooner. She wants doctors to listen when older women describe chronic pain that does not go away.
Bone density scans exist. Early intervention works. The disease is manageable when caught in time.
Jane Alexander broke her spine in a Pilates class at 62. She is turning that experience into a warning every woman over 50 needs to hear.
If something in your back has been bothering you for a while — ask your doctor about a bone density scan. Do not wait for a snap to tell you something was wrong all along.

06/05/2026

Mouth breathing harms the oral microbiome. It allows bacteria to thrive in the gums and oral tissue. And it depletes oxygenation to the heart. These things affect your energy, your healthy and your lifespan. Practice breathing through your nose constantly. If you don’t exercise this ability, it will stop working, but you can change it by being aware of breathing habits. See me to discuss further.

Nasal breathing raises arterial oxygenation about 10% compared to mouth breathing in healthy subjects. The mechanism involves nitric oxide produced continuously in the paranasal sinuses, inhaled with each nasal breath, that selectively dilates pulmonary vessels in well-ventilated alveoli. Mouth breathing bypasses the entire pathway.

This was characterized by Lundberg and colleagues at the Karolinska Institute in the 1990s, with the most direct measurement published in Acta Physiologica Scandinavica in 1996. The paranasal sinuses contain epithelium that constitutively expresses an isoform closely related to inducible nitric oxide synthase, which produces NO at high concentrations into the nasal airway. This NO production is continuous and is not significantly affected by glucocorticoids, unlike the inducible isoform expressed elsewhere in the body. With each nasal inhalation, this sinus-derived NO is carried into the lower airways and lungs.

In the lungs, NO is a potent local vasodilator. It selectively widens pulmonary vessels in alveoli that are well-ventilated, which improves the matching between ventilation and perfusion. Better V/Q matching means more of the inhaled oxygen gets transferred to blood, which raises arterial oxygenation. This is the same physiologic principle behind clinical inhaled NO therapy used in pulmonary hypertension and severe ARDS, except that the body produces and inhales its own low-dose NO continuously through nasal breathing.

The Lundberg 1996 study measured this in two groups. In 8 healthy adult subjects, transcutaneous oxygen tension was measured during alternating periods of nasal and oral breathing. Six of the 8 subjects showed approximately 10% higher tcPO₂ during nasal breathing compared to oral breathing. In a second experiment, 6 long-term intubated patients (who had been deprived of nasal NO because the ventilator bypassed their nose) had their own nasal air aspirated and routed back into the inhalation limb of the ventilator. All 6 patients showed increased arterial oxygenation when nasal NO was reintroduced. The mechanism is the same in both: NO from the sinuses, delivered to the lungs, improves V/Q matching and raises arterial oxygenation.

A few caveats. The original healthy subject study was small, with only 8 participants, of whom 6 showed the effect. The magnitude of 10% is from this small sample and the precise number varies between individuals. The intubated patient finding is more consistent (6 of 6) but represents a different physiologic state. The broader principle that nasal-derived NO contributes to pulmonary function is well-supported across the Lundberg group's work and subsequent literature, but a large-scale quantitative replication in healthy adults has not been the focus of follow-up research.
There are several practical implications. Chronic mouth breathing, whether from nasal obstruction, habit, or training (e.g., sleeping with an open mouth), bypasses the NO delivery pathway. The body still produces NO in the sinuses, but it doesn't reach the lungs. Whether this matters clinically depends on baseline pulmonary function and the duration of exposure. In healthy adults, the effect is small but measurable. In compromised respiratory states (high altitude, sleep apnea, intubation, exercise at altitude), the contribution of nasal-derived NO to oxygenation may matter more.

What this establishes. The body has a built-in NO delivery system from the paranasal sinuses to the lungs, active only during nasal breathing. The functional payoff is approximately 10% higher arterial oxygenation in healthy subjects. The mechanism is V/Q matching, the same principle as clinical inhaled NO therapy. Mouth breathing is not equivalent to nasal breathing at the level of pulmonary physiology, even with the same lungs and the same minute ventilation.

The practical lever is straightforward. Breathe through your nose when you can. Address chronic nasal obstruction if it's present. The mechanism your body is using to optimize gas exchange runs continuously when the nose is open and stops running when it isn't.

Lundberg et al., Acta Physiologica Scandinavica, 1996

26/04/2026

An overview of research to settle the krill vs fish oil debate. At low doses, krill oil offers more bio-availability, but if taking more than 2g of fish oil, the fish oil becomes better. For me, I always prescribe above 2g, as am looking for the anti-inflammatory and cholesterol lowering effects which this can support, so will always achieve better results with fish oil. And whilst I am a fan of astaxanthin for anti-ageing, I offer a collagen powder with this in it. For top quality high dose (750mg EPA, 250mg DHA) fish oil capsules, please see me in clinic.

Krill oil contains EPA and DHA bound primarily to phospholipids. Standard fish oil delivers EPA and DHA as triglycerides or, in concentrated products, as ethyl esters. The phospholipid-form difference is the basis of bioavailability claims that range from "two to three times more" to "eight times more" depending on the source. Per gram of EPA+DHA, krill oil typically retails for five to ten times more than standard fish oil.

The bioavailability claim has a specific origin. Bunea and colleagues published a study in 2004 (Alternative Medicine Review) comparing krill oil to menhaden fish oil in 120 patients with elevated cholesterol. The study measured lipid changes (total cholesterol, LDL, HDL, triglycerides), not EPA+DHA bioavailability directly. Krill produced larger reductions in lipid markers, and bioavailability claims drew on those results indirectly. The doses weren't matched. The krill arms received 1 to 3 grams per day. The fish oil arm received 3 grams. Lipid endpoints aren't a direct readout of how much EPA and DHA reached the bloodstream. Maki and colleagues (2009) ran a follow-up trial that compared 2 grams of krill oil to 2 grams of menhaden oil, but the products contained different EPA+DHA concentrations per gram, so the dose of the active compounds still wasn't matched.

When the dose was matched and plasma EPA+DHA was measured directly, the difference between forms was small.
Yurko-Mauro and colleagues (2015, Lipids in Health and Disease) ran a three-arm randomized trial in 66 healthy adults. Each arm received 1.3 grams per day of EPA+DHA for four weeks: krill oil, fish oil triglyceride form, or fish oil ethyl ester form. After four weeks, plasma EPA+DHA was 118 µg/mL on krill, 108 on fish oil triglyceride, and 91 on fish oil ethyl ester. The differences between the three groups were small enough that they could plausibly be chance. Bioavailability differed by less than 24% across all three forms. Red blood cell omega-3 indexes were comparable across all three. Four of the six authors of this trial are employees of DSM Nutritional Products, which is a major fish oil supplier.
Earlier work from Ulven and colleagues (2011, Lipids) reached a similar conclusion. They randomized 113 subjects to krill oil at 543 mg EPA+DHA per day, fish oil at 864 mg EPA+DHA per day, or no supplement. The krill arm received 63% of the EPA+DHA dose of the fish oil arm. Plasma EPA, DHA, and DPA increased equivalently in both groups. Krill produced parity with fish oil at a meaningfully lower dose, suggesting a real phospholipid-form advantage at lower dose ranges.

A 2024 network meta-analysis pooled 26 studies and found krill oil shows superior bioavailability overall, with one important caveat. At doses under 2,000 mg, krill outperforms fish oil on omega-3 absorption. Above that threshold, fish oil and krill oil reach comparable omega-3 indexes. Whether the low-dose pharmacokinetic edge translates into a difference in long-term cardiovascular or cognitive outcomes has not been demonstrated.
Krill oil also costs more to produce than fish oil. Antarctic krill comes from a remote, quota-limited fishery. The endogenous lipases in krill degrade the phospholipids quickly, so processing has to happen at sea or under tight cold chain. The gentler extraction methods needed to preserve phospholipid structure have lower throughput than standard fish oil refining. A production-cost premium of roughly two to three times standard fish oil is reasonable. The retail premium of five to ten times reflects positioning beyond production cost.

Two caveats. First, the Yurko-Mauro between-group difference was right at the edge of statistical significance, trends-level rather than firmly null. The matched-dose data does not formally prove equivalence. It shows a difference too small to reach significance with that sample size. Second, krill oil contains astaxanthin and choline, which fish oil generally does not. Whether those additional compounds confer independent benefit at the doses present in commercial krill products has not been established.

For someone targeting a specific omega-3 index at typical clinical doses (1.5 to 3 grams of EPA+DHA per day), the matched-dose evidence indicates that any well-formulated EPA+DHA source will get them there. For someone using lower doses (under 2 grams per day) and prioritizing pharmacokinetic uptake, krill has a defensible edge.

Yurko-Mauro et al., Lipids in Health and Disease, 2015
Ulven et al., Lipids, 2011
Pham et al., Food Chemistry: X, 2024
Bunea et al., Alternative Medicine Review, 2004