Revive Your Health Naturopathic

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

20/04/2026

Interesting new research into the reason for the increase in autism. In my view, it’s never one thing, it’s a combination, but this research does give reason to question the safety of medication during pregnancy, and beyond.

“These sterol biosynthesis–inhibiting medications (SBIMs) include certain antidepressants, antipsychotics, anxiolytics, beta-blockers and statins. These are the generic names of the 14 medications studied: aripiprazole, atorvastatin, bupropion, buspirone, fluoxetine, haloperidol, metoprolol, nebivolol, pravastatin, propranolol, rosuvastatin, sertraline, simvastatin and trazodone. Many of these are among the most commonly prescribed medications in the United States, accounting for more than 400 million annual prescriptions.

Key findings include:

Mothers prescribed at least one SBIM during pregnancy had a 1.47-fold higher risk of having a child diagnosed with ASD. Risk increased in a dose-dependent manner. For each additional SBIM co-prescribed, there was a 1.33 times increased risk of ASD, reaching 2.33-fold risk when four or more SBIMs were prescribed simultaneously.
Among the 196,447 children diagnosed with ASD in the cohort, 14.2% had prenatal SBIM exposure.
Use of SBIMs during pregnancy increased sharply over time, rising from 4.3% of pregnancies in 2014 to 16.8% in 2023.”

A landmark study led by researchers at the University of Nebraska Medical Center (UNMC) and published in Molecular Psychiatry has identified a significant association between prenatal prescription of commonly utilized medications and the risk of autism spectrum disorder (ASD) in children.

08/04/2026

An article in The Age today about sleeping positions. I talk with patients about this all the time. We spend hours in bed - it is essential to be supporting our hips and spine, not stressing them. Come in for a massage and discuss your sleeping habits and revive your sleep! Book Now at www.reviveyourhealth.com.au

“Sleeping on top of a memory foam or gel mattress pad can help by distributing your weight more evenly, he says. Placing a pillow between your knees can also reduce hip, knee and lower back pain by keeping your legs and hips aligned.”

“Strategic placement of pillows, special cushions or devices can help keep you in one position throughout the night, Gurubhagavatula says. To stay on your side, try placing a body pillow behind you, she suggests. There are also cushions that strap onto your back to keep you on your side, and electronic devices that vibrate when they sense that you’ve rolled onto your back. They’re the technological equivalent of getting elbowed by your bed partner, Yadollahi says.”

https://www.theage.com.au/lifestyle/health-and-wellness/the-sleeping-position-that-might-be-to-blame-for-your-back-pain-20260407-p5zltr.html

There is no “right” way to sleep, but some positions may cause more discomfort.

04/04/2026

Epstein-Barr virus is the background villain to many later in life diseases. Whilst it is not a definitive pathway, if you know or can see from doing blood treats that you have had EBV, it is worth doing ongoing work to support your immune response and keep inflammation at bay. This involves maintains good gut health, some supplements and being aware of symptoms in order to fend off issues. You may not be able to avoid getting auto immune diseases, but it is possible to reduce the impact. Please see me in clinic to discuss further. www.reviveyourhealth.com.au and click on “Book Now”.

Scientists may have finally found the trigger behind virtually every case of lupus.

For centuries, lupus has remained a "cruel mystery," but researchers at Stanford University may have finally identified its primary trigger.

A landmark study suggests that the Epstein-Barr virus (EBV)—the common pathogen responsible for mononucleosis—underlies nearly every case of the chronic autoimmune disease. Using advanced sequencing techniques, scientists discovered that EBV directly infects and reprograms B cells, flipping a biological "switch" that turns these immune cells into pro-inflammatory agents. In lupus patients, the concentration of these infected cells is 25 times higher than in healthy individuals, causing the immune system to mistakenly attack the body's own healthy tissues.

This discovery provides a long-awaited mechanistic explanation for why lupus symptoms flare and settle in unpredictable cycles. Beyond lupus, the findings offer a roadmap for understanding other autoimmune disorders linked to EBV, such as multiple sclerosis and long COVID. By pinpointing how the virus hijacks the immune system's memory cells, researchers can now focus on targeted therapies that hunt down and replace these faulty B cells. Lead researcher William Robinson describes the finding as the most impactful of his career, signaling a major shift from merely managing symptoms to potentially addressing the underlying viral cause of the disease.

source: Cassella, C. (2025). Scientists Trace Lupus to One of The World's Most Common Viruses. ScienceAlert. Original research: Younis, S., et al. (2025). Science Translational Medicine.

02/04/2026

Great reference on using collagen with vitamin C to stabilise collagen. I am very particular about the forms of collagen that I prescribe to patients, and will often co-prescribe vitamin C and zinc, as they are easy to take in combination, and vitamin C gives a good flavor. Please see me in clinic to discuss your joint support needs. Book online at www.reviveyourhealth.com.au

Your body makes collagen constantly. But the version it assembles first isn't finished. Before collagen can hold its shape, an enzyme has to modify specific amino acids in the chain. That enzyme needs vitamin C to work.

Here's what vitamin C actually does: it enables the chemical modification (hydroxylation) that allows three collagen chains to lock together into a stable triple helix. Without that modification, the collagen structure is so weak it falls apart below body temperature. Literally. Unhydroxylated collagen melts at about 24°C. Your body runs at 37°C. The only thing keeping your collagen intact at body temperature is the modification that vitamin C makes possible.

This is why scurvy causes bleeding gums, loose teeth, poor wound healing, and joint pain. Your body is still making collagen. It just can't hold together.

Vitamin C isn't recycled in this process. It's consumed each time. Your supply has to be continuously replenished.

Most collagen supplement studies co-administer vitamin C. The ones that don't rarely account for baseline vitamin C status. If you're taking collagen without adequate C, you're supplying the raw material without the tool that finishes it.

Sources: Peterkofsky, Am J Clin Nutr, 1991. Shoulders & Raines, Annu Rev Biochem, 2009.

25/03/2026

This study shows that getting UTI’s or having poor dental health, particularly in older age, may have correlation with developing dementia. The key here would be prevention and staying on to of arising infection. Staying well hydrated, brushing and flossing teeth are good starting points, alongside considering ongoing nutrient and herbal support, to support the body’s ability to fend off infection. Please see me in clinic to discuss further. www.reviveyourhealth.com.au and click on “Book Now”.

Severe cystitis, pneumonia or tooth decay could increase your risk of developing dementia over the next five to six years.

11/03/2026

I saw this and instantly thought “magnesium deficiency”. Did you know that other signs of low magnesium can be chocolate cravings, cramps in the feet or legs, and twitching in back of hand or eyebrow. And then there’s stress.. There are even specific indications in the tongue and iris. You can’t test for low magnesium using a blood test, as less than 1% of the body’s magnesium is in the blood. For help with discerning low magnesium, and prescribing appropriate high quality magnesium, please see me in clinic. www.reviveyourhealth.com.au and click on “Book Now”.