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A bespoke, science-led retreat for midlife renewal.

Combining nutrition, movement, and meaningful travel - guided by science, soul, and strategy. ๐ŸŒฟ

๐Ÿง  Can nutrition influence neurodegeneration, not just cognition?This new pilot study caught my attention.Not because I t...
09/10/2026

๐Ÿง  Can nutrition influence neurodegeneration, not just cognition?

This new pilot study caught my attention.

Not because I think we've discovered a new treatment for Alzheimer's disease. We haven't.

But because the researchers found something worth following. ๐Ÿ”ฌ

In a six-month randomised, double-blind, placebo-controlled trial, 54 older adults with cognitive impairment ranging from MCI to mild/moderate dementia received either placebo or a nutraceutical containing DHA (1,000 mg/day), Boswellia-derived compounds, beta-caryophyllene from clove and compounds from myrrh.

After six months, the intervention group showed improvements in MMSE and Clinical Dementia Rating compared with placebo.

Interesting.

But what really caught my attention was that two blood biomarkers associated with neurodegeneration, neurofilament light (NfL) and phosphorylated tau (p-tau), also decreased relative to placebo.

So could a nutritional intervention potentially influence the underlying biology as well as cognitive function? ๐Ÿงฌ

Possibly. But we're certainly not there yet.

This was a small pilot study. Only 54 people were randomised. The trial was retrospectively registered, there was an imbalance in polypharmacy between the groups, and we don't know which ingredient, if any, was responsible for the effect. The authors appropriately call for larger trials.

DHA already has a substantial research history in brain health, although supplementation trials have produced mixed results. Other nutritional interventions including B vitamins, Ginkgo, polyphenols and multinutrient formulations have also been investigated, again with variable evidence.

The botanical components here are fascinating too, particularly the proposed anti-inflammatory and neuroprotective actions of boswellic acids and beta-caryophyllene. But much of that mechanistic evidence remains preclinical. ๐ŸŒฟ

The supplement appeared well tolerated in this small study, but 27 treated participants is nowhere near enough to establish long-term safety.

So what would I like to see next? ๐Ÿ”Ž

A larger, prospectively registered and independently replicated trial. Longer follow-up. Better characterisation of Alzheimer's pathology. And ideally studies that help tease apart the contribution of DHA versus the botanical components.

Most importantly: does any improvement translate into slower cognitive and functional decline over years, rather than simply moving a test score or biomarker?

That's the outcome that matters. ๐ŸŽฏ

๐Ÿ”Ž ONE STEP TOWARD OPTIMAL

Don't rush out and buy the supplement. Do stay curious. Good pilot research gives us a reason to investigate, not a reason to prescribe.

Reference:
Trabace L, Morgese MG, Tucci P, et al. The impact of GeNeurofilโ„ข nutraceutical supplementation on psychometric assessment and biomarkers of neurodegeneration in cognitive impaired patients: a pilot study. European Journal of Clinical Nutrition. 2026;80:943โ€“948. doi:10.1038/s41430-026-01791-6.


Iโ€™m guest editing a Special Issue of Current Oncology on: ๐—ก๐˜‚๐˜๐—ฟ๐—ถ๐˜๐—ถ๐—ผ๐—ป๐—ฎ๐—น ๐—ฆ๐˜‚๐—ฝ๐—ฝ๐—ผ๐—ฟ๐˜ ๐—ถ๐—ป ๐—ข๐—ป๐—ฐ๐—ผ๐—น๐—ผ๐—ด๐˜†: ๐—˜๐˜ƒ๐—ถ๐—ฑ๐—ฒ๐—ป๐—ฐ๐—ฒ ๐—ฎ๐—ป๐—ฑ ๐—ฃ๐—ฟ๐—ฎ๐—ฐ๐˜๐—ถ๐—ฐ๐—ฒ One of ...
06/10/2026

Iโ€™m guest editing a Special Issue of Current Oncology on: ๐—ก๐˜‚๐˜๐—ฟ๐—ถ๐˜๐—ถ๐—ผ๐—ป๐—ฎ๐—น ๐—ฆ๐˜‚๐—ฝ๐—ฝ๐—ผ๐—ฟ๐˜ ๐—ถ๐—ป ๐—ข๐—ป๐—ฐ๐—ผ๐—น๐—ผ๐—ด๐˜†: ๐—˜๐˜ƒ๐—ถ๐—ฑ๐—ฒ๐—ป๐—ฐ๐—ฒ ๐—ฎ๐—ป๐—ฑ ๐—ฃ๐—ฟ๐—ฎ๐—ฐ๐˜๐—ถ๐—ฐ๐—ฒ

One of the things that continues to stand out in oncology nutrition is that the evidence base has advanced significantly, but implementation in real-world care is still highly variable.

We know nutrition influences treatment tolerance, recovery, body composition, survivorship outcomes, and quality of life.

The challenge now is translating that evidence into practical, scalable, and integrated models of care.

This Special Issue is focused on that intersection between evidence and implementation.

Weโ€™re welcoming submissions across areas, including:

โžก๏ธ oncology nutrition and malnutrition
โžก๏ธ cancer cachexia and metabolic changes
โžก๏ธ body composition and nutritional risk
โžก๏ธ nutrition interventions during and after treatment
โžก๏ธ survivorship and supportive care
โžก๏ธ implementation within oncology pathways

Original research, reviews, and short communications are all welcome.

If youโ€™re working in this space and considering submitting work, Iโ€™d be very pleased to hear from you.

Submissions are open until 31 December 2026.

๐Ÿ”— Details here: https://lnkd.in/gBEMSmZ2

Looking forward to seeing the next wave of work helping shape nutritional care in oncology.

Excited to be sharing the stage with multidisciplinary experts at   in Sydney this November.Iโ€™ll be discussing Nutrition...
02/10/2026

Excited to be sharing the stage with multidisciplinary experts at in Sydney this November.

Iโ€™ll be discussing Nutrition Conversations in Cancer Care: Navigating Complexity, Evidence, and Patient Perspectives - exploring how we can navigate the often confusing nutrition landscape, communicate what we know and donโ€™t know, and make nutrition advice meaningful for each patient.

Register at cosaasm.org.au/register and see you there! Clinical Oncology Society of Australia - COSA

1 October is the International Day of Older Persons. Healthy ageing isn't simply about living longer. It is about mainta...
01/10/2026

1 October is the International Day of Older Persons.

Healthy ageing isn't simply about living longer.

It is about maintaining the strength, function and independence that allow people to keep doing the things that matter to them.

๐Ÿ’ช Muscle health plays an important part in that.

As we age, changes in muscle strength, mass and physical function can increase the risk of falls, frailty, disability and loss of independence. But waiting until significant decline has occurred before we pay attention to muscle health may mean we've missed an opportunity to act earlier.

Nutrition has a role to play - but the answer isn't simply to tell older adults to eat more protein.

Maintaining muscle and function requires a broader approach: adequate nutrition alongside resistance exercise, physical activity and appropriate assessment.

And the evidence consistently shows that combined approaches can offer greater benefits than nutrition or exercise in isolation.

๐Ÿ”นSimple measures such as handgrip strength, chair stands and gait speed can provide useful information about changes in physical function and help identify people who may benefit from earlier assessment and support.

Increasingly, the focus is shifting from treating established sarcopenia towards promoting muscle health earlier in the ageing process - recognising changes in strength and function before they translate into falls, disability or loss of independence, while there is still meaningful opportunity to act.

This is something that connects directly to our research on nutrition and muscle health across ageing and chronic disease.

Healthy ageing isn't just about adding years to life.

It is also about preserving the capacity to live well in those years.

๐Ÿ”Ž ONE STEP TOWARD OPTIMAL

Do something this week that asks your muscles to work. Try a strength-training session, a few chair stands, or an activity that challenges your muscles safely. Small, consistent actions can help preserve the capacity to keep doing what matters to you.

Sarcopenia and frailty are often discussed together. But they aren't the same thing. Sarcopenia is a muscle condition, c...
29/09/2026

Sarcopenia and frailty are often discussed together.

But they aren't the same thing.

Sarcopenia is a muscle condition, characterised primarily by reduced muscle strength, with changes in muscle quantity or quality and physical performance also considered in assessment.

Frailty is broader. It reflects reduced physiological reserve and increased vulnerability to stressors, and can involve physical, nutritional, cognitive, psychological and social factors.

The two frequently overlap. But someone can have sarcopenia without being frail. And someone can be frail without meeting the criteria for sarcopenia.

Why does that distinction matter?

Because the distinction helps us choose the right assessment and tailor the intervention to the person.

For someone with sarcopenia, nutrition and resistance exercise may be central to addressing declining muscle health. For someone who is frail, these may still be important - but they are unlikely to address the whole picture. Comorbidities, polypharmacy, cognitive changes, social isolation and other factors may also need attention.

Both conditions can benefit from multimodal care. But understanding whether we're looking at a muscle problem, broader vulnerability, or both helps us think about what support is most appropriate for that person.

That distinction matters if we want nutrition and exercise interventions to be meaningful for the individual patient.

๐Ÿ”Ž ONE STEP TOWARD OPTIMAL

If strength or function is changing, don't assume it's simply โ€œgetting olderโ€. Consider whether a proper assessment could help identify what is contributing.

Clinical nutrition has a substantial evidence base. We have evidence showing that nutrition intervention can improve cli...
25/09/2026

Clinical nutrition has a substantial evidence base.

We have evidence showing that nutrition intervention can improve clinical outcomes. We know that malnutrition screening is valuable when it is followed by assessment and appropriate care. Nutrition is a core component of wound management, cancer care, aged care and rehabilitation.

The harder question is what happens when that evidence meets routine clinical practice.

A nutrition intervention may be well supported by research, but delivering it consistently depends on everything around the intervention: how care is organised, who is responsible for it, whether it fits within clinical workflows, what resources are available, and what is realistic for the patient.

These factors can determine whether evidence-based care is adopted, delivered as intended, followed up and sustained.

This is particularly visible in nutrition, where, in some areas, the evidence has advanced faster than the systems needed to deliver it consistently.

Implementation science offers a different set of questions.

๐Ÿ”น What are the barriers and enablers in this specific clinical context?
๐Ÿ”น Which strategies are most likely to support consistent delivery?
๐Ÿ”น How do we measure whether care is actually reaching the patients who need it?

This is something I think about a great deal in our research - because identifying which patients benefit from which nutrition interventions is only part of the challenge.

We also need to understand how to embed that knowledge into clinical practice so that evidence-based care can be delivered consistently, adapted to context, and sustained over time.

For me, that is an important part of where clinical nutrition needs to go next: translating the evidence we have into the care patients actually receive.

Knowing what the evidence says is important. But making it work in the real world is part of the science too.

๐Ÿ”Ž ONE STEP TOWARD OPTIMAL

Ask not only โ€œWhat does the evidence say?โ€ but โ€œWhat will help us actually deliver it?โ€


An interesting new study made me think about how quickly we attribute the benefits of fermented foods to their live micr...
22/09/2026

An interesting new study made me think about how quickly we attribute the benefits of fermented foods to their live microbes.

In this randomised crossover trial, 87 healthy adults consumed 100 g of sauerkraut every day for four weeks, first fresh or pasteurised, with a washout period between interventions.

Fresh sauerkraut contained live lactic acid bacteria. The pasteurised version had been heat-treated, with viable bacteria below the detection limit.
Yet both produced a small reduction in systolic blood pressure of around 1.5โ€“2.5 mmHg, with no significant difference between them.
Interestingly, neither produced appreciable overall improvements in inflammatory markers, glycaemic control or markers of gut barrier integrity in these healthy participants.

So what was responsible for the blood pressure effect? ๐Ÿงช

The authors discuss several possibilities, including organic acids, phenolic compounds and bioactive peptides. Fermentation can change a food and produce biologically active compounds that remain even when the microorganisms themselves are no longer alive.

This fits with the growing interest in postbiotics and the idea that beneficial microbial effects don't necessarily require us to consume live organisms.
But I also found myself wondering about a much simpler explanation.

What about the food itself? ๐Ÿฅฌ

Cabbage brings its own nutritional package, including fibre and potassium. Without an unfermented cabbage control, we can't determine how much of the effect came from fermentation, fermentation products or simply the underlying food.

And that's what I like about this study. It challenges an increasingly common assumption:
Fermented food โ†’ live bacteria โ†’ gut microbiome โ†’ health benefit.

Biology is rarely quite that tidy. ๐Ÿ”ฌ

Perhaps the better question isn't simply โ€œAre the bacteria alive?โ€ but:
What changed in the food during fermentation, what remains when the bacteria are gone, and which component is actually responsible for the effect?

๐Ÿ”Ž ONE STEP TOWARD OPTIMAL
Enjoy fermented foods if you like them, but don't forget the bigger picture. Variety, whole foods and the overall dietary pattern probably matter more than whether every mouthful contains live microbes.

Reference:
Schropp N, Bauer A, Stanislas V, Michels KB. Fermented foods and inflammation: a crossover intervention trial with fresh and pasteurized sauerkraut. European Journal of Clinical Nutrition. 2026;80:928โ€“935. doi:10.1038/s41430-026-01776-5.

When someone loses weight intentionally, how do we know whether the weight lost is the weight we actually wanted them to...
18/09/2026

When someone loses weight intentionally, how do we know whether the weight lost is the weight we actually wanted them to lose?

GLP-1 medications can produce substantial weight loss, and much of that loss comes from fat mass.

But some lean mass is also lost.

Recent evidence suggests that lean mass may account for approximately 25% of total weight lost, with some studies reporting higher proportions, around 40%.

Importantly, lean mass is not the same as skeletal muscle mass, and changes in muscle size do not necessarily translate directly into changes in muscle function.

So the number on the scales only tells us part of the story.

A recent review highlighted that, in certain clinical trials, participants receiving incretin-mimetic medications lost 10% or more of their muscle mass over 68โ€“72 weeks, a magnitude approximately equivalent to 20 years of age-related muscle loss.

This does not mean the medications accelerate ageing by 20 years. Rather, it highlights why muscle health deserves attention, particularly in older adults and people who already have lower muscle reserves or are at risk of sarcopenia.

As these treatments are used across increasingly diverse populations, we are still learning about their long-term effects on body composition and physical function.

This reinforces the importance of a multidisciplinary approach. Appropriate nutrition support, adequate protein intake, resistance exercise and monitoring of body composition and physical function all have a role in supporting patients throughout weight loss.

GLP-1 medications are powerful and effective tools.

The question isn't whether we should use them.

It's whether we're supporting patients well enough to ensure the weight they lose contributes to better health and function, not simply a lower number on the scales.

๐Ÿ”Ž ONE STEP TOWARD OPTIMAL

If you're losing weight with a GLP-1 medication, ask whether muscle health and physical function are being considered alongside the number on the scales.

For clinicians, how are you incorporating nutrition and resistance exercise into GLP-1 weight-management care? What barriers are you seeing in practice?

References

Karakasis P, et al. Effect of glucagon-like peptide-1 receptor agonists and co-agonists on body composition: Systematic review and network meta-analysis. Metabolism. 2025;164:156113. doi:10.1016/j.metabol.2024.156113.

Mechanick JI, et al. Strategies for minimizing muscle loss during use of incretin-mimetic drugs for treatment of obesity. Obesity Reviews. 2025. doi:10.1111/obr.13841.

Bridge to Brisbane 10K done! ๐Ÿƒโ€โ™€๏ธOne of the things I love most about events like this is seeing people from all walks of...
15/09/2026

Bridge to Brisbane 10K done! ๐Ÿƒโ€โ™€๏ธ

One of the things I love most about events like this is seeing people from all walks of life, all ages, shapes and fitness levels, just getting out there and giving it a go.

Itโ€™s such a great reminder that movement doesnโ€™t have to be about being the fastest or the fittest. Sometimes showing up, moving your body and enjoying the experience is more than enough. โค๏ธ

Malnutrition screening is now routine in many healthcare settings. So why do we still miss so much malnutrition? Screeni...
15/09/2026

Malnutrition screening is now routine in many healthcare settings.

So why do we still miss so much malnutrition?

Screening tools such as MUST, MST and NRS-2002 are designed to identify patients at nutritional risk. They are an important first step. But they are only the first step.

A positive screen is not a diagnosis. And identifying risk achieves very little if it doesn't reliably lead to what comes next.

The clinical pathway looks straightforward:

๐Ÿ”น Screen - identify those at risk
๐Ÿ”น Assess - understand severity, causes and contributing factors
๐Ÿ”น Diagnose - apply structured criteria to confirm malnutrition
๐Ÿ”น Intervene - deliver an individualised nutrition care plan
๐Ÿ”น Monitor - track response and adjust accordingly
In practice, the pathway can break down at any of these stages.

Positive screens are documented but not always acted on. Assessment may be delayed or not completed. Responsibility for nutrition care may be unclear across teams. Interventions may be started but never reviewed. And there may be no systematic feedback loop to determine whether patients are actually receiving the care they need.

The result is that malnutrition remains underdiagnosed and undertreated - not because we aren't screening, but because screening alone is not enough.

For the patient, being identified as โ€œat riskโ€ only matters if something happens next.

We have evidence-based approaches to identify and manage nutritional risk. The challenge is building clinical systems where identification of risk reliably translates into assessment, diagnosis, and timely, monitored care.

Because a screening tool that doesn't reliably trigger the next step is not solving the problem.

It is documenting it.

๐Ÿ”Ž ONE STEP TOWARD OPTIMAL

If someone is identified as being at nutritional risk, ask: what happens next?

This is an area I have been interested in throughout my research. In our work in residential aged care, we found that the Malnutrition Screening Tool (MST) could be useful for identifying residents at nutritional risk. Further work explored how screening and assessment methods can guide appropriate nutrition care.

These studies, undertaken with colleagues including Judith Bauer, Merrilyn Banks and Maree Ferguson, reinforced an important principle: screening is valuable, but it is only the beginning of the nutrition care pathway.

The challenge is ensuring that identifying risk leads to appropriate assessment, diagnosis, intervention and monitoring.

References: Isenring EA, Bauer JD, Banks M, Gaskill D. The Malnutrition Screening Tool is a useful tool for identifying malnutrition risk in residential aged care. Journal of Human Nutrition and Dietetics. 2009;22(6):545โ€“550. doi:10.1111/j.1365-277X.2009.01008.x.

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