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At McKesson IdeaShare 2025, Lara Zakaria, PharmD, MS, CNS, CDN, IFMCP, delivered a compelling presentation calling for a reimagining of pharmacists’ role in patient nutrition. As the founder of Foodie Farmacist, LLC, and the creator of the concept of pharmaconutrition, Zakaria advocates for a future where pharmacists are recognized as trusted nutrition experts in their communities.¹

“I want to make this a thing,” she said. “I want this to be the way that we are thought of in our communities, that we are that pharmacy team that makes sure that we talk about nutrition at every opportunity that we can.”¹

Zakaria emphasized how food and nutrition have become moralized, affecting societal perceptions of body size and obesity. She pointed to the limitations of body mass index (BMI) as a health metric, noting it fails to reflect the quality of body composition.¹

“Under-nutrition is just as dangerous as over-nutrition, and that’s something we need to pay attention to,” she said, citing data showing mortality risks at both low and high BMI ranges.²

Rethinking Diet Quality and the Role of Ultra-Processed Foods

Ultra-processed foods (UPFs) were another focus of the presentation. Zakaria referenced a narrative review published in Nutrients that found no studies linking UPFs to health benefits but considerable evidence linking them to adverse outcomes such as obesity, cardiovascular disease, and cancer.³ With their heavily altered ingredients, UPFs complicate traditional calorie-based thinking.

“There’s a whole spectrum of connections between the increase of UPF in our diet and this increased risk, so we can no longer really afford to just look at this as a ‘calories in, calories out’ problem,” she explained. “We have to start thinking about this in a more nuanced way, and we have to start thinking about quality [of food] as well.”

Zakaria encouraged pharmacists to use patient interactions to “plant some seeds” about nutrition, tying advice to each patient’s broader health goals. For instance, the Mediterranean diet can reduce cardiovascular risk and improve metabolic and inflammatory markers. Drawing from the PREDIMED study, she cited a 30% risk reduction in cardiovascular disease⁴ and emphasized the role of phytonutrients, polyphenols, and the cultural aspects of food.

“There’s something to be said about how we eat and how it affects how we view our food, and it might be part of why the Mediterranean diet is so effective.”¹

Addressing Nutrient Depletion, Drug Interactions, and Gut Health

Zakaria highlighted the importance of macronutrients, micronutrients, and phytonutrients—natural compounds found in foods that influence microbiome function and gene expression. Most people, she noted, are deficient in several key minerals, especially potassium. She also added that there has been an overwhelming number of conflicting headlines about macronutrients, leaving patients confused about whether to consume carbohydrates and fats.¹

Biological and external factors also influence nutritional status. Chronic disease, strenuous physical activity, genetic variations, and environmental exposures all affect nutrient absorption and metabolism. Drug-induced nutrient depletions (DIND), however, are a key concern. Many medications can directly or indirectly impair how the body absorbs or utilizes nutrients. Patients often report symptoms to their physician and start a medication, which eventually leads to different symptoms as a result of depletion. Introducing DIND and nutrition earlier in that conversation can stop this cascade.¹

She also described the stages of nutritional deficiency, noting the importance of early detection before permanent damage occurs. Common drug culprits include proton pump inhibitors, statins, metformin, estrogens, angiotensin-converting enzyme inhibitors, and even caffeine and alcohol.¹

“What we want to do is try to catch those deficiencies as early as possible, before they get to the point where they impair metabolism or cause damage.”¹

Zakaria concluded with some simple food-as-medicine interventions that support gut health and immune function, noting that addressing nutritional issues does not have to be overwhelming for patients. Ingredients like ginger, fennel, turmeric, aloe vera, and epigallocatechin gallate (found in green tea) were highlighted for their anti-inflammatory and digestive benefits and can be easy to incorporate into patients’ diets.¹

With pharmaconutrition, Zakaria hopes to lead a movement that empowers pharmacists to guide patients toward better health, 1 conversation at a time.¹

Starting With the Foundations: Practical Steps for Patient Engagement

To put pharmaconutrition into practice, Zakaria advised pharmacists to start with foundational strategies. The Mediterranean diet can be an accessible and enjoyable starting point—it’s familiar to many patients, doesn’t require excessive counting or measuring, and is widely supported by evidence.¹

Simple lifestyle modifications can also go a long way. Zakaria recommended encouraging patients to take a 20-minute walk after dinner, incorporate movement throughout the day, and engage in basic exercise. Assessing sleep quality and ruling out sleep apnea is another key step in supporting overall health.¹

Finally, pharmacists should guide patients in reducing alcohol and caffeine consumption and support tobacco cessation. These basic yet powerful changes, she emphasized, can have significant ripple effects on patient outcomes and well-being.¹

REFERENCES

1. Zakaria L. The Nutrition Games: A Tribute to Nutrient and Medication Collaboration. Presented at: McKesson IdeaShare 2025. Nashville, TN; July 10, 2025.

2. Visaria A, Setoguchi S. Body mass index and all-cause mortality in a 21st century US population: a national health interview survey analysis. PLoS One. 2023;18(7):e0287218. doi:10.1371/journal.pone.0287218

3. Elizabeth L, Machado P, Zinöcker M, Baker P, Lawrence M. Ultra-processed foods and health outcomes: a narrative review. Nutrients. 2020;12(7):1955. doi:10.3390/nu12071955

4. Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet supplemented with extra-virgin olive oil or nuts. N Engl J Med. 2018;378:e34. doi:10.1056/NEJMoa1800389

July 10, 2025 — A study led by scientists at King’s College London has revealed how the physical orientation of the heart inside the chest dramatically influences the electrical signals captured in an electrocardiogram (ECG) — a discovery that could pave the way for more personalized and accurate heart diagnostics. 

With data from more than 39,000 participants from the UK Biobank, this is one of the largest population-based studies to date exploring the relationship between heart anatomy and electrical activity. By combining 3D heart imaging with ECG data, the team created simplified digital twins of each participant’s heart. These personalized models allowed researchers to explore how the heart’s anatomical position, known as the anatomical axis, aligns with a spatial metric of electrical activity, or electrical axis.  

Digital twins are emerging as a powerful tool in cardiovascular research, enabling scientists to simulate and study the heart’s structure and function in unprecedented detail. In this study, they were key to revealing how natural variations in heart orientation, shaped by factors such as body mass index (BMI), sex, and hypertension, can significantly influence ECG readings. 

The researchers proposed new, standardized definitions for both anatomical and electrical axes based on their alignment in 3D space. They found that people with higher BMI or high blood pressure tend to have hearts that sit more horizontally in the chest, and that this shift is mirrored in their ECG signals. The study also revealed clear differences between men and women: male hearts were generally more horizontally oriented than female hearts, a structural difference that was reflected in their surface electrical activity. These sex-based variations highlight the need for more tailored approaches to ECG interpretation. 

By identifying and quantifying this variability across a large population, the study highlights the importance of distinguishing between normal anatomical differences and early signs of disease. This could help clinicians detect conditions such as hypertension, conduction abnormalities, or early heart muscle changes sooner and more precisely – especially in patients whose heart orientation deviates from standard assumptions. 

The findings point to a future where ECGs are no longer interpreted using a one-size-fits-all approach, but instead tailored to each patient’s unique anatomy. This personalized perspective could reduce misdiagnoses and support earlier, more targeted interventions. 

Mohammad Kayyali, lead author and PhD student at the King’s School of Biomedical Engineering & Imaging Sciences, said: “Large-scale biomedical resources like the UK Biobank are paving the way for patient-centric disease characterization by enabling detailed analysis of anatomical and electrophysiological variability across the population. This work demonstrated differences in cardiac axes among healthy and diseased individuals, highlighting the potential to enhance digital twin personalization and improve disease prediction and characterization, ultimately supporting more tailored clinical care.” 

Professor Pablo Lamata, report author and professor of biomedical engineering at King’s, said: “The ability to build personalized models (i.e. digital twins) of the cardiovascular system is an exciting research area, where we hope to find new parameters that can better inform about prevention, diagnosis and risks of cardiovascular diseases. In this work, we start to explore these uncharted waters, and we hope we will soon propose new ways to early detect conditions such as electrical conduction disorders.”

Results from a recently published, 52-week, phase 2, double-blind, placebo-controlled study showed that ambroxol, a chaperone for β-glucocerebrosidase, was safe in patients with Parkinson disease dementia (PDD); however, its effects on cognition were not confirmed. Positive data revealed stabilization of neuropsychiatric symptoms and plasma glial fibrillary acidic protein (GFAP) levels, a marker of neurodegeneration.¹

After excluding the low-dose group due to recruitment challenges, the study featured a cohort of patients with PDD who were randomly assigned 1:1 to either high-dose ambroxol at 1050 mg (n = 22) or placebo (n = 24) for a 52-week period, with an additional 26-week open-label extension. All told, change in Alzheimer Disease Assessment Scale–cognitive subscale 13 (ADAS-Cog13) and Clinician Global Impression of Change (CGIC), the study’s primary outcomes, were not different between the groups at week 26 or week 52.

In the study, investigators observed no statistical between-group differences on secondary outcomes as well, which included Clinical Dementia Rating Scale, Parkinson’s Disease Cognitive Rating Scale, Trail Making Test, and Stroop test, among many others. The study authors did observe a trend in total Neuropsychiatry Inventory (NPI) score (t = –1.86; P = .07), where the placebo group worsened from baseline to week 52 while those in the ambroxol group remained stable. NPI score among GBA1 carriers revealed that 2 patients taking placebo changed by 0 and +10 points, whereas patients taking high-dose ambroxol showed score reductions of –1, –8, –12, and –15 points at week 52.

Led by senior author Stephen H. Pasternak, MD, PhD, the study aimed at testing the safety and tolerability of ambroxol, as well as its effects in slowing the progression of cognitive deficits in PDD. Ambroxol, an over-the-counter expectorant with documented safety profile, has been identified as a high throughput screen as a pharmacological chaperone of GCase and an inhibitor that binds and increases levels of GCase, while dissociating from GCase in the acidic environment of the lysosome. Prior to this study, ambroxol has shown an ability to increase GCase and reduce alpha-synuclein in mice and nonhuman primate brains.

Ambroxol was shown to be safe in patients with PDD, as those on the drug had a similar rate of adverse events (AEs) than those in the placebo group. Overall, 8 patients on ambroxol (2 low-dose; 6 high-dose) and 3 patients taking placebo (12.5%) withdrew because of AEs. There were 7 hospitalizations, considered a serious AE, found in the ambroxol group. These included one patient on low-dose admitted twice for delirium, and other participants admitted to urinary tract infection (low-dose), worsening hallucinations and recurrent falls (high dose), infection after elective surgery (low dose), rigidity and worsening hallucinations (high dose), and severe leg weakness (high dose).

READ MORE: FDA Approves Updated Label for Alzheimer Therapy Donanemab to Lower ARIA-E Risk

For gastrointestinal disorders, 12% of ambroxol-patients reported these vs 5% of those taking placebo. In addition, there were more psychiatric AEs in the placebo group (23%) compared with the ambroxol group (16.6%), as well as more injuries/falls (29.7% vs 22.8%).

The plasma biomarker analysis comprised 15 patients on high dose ambroxol and 20 on placebo, all who had baseline and week 52 samples. When excluding those who had a clinically significant AE or were not taking treatment within 1 month of the end of trial (6 taking ambroxol and 3 taking placebo excluded), the placebo group demonstrated an increase in GFAP from baseline over the 52 weeks (mean: 135.07 pg/mL to 167.90 pg/mL) whereas those on ambroxol high dose did not (mean: 127.95 pg/mL to 118.05 pg/mL).

At week 26, GCase levels were significantly higher in the ambroxol group vs placebo (12.45 ± 1.97 vs 8.50 ± 1.96 nmol/h/mg; 91% CI, 11.54–13.36 vs 7.65–9.34; P = .05), and remained elevated but not statistically different at week 52 (11.45 ± 1.59 vs 8.59 ± 1.56 nmol/h/mg; 95% CI, 10.61–12.28 vs 7.86–9.31). Considerable inter-patient variability was observed, including at baseline.

“In conclusion, results of this randomized clinical trial reveal that ambroxol was deemed safe and well tolerated in PDD. Sufficient drug levels were achieved, and target engagement was demonstrated based on increased white blood cell GCase activity levels,” Pasternak et al wrote. “Future studies should attempt to reduce the heterogeneity in study population, focus on recruiting more GBA1 carriers, and assess GFAP as a potential biomarker to be used in PD clinical trials.”

REFERENCE
1. Silveira CRA, Coleman KKL, Borron K, et al. Ambroxol as a treatment for Parkinson disease dementia: a randomized clinical trial. JAMA Neurol. Published online June 30, 2025. doi:10.1001/jamaneurol.2025.1687

July 10 (UPI) — They say age is all in your mind — and that might literally be true, a new study reveals.

People with “young” brains — brains aging more slowly than their actual age — are much less likely to die or develop Alzheimer’s disease than those with “old” brains suffering from accelerated aging, researchers reported Wednesday in the journal Nature Medicine.

Results show that having an extremely aged brain nearly triples a person’s risk of dying during a roughly 15-year period.

At the same time, people with extremely youthful brains had a 40% lower risk of early death, researchers found.

In other words, the biological age of the brain plays an outsized role in determining how long a person has left to live, said senior researcher Tony Wyss-Coray, director of the Knight Initiative for Brain Resilience at Stanford Medicine.

“The brain is the gatekeeper of longevity,” he said. “If you’ve got an old brain, you have an increased likelihood of mortality. If you’ve got a young brain, you’re probably going to live longer.”

Previous research has shown that a person’s body can age from wear-and-tear more rapidly that what is reflected by their birth date. Essentially, a person’s biological age can be older than their calendar age.

For this study, researchers analyzed blood samples from nearly 44,500 people 40 to 70 participating in the UK Biobank, a large-scale health research project in the United Kingdom.

Researchers used proteins found in the blood samples to estimate the biological age of 11 distinct organs or organ systems for each person, including the brain.

About 6% to 7% of participants had “extremely youthful” brains, and a similar proportion had “extremely aged” brains.

Overall, researchers found that any organ’s biological age increased its likelihood of disease.

For example, an extremely aged heart increased risk of abnormal heart rhythm or heart failure, and aged lungs increased COPD risk.

But the association between an aged brain and Alzheimer’s was particularly powerful – more than three times that of a person with a normally aging brain, researchers said.

On the other hand, people with youthful brains had a quarter of the Alzheimer’s risk linked to brains that were aging normally, the study found.

In other words, someone with a biologically old brain is about 12 times as likely to be diagnosed with Alzheimer’s as a person the same age with a biologically young brain, researchers concluded.

These results could open the door to new medical screenings that could determine people’s risk for various diseases based on the biological age of their organs, Wyss-Coray said.

Future research also could figure out whether existing approved drugs might restore organ youth before people develop a disease based on that aging organ, he added.

“This is, ideally, the future of medicine,” Wyss-Coray said. “Today, you go to the doctor because something aches, and they take a look to see what’s broken. We’re trying to shift from sick care to health care and intervene before people get organ-specific disease.”

Wyss-Coray plans to commercialize the blood sample test, working with companies to get it on the market within a few years.

“The cost will come down as we focus on fewer key organs, such as the brain, heart and immune system, to get more resolution and stronger links to specific diseases,” he said.

More information

The Mayo Clinic has more on biological versus chronological age.

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A recent study found no significant difference in dementia incidence over a 20-year follow-up among individuals who had or did not have a transient ischemic attack.¹

“Our findings challenge our initial hypothesis and diverge from certain existing literature studies that have proposed persistent cognitive decline following [transient ischemic attack],” wrote investigators, led by Vasileios‐Arsenios Lioutas, MD, from the department of neurology at Beth Israel Deaconess Medical Center, Harvard Medical School. “It is noteworthy, however, that other studies suggest cognitive impairment after [transient ischemic attack] is a transient phenomenon, potentially part of an acute confusional state or delirium.”

According to the Cleveland Clinic, multi-infarct dementia results from a series of small strokes—transient ischemic attacks.² Transient ischemic attacks and strokes share symptoms, but the former may be milder. Risk factors for multi-infarct dementia include hypertension, diabetes, conditions that can cause blood clots (atherosclerosis, coronary heart disease, heart valve disease, and carotid artery disease), hyperlipidemia, and smoking.

Despite existing data, the link between transient ischemic attack and dementia is still under-characterized. Investigators aimed to determine the long-term incidence of dementia following a transient ischemic attack and whether the attack prompts changes in vascular risk factors. The primary outcome was the 20-year incidence of all-cause dementia.

The team recruited participants from a nested, matched, longitudinal cohort study within the community-based Framingham Heart Study. Participants without dementia or transient ischemic attack (n = 1485) were matched 5:1 by age and sex to 297 participants with first incident transient ischemic attack at > 60 years. The arm with incident transient ischemic attack had a sample of 47% men and a mean age of 72.7 ±7.7 years. Participants with transient ischemic attack were more likely to have hypertension (78% vs 67%; P = .0006), coronary heart disease (37% vs 7%; P = .018), and atrial fibrillation (11% vs 7%; P = .018).

Over a follow-up of 8.9 years, 19% and 24% of patients with and without transient ischemic attack, respectively, developed dementia (hazard ratio [HR], 0.93; 95% confidence interval [CI], 0.71 – 1.24; P = .063). The association remained after adjusting for strokes and the competing risk of death. Once the team removed case-control sets with interim stroke, 25% and 24% of participants with and without transient ischemic attack, respectively, developed dementia (HR, 1.17; 95% CI, 0.78 – 1.73; P = .448).

“It is still unclear whether this represents a true lack of association between [transient ischemic attack] and cognitive decline or a true but relatively small risk exists but can be mitigated by early initiation and consistent adherence with secondary prevention,” the team wrote.

The analysis showed that participants with transient ischemic attack were more likely to have a reduction in the frequency of smoking (18% to 11%; P = .025), an increase in anticoagulant use (3% to 18%; P = .0005), and a slight increase in aspirin use (46% to 61%; P = .052).

Furthermore, participants who started anticoagulation after transient ischemic attack had a greater likelihood of developing dementia (HR, 4.71; 95% CI, 1.89 – 11.71; P < .001). This was observed after adjusting for atrial fibrillation (HR, 4.01; 95% CI, 1.57–10.20; P = .0005).

No participants in either arm experienced changes in their mean SBP or had high systolic SBP (SBP > 149 mm Hg).

“Prospective studies with well‐matched controls, active cognitive surveillance, and sufficiently long follow‐up are necessary to better characterize the cognitive repercussions of [transient ischemic attack] and the impact of secondary stroke prevention in cognitive health,” investigators wrote.

References

1. Lioutas VA, Peloso G, Romero JR, et al. Long-Term Incidence of Dementia Following Transient Ischemic Attack: A Longitudinal Cohort Study. J Am Heart Assoc. Published online July 3, 2025. doi:10.1161/JAHA.124.037817

2. Multi-Infarct Dementia. Cleveland Clinic. July 10, 2025. https://my.clevelandclinic.org/health/diseases/6063-multi-infarct-dementia. Accessed July 10, 2025