Endocrine Wellness

03/12/2026

Listen, I know I share A LOT of Kerry Bone’s posts but he’s just so brilliant!!! And I don’t need to try to repeat research he has already done. So with that out of the way….I LOVE LOVE LOVE Rhodiola. 🥰. It is one of my favorite herbs of all time. And the more I learn about it, the more I love it! Quality and strength can make a world of difference when it comes to dosing and efficacy. I haven’t found a better source for Rhodiola than MediHerb. The Rhodiola & Ginseng is my “go to” support for stress, improved mood and resiliency. 💗💗💗

A group of US scientists conducted a randomised, double blind, crossover, placebo-controlled trial in resistance-trained adults (13 men, 14 women; n = 27 total) to examine the short-term dose-response effects of Rhodiola rosea on strength and cognition. Participants completed four 7-day scenarios separated by 7-day washouts: capsule-free control, placebo (1.5 g/day maltodextrin), low-dose Rhodiola extract (200 mg/day), and high-dose Rhodiola extract (1500 mg/day). The extract was standardised to 3% salidroside and 1% rosavin (6 mg vs 45 mg salidroside/day). The final dose was administered 60 minutes before testing. Primary endpoints included bench press and leg press 1RM, set-3 repetitions to failure at 60% 1RM, Tendo-derived power, and Stroop executive function. Secondary outcomes included Wingate anaerobic performance, haemodynamics, perceived exertion and tolerability. 1RM, one-repetition maximum, is considered the gold standard for measuring maximal muscular strength.

Resistance outcomes favoured the lower dose in several key measures. The 200 mg/day condition significantly improved bench press 1RM, repetitions to failure, set-3 volume, and mean power, with moderate-to-large effect sizes. The 1500 mg/day dose improved leg press 1RM and peak power and also enhanced repetitions, but generally less consistently than the lower dose. Neither dose improved Wingate sprint performance, suggesting the ergogenic effect was more relevant to resistance-based fatigue tolerance than maximal anaerobic cycling output. Importantly, a clear linear dose–response pattern was not observed. In several outcomes, the lower dose performed as well as or better than the higher dose, suggesting a possible hormetic or non-linear response typical of adaptogenic agents rather than a simple “more is better” relationship.

Cognitive findings were robust. Both doses significantly improved Stroop Word, Colour, Colour-Word, and total scores compared with control, and both exceeded placebo on key contrasts. Improvements were statistically strong and consistent across sections, supporting enhanced executive processing under testing conditions. Again, no consistent superiority of the higher dose was demonstrated; in some Stroop domains, gains appeared comparable between doses.

Haemodynamic measures showed no meaningful or consistent changes in heart rate or blood pressure, and tolerability was good, with no serious adverse events reported.

Strengths of the study include its crossover structure, within-subject comparisons, standardised extract, and inclusion of two active doses. Limitations include small sample size, short intervention duration, absence of mechanistic biomarkers, and restriction to young, trained adults, limiting generalisability. Independent verification of extract composition was not performed. Clinically, the findings suggest that short-term supplementation with standardised Rhodiola rosea extract—particularly around 200 mg/day—may enhance resistance-training work capacity and executive function without cardiovascular concerns.

In terms of any s*x-specific effects, absolute strength was higher in males (as expected), but relative improvements with Rhodiola were comparable across s*xes. Moreover, the ergogenic and cognitive effects were not s*x-specific in this trained cohort.

The absence of a clear positive dose-response relationship strengthens the interpretation of Rhodiola as an adaptogen with a potentially optimal moderate dose rather than an agent exhibiting proportional dose-dependent gains.

For more information see: https://pubmed.ncbi.nlm.nih.gov/41374026/

03/12/2026

Here’s another thing to consider…a drug might give you one thing that you are looking for but also 20 unwanted effects. A herb might be taken for one specific purpose but then there’s 20 bonuses for the rest of your system! Now, I know it isn’t exactly 20 for either one, but you get the point. 😉. Choose real food and plants!!! 🌱🫚

03/10/2026

We had a blast this past weekend! It’s always a joy and a privilege to be able to nerd out and teach other practitioners about functional wellness and better ways to support our patients! See you next time Springfield, MO!

If you missed Dr. Annette this past weekend, she’ll be speaking at the Logan Symposium the beginning of May.

03/05/2026

Practitioners, if you haven't already signed up for Dr. Annette's seminar in Springfield, MO this Saturday don't worry, there is still time! Hit the link below and register to learn how to naturally support your peri-menopausal and menopausal patients!

https://my.standardprocess.com/Event?Id=4183

03/02/2026

Happy March! Spring is right around the corner as this month holds the Spring Equinox!!! 🌱🌞🌚🌱

To celebrate, here at Endocrine Wellness we’ve decided to change things up a bit. Getting away from the overly commercialized and high pressure New Year cleanse/detox season, we are going to honor our natural rhythms and start doing a 3 Week Reset in the Spring (and Fall)!

This cleanse is different from most others; another reason we wanted to change up our usual timing. For those who haven’t done one with us yet, you won’t be running to the bathroom, or starving for 3 weeks. This cleanse is made to be gentle, but effective, and give your body a break, all while cleansing toxins and help with sleep, mood, energy, hormone balance etc.

We invite everyone to join us for a Group Reset starting April 6! For more information or to sign up please contact us at endocrinewellness@gmail.com or contact either the IL office at 217-370-5060, or MO office at 417-590-2151.

Not ready to join our Spring Reset, no worries, we’ll be doing a second round in the fall! 🍁

03/01/2026

As daunting as this post might seem, please read the next to the last paragraph! Having a risk doesn’t mean you are destined to get Alzheimer’s or dementia. Focus on reducing neuro inflammation and a strong blood brain barrier would be a great place to start. AND we need to think about these things well before there are any signs of dementia or AD!!! More to come on this topic…

A new analysis led by researchers at University College London (UCL) suggests that Alzheimer disease (AD) may depend far more heavily on one gene than scientists once believed. The study estimates that more than 90% of Alzheimer cases might not develop without the influence of a single gene called APOE. Moreover, the impact appears to extend beyond AD alone. Researchers found that nearly half of all dementia cases may also rely on this gene’s contribution.

The APOE gene has been linked to Alzheimer’s disease for many years. It exists in three common forms, or alleles, known as ε2, ε3, and ε4. Each person inherits two copies of APOE, which results in six possible combinations of these variants. The six combinations of the APOE gene are: ε2+ε2; ε2+ε3; ε2+ε4; ε3+ε3; ε3+ε4; ε4+ε4. The variants are more commonly referred to as APOE2, APOE3, APOE4, which more correctly describes the APOE protein type produced from the gene (apolipoprotein E). APOE4 is thought to be the ancestral form; APOE3 and APOE2 evolved later.

Research in the 1990s established that people who carry one or more ε4 variants (producing mainly APOE4) face a much higher risk of AD compared with those who have two copies of the more common ε3 variant. People with ε2 generally had a lower risk than ε3 carriers. However, the new study goes much further than this.

Lead author Dr. Dylan Williams (UCL Division of Psychiatry and Unit for Lifelong Health and Ageing at UCL) said: “We have long underestimated how much the APOE gene contributes to the burden of Alzheimer’s disease. The ε4 variant of APOE is well recognised as harmful by dementia researchers, but much disease would not occur without the additional impact of the common ε3 allele, which has been typically misperceived as neutral in terms of Alzheimer’s risk.

“When we consider the contributions of ε3 and ε4, we can see that APOE potentially has a role in almost all Alzheimer’s disease. Consequently, if we knew how to reduce the risk that the ε3 and ε4 variants confer to people, we may be able prevent most disease from occurring.”

The study represents the most detailed modelling so far of how common APOE variants contribute to Alzheimer’s and dementia across the population. Researchers combined evidence linking the ε3 and ε4 alleles to Alzheimer’s disease, all-cause dementia, and the brain changes that precede Alzheimer’s.

A critical element of the analysis was access to data from four very large studies involving more than 450,000 participants. This allowed researchers to identify a sizable group of people with two ε2 copies, an uncommon but low risk group, and use them as a reference point in their calculations for the first time in this type of research. Specifically, the researchers analysed electronic health record data from 171,105 older adults in the UK Biobank cohort and 289,150 older adults in the FinnGen study to determine Alzheimer and all-cause dementia diagnoses. They also examined baseline amyloid PET scans of 4,415 participants in the A4 trial and analysed data from 5,007 participants in the Alzheimer's Disease Genetics Consortium (ADGC) of autopsy-confirmed Alzheimer cases and controls to provide a comprehensive view.

Based on their analysis, the researchers estimated that 72 to 93% of Alzheimer cases would not have occurred without the ε3 and ε4 variants of APOE. They also found that roughly 45% of all dementia cases might not arise without the gene’s influence.

These estimates exceed earlier assessments of APOE’s impact, largely because the new study evaluated the combined effects of both ε3 and ε4 rather than focusing only on ε4.

Results differed somewhat across the four studies included in the analysis. These differences reflected how AD and dementia were defined and measured, including whether cases were identified through medical diagnoses, other dementia classifications, or signs of amyloid buildup seen on brain scans. Variation in follow-up length and possible recruitment biases also contributed. When considered together, the evidence suggests that APOE is likely responsible for at least three quarters of Alzheimer cases, and potentially more.

The findings indicate that APOE should receive greater attention in research aimed at understanding disease mechanisms and developing new treatments and prevention options.

APOE is a lipoprotein-binding protein that helps transport cholesterol, triglycerides and phospholipids. It acts as a ligand for LDL (low density lipoprotein) receptors and related receptors, helping shuttle lipids between tissues, particularly the brain, the vascular system and the liver. In the brain, APOE is produced mainly by astrocytes and helps redistribute cholesterol to neurons for membrane repair and synapse maintenance.

The APOE ε4 variant is thought to increase dementia risk by impairing amyloid-β clearance, amplifying tau pathology and neuroinflammation, disrupting brain lipid transport and synaptic repair, and compromising vascular integrity, thereby lowering the brain’s resilience to age-related neurodegenerative stress over time. Further research is needed to confirm these processes and to explain why ε3 increases dementia risk compared with ε2.

Despite its strong influence, APOE is not the sole cause of Alzheimer or other dementias. Even among people with the highest genetic risk, those who carry two ε4 variants, lifetime risk of AD is still estimated to be below 70%. See my recent posting on the 14 modifiable risk factors in AD and the key role they play.

This invites some more sober commentary on the study’s findings. For example, claiming that most Alzheimer cases would not occur without the contribution of APOE was a bit like saying most road traffic deaths wouldn't occur without the contribution of cars, according to geneticist Dr Timothy Frayling of the University of Geneva. (This is not entirely true because only ε3 and ε4 appear to account for risk.) "People should not worry if they have the risk versions of the gene, because 99.4% of us do," he added.

To my mind, the true value of this study lies in the mechanistic lens it provides. Specifically, are there any natural interventions that can mitigate the risk imposed by APOE variants? See my next posting for a few promising leads.

For more information see: https://bit.ly/40837KO
and
https://scitechdaily.com/one-overlooked-gene-may-shape-nearly-all-alzheimers-risk/

02/22/2026

Eating a more Mediterranean type diet with lots of tomatoes could help in multiple ways!!! Don’t forget the mushrooms and bitter spices!

Chronic periodontal disease is strongly associated with systemic inflammation and has been linked in cohort and mechanistic studies to increased risk of cardiovascular disease, type 2 diabetes, adverse pregnancy outcomes, rheumatoid arthritis, and even cognitive decline, largely via pathways involving bacterial translocation (such as for Porphyromonas gingivalis), endotoxaemia, endothelial dysfunction, and heightened cytokine signalling.

A large cross-sectional analysis of 1,227 US adults aged 65 to 79 used NHANES (National Health and Nutrition Examination Survey) 2009 to 2014 data to explore whether dietary lycopene intake was associated with severe periodontitis (PD).

Lycopene intake was derived from two 24-hour dietary recalls and categorised as sufficient (≥ 8 mg/day) or insufficient. Periodontal status was assessed by standardised examination in NHANES mobile examination centres. Survey-weighted multinomial logistic regression models adjusted for age, s*x, race, smoking status, education and BMI.

Overall, 77.9% of participants had insufficient lycopene intake and 5.6% had severe PD. After adjustment, sufficient lycopene intake was associated with markedly lower odds of severe PD (odds ratio, OR 0.33). Current smoking showed the expected strong association (OR 3.29) and the association between sufficient lycopene intake and severe PD was strongest in non-Hispanic White participants (OR 0.13) and not statistically significant in non-Hispanic Black participants.

The magnitude of these associations is large for a single dietary component and therefore warrants careful interpretation. The principal limitation is the cross-sectional design: exposure and outcome were measured at the same time, so temporality and causality cannot be established. Reverse causation is plausible, as individuals diagnosed with periodontal disease may have altered their diets. Lycopene intake was based on two-day recall rather than biomarker measurement, and the ≥ 8 mg cutoff was derived from other disease contexts rather than periodontal outcomes. Critically, the models did not adjust for overall dietary pattern (such as fruit/vegetable intake, Healthy Eating Index, fibre, total carotenoids), dental care access, oral hygiene behaviours, or detailed socioeconomic factors. Given that lycopene intake typically tracks with higher diet quality and healthier lifestyles, substantial residual confounding is likely.

Taken together, this study provides a statistically robust association between higher reported lycopene intake and lower prevalence of severe PD in older adults, but it is best interpreted as hypothesis-generating. The large effect size suggests that lycopene may function partly as a marker of a phytonutrient-rich, Mediterranean-style dietary pattern rather than acting as an isolated causal agent. Biological plausibility exist, lycopene has antioxidant and anti-inflammatory properties, but the magnitude observed here likely overestimates any true independent effect. Clinically, the findings support encouraging whole-food, carotenoid-rich diets in older adults; however, they do not justify lycopene supplementation as a stand-alone periodontal intervention without new longitudinal or randomised trial evidence.

This is a well-executed analysis using nationally representative data and appropriate complex-survey statistics, but it remains observational and does not establish causality. However, the large effect size suggests a real association, at least with a phytonutrient rich diet.

For more information see: https://scitechdaily.com/could-a-tomato-nutrient-help-prevent-severe-gum-disease-in-older-adults/

https://pubmed.ncbi.nlm.nih.gov/41391269/

02/17/2026

✨Attention all practitioners, Dr. Annette has a seminar coming up you won't want to miss! Make a trip to Springfield MO for her March 7th seminar or to one of the other locations later this year, and learn how to support your female patients!✨

02/16/2026

Small daily habits add up over time! Ditch the sweet milk chocolate for the dark and bitter chocolate! It helps to slowly work your way up to 75-80% cacao.

Notice that I waited until AFTER Valentine’s Day to share this post. You’re welcome! 😍

One of the core components of my microcirculation phytonutrient diet is cocoa, usually as very dark chocolate (85 to 90%), chosen for its higher flavanol density and lower sugar load. A 2025 systematic review rigorously evaluated the clinical evidence to determine whether cocoa flavanols meaningfully enhance microvascular function. The review included 19 randomised, placebo-controlled human trials, comprising 13 acute studies and 7 chronic studies (with one study containing both phases), spanning effects on skin, skeletal muscle, cerebral and retinal microvascular beds.

Participants were not simply eating ordinary chocolate. Most of the trials used standardised, high-flavanol cocoa beverages, concentrated cocoa extracts in capsules, or specially prepared high-percentage dark chocolate, delivering pharmacological doses of flavanols. Acute doses commonly ranged from 500 to 1350 mg total flavanols (with 45 to 255 mg of (-)-epicatechin), and some chronic studies delivered up to 900 to 1800 mg/day.

A conventional meta-analysis was not possible because the studies varied widely in assessed vascular beds, measurement techniques (Laser Doppler, plethysmography etc), and stimulus conditions (reactive hyperaemia, hypoxia, mental stress, exercise). The authors therefore used vote counting, a Cochrane-recognised fallback method. In this approach, each study subgroup was assigned a “vote” based solely on whether cocoa performed better than placebo (1) or not (0), regardless of statistical significance or effect size. They then tested whether the proportion of positive directions exceeded chance (50%).

Using vote counting (direction-of-effect analysis), 12 of 14 acute subgroups (85.7%) showed improved vasodilator responses with cocoa flavanols, a proportion significantly greater than chance (p = 0.013), with 100% of the low-risk-of-bias (higher quality) acute studies favouring cocoa. For chronic supplementation, the direction was also generally favourable but less robust: 8 of 11 subgroups (72.7%) showed improved vasodilator responses and 7 of 9 (77.7%) favoured cocoa at rest, but these proportions did not reach statistical significance. (Note that some trials generated more than one subgroup for analysis.)

Hence the strongest signal was for acute enhancement of microvascular reactivity within 1 to 3 hours after ingestion, coinciding with peak circulating flavanol metabolites and nitric oxide-related activity. Chronic effects were less consistent, and there was little evidence of structural microvascular remodelling or reversal of established disease. The current clinical data therefore position high-dose cocoa flavanol extracts as performance enhancing short-term endothelial modulators that may enhance vascular responsiveness under stress (cognitive demand, hypoxia, reactive hyperaemia).

The fact that the clinical evidence favours acute effects from cocoa does not rule out benefits from long-term chronic intake. However, it does highlight that the use of a multicomponent sustained input, as per my microcirculation diet, is more likely to have the greatest impact on chronic microvascular compromise.

For more information see: https://pubmed.ncbi.nlm.nih.gov/40217225/

01/31/2026

Love this!!!

01/29/2026

This!!!! ♥️♥️♥️

A new paper has revealed a clear human fingerprint on medicinal plant diversity and reframes herbal medicine as an emergent, co-evolved system, rather than an accidental pharmacological curiosity.

The human fingerprint of medicinal plant species diversity argues that the global distribution of medicinal plant diversity is not simply a reflection of overall plant biodiversity or ecological richness, but is strongly shaped by long-term human cultural, medical and historical factors. The authors show that regions with high medicinal plant diversity often correspond to areas with deep, continuous traditions of human settlement, healing systems and ethnomedical knowledge, rather than just botanical “hotspots” alone.

Using global datasets, the paper demonstrates that medicinal floras are disproportionately enriched in certain plant lineages and regions, reflecting selective human use over millennia. In other words, humans have acted as powerful evolutionary and ecological filters: repeatedly identifying, cultivating, trading and conserving plants with perceived therapeutic value. This has created a distinctive “human fingerprint” on medicinal plant diversity that differs from patterns seen in non-medicinal plant species.

They write: “A key unexplored topic is whether variation in the duration of human interactions with a flora has influenced regional heterogeneity in medicinal plant knowledge and diversity. Here, we investigate and compare these influences on the distribution and diversity of 32,460 medicinal plant species and on global vascular plant distributions. We identify significant regional variation in medicinal plant diversity, including "hotspots" (India, Nepal, Myanmar, and China) and "coldspots" (the Andes, New Guinea, Madagascar, the Cape Provinces, and Western Australia) of diversity. Regions with long histories of human settlement typically boast richer medicinal floras than expected.”

The study also highlights that medicinal plant diversity is tightly linked to cultural diversity and traditional knowledge systems, and that erosion of indigenous and local knowledge threatens not just cultural heritage, but the functional diversity of medicinal floras themselves.

Overall, the paper reframes medicinal plants as a biocultural phenomenon—emerging from long co-evolution between humans and plants—rather than a random subset of the world’s flora. This has major implications for conservation, emphasising that protecting medicinal plant diversity requires safeguarding both ecosystems and the human knowledge systems that shape them.

Australia presents as an apparent anomaly in the analysis, showing a low recorded medicinal plant diversity signal despite one of the longest continuous human occupations on Earth. This pattern does not contradict human-plant co-development, but instead exposes limitations in how medicinal knowledge is captured in global datasets. Aboriginal medicinal systems were profoundly disrupted by colonisation, leaving extensive therapeutic knowledge undocumented or fragmented. In addition, Australian healing traditions emphasise holistic, ecological, and spiritual frameworks—a cultural sophistication poorly reflected in Western-style materia medica inventories. Rather than a true exception, Australia illustrates how low recorded medicinal plant diversity may arise from disrupted documentation and knowledge transmission, especially from an oral tradition, not from an absence of deep human-plant co-development.

The authors write: “By contrast, colonial influences and modernization may have contributed to geographically uneven erosion or non-documentation of this knowledge, highlighting the need to better preserve and explore traditional ethnobotanical practices. For instance, profound demographic collapse in Latin America and Australia from colonization likely led to significant losses in ethnobotanical knowledge, thereby weakening the continuity of medicinal practices. By comparison, Africa and much of Asia retained stronger cultural resilience, allowing traditional practices to persist more robustly and continue shaping medicinal plant diversity.” And they later conclude: “Regions we identified as medicinal plant diversity coldspots, such as the Andes, New Guinea, Madagascar, the Cape Provinces, and Western Australia, likely have unrecorded or unrecognized medicinal plant resources and therefore require knowledge revitalization.”

What this study shows overall is that medicinal plants are not chance. Over millennia, humans have acted as powerful selective forces—identifying, protecting, propagating and trading plants with meaningful bioactivity. In turn, these plants shaped medical traditions, therapeutic intuition and systems of care. Medicinal floras are therefore not random subsets of biodiversity, but biocultural archives.

This study makes it clear that herbal medicine is not a discarded relic of pre-scientific thinking, but a living knowledge system embedded in human psychology, culture and practice. The global patterns of medicinal plant diversity it reveals reflect enduring human selection, memory and meaning, not historical accident.

Herbal medicine persists because it aligns with how humans perceive illness, healing, and the natural world—shaped by a long co-evolution that is not superseded by modern biomedicine. Far from being obsolete, it remains relevant precisely because it is woven into the ecological, cognitive and cultural architecture of human health.

For more information see: https://pubmed.ncbi.nlm.nih.gov/41151580/

11/23/2025

Why is it that women experience stress more intensely than men? Drs. Daina Parent and Annette Schippel discuss the connection between women's hormones and the effects of stress on the female body. Dr. Schippel offers invaluable clinical tools and takeaways to create a strong foundation for any woman to navigate stress management and optimal wellness with nutrition, herbs, lifestyle and more.

Why is it that women experience stress more intensely than men? Drs. Daina Parent and Annette Schippel discuss the connection between women’s hormones and th...