Endocrine Wellness

04/02/2026

More reasons to love coffee and chocolate! Tea too…I guess if you like it. 😝. But I’m sticking with my coffee!!! 😜☕️🍫

Across human history, our relationship with plant alkaloids has been intimate, ambivalent and profoundly influential. These often bitter, physiologically potent nitrogen-containing compounds have shaped medicine, ritual, warfare, agriculture and addiction alike. From caffeine in tea and coffee, to morphine from o***m poppy, quinine from cinchona, ni****ne from to***co, and atropine from belladonna, alkaloids have altered mood, perception, pain, immunity and cardiovascular tone with a potency and specificity that conceptually foreshadowed modern pharmacology.

Most alkaloids are biologically potent precisely because they are toxic in higher doses. Many were designed by the plant as defence chemicals able to interfere with neural transmission, ion channels or enzymatic pathways. Their therapeutic window is often narrow. The major exception in everyday human use is the xanthine alkaloids, caffeine in tea and coffee, and theobromine (with small amounts of caffeine) in cocoa, which are comparatively mild central nervous system stimulants with a wide safety margin at customary dietary intakes. One might even say that human cultures appear to have instinctively selected and preserved xanthine-alkaloid-containing plants as daily companions: an implicit, cross-civilisational recognition that their gentle properties confer functional benefits without crossing into the toxicity that characterises most other alkaloids.
Now two recent studies add weight to the assertion that there might be substantial health benefits from the regular consumption of xanthine alkaloids. A 2025 population-based study examined whether circulating theobromine was associated with epigenetic markers of biological ageing in two European cohorts. In the discovery TwinsUK sample (n = 509), each unit increase in metabolomically derived circulating theobromine was associated with 1.6 fewer years of GrimAge acceleration (p = 3.99 × 10⁻⁶) and significantly longer DNA methylation-based telomere length (DNAmTL , p = 0.0029). These findings were replicated in the larger KORA cohort (n = 1,160), where theobromine was associated with approximately 1.1 fewer biological years of GrimAge acceleration (p = 7.2 × 10⁻⁸) and longer DNAmTL (p = 0.007). Note the extraordinarily low p values, indicating very high statistical significance.

Importantly, theobromine was not measured using a targeted quantitative chemical assay, nor was cocoa intake directly assessed; instead, its exposure was identified through blood metabolomic profiling. So, the association reflects circulating levels at a single time point using an objective exposure marker, but one shaped by recent intake and individual metabolism rather than a precise measure of long-term cocoa consumption. However, the authors regarded their metabolomic profiling of circulating theobromine as a more biologically integrated and objective measure of systemic exposure, arguably more reflective of intake and metabolism than self-reported dietary data. Sensitivity analyses including covariates of other cocoa and coffee metabolites suggested that the observed effects were specific to theobromine.

Biologically, the results for theobromine are plausible from its known properties and consistent with contemporary ageing mechanisms. While observational and not proof of causality, the magnitude (roughly 1 to 1.5 years difference in epigenetic age acceleration across exposure variation) is statistically robust yet biologically modest. It positions theobromine as just one among many phytonutrients that, when combined (like in my microcirculation diet), might substantially decelerate biological ageing.

The second study was a new prospective cohort study. Researchers sought to clarify the relationships between tea and coffee consumption and cognitive decline using repeated, detailed dietary assessments across two independent cohorts. Participants in the National Health Service (NHS) (n = 86,606 women; mean age at baseline, 46.2 years) and the Health Professionals Follow-up Study (n = 45,215 men; mean age at baseline, 53.8 years) completed repeated food frequency questionnaires every 2 to 4 years to assess caffeinated and decaffeinated coffee and tea intake.

Over a follow-up period of up to 43 years, 11,033 participants developed dementia. Moderate caffeinated coffee intake of about 2 to 3 cups/day was associated with an 18% lower risk for incident dementia compared with no coffee (hazard ratio [HR], 0.82; 95% CI, 0.76 to 0.89). Tea consumption showed a similar pattern, with participants who reported moderate tea intake (1 to 2 cups/day) showing a 14% lower risk for dementia than those who drank no tea (HR, 0.86; 95% CI, 0.83 to 0.90).

In contrast, decaffeinated coffee intake was not associated with a reduced risk for dementia.

“The decaf findings suggest that caffeine may be an important contributor because caffeinated coffee and tea showed more consistent associations than decaffeinated coffee,” lead author Zhang said.

Both green tea and cocoa (ideally as 85 to 90% dark chocolate) form core pillars of my microcirculation diet. The evidence supporting their broad vascular and cardiometabolic benefits continues to strengthen, and is now further enriched by the emerging data suggesting that the resultant coincidental intake of xanthine alkaloids may also meaningfully contribute to healthy ageing biology.

For more information see:
https://pubmed.ncbi.nlm.nih.gov/41397115/
https://www.medscape.com/viewarticle/coffee-and-tea-may-protect-against-dementia-hold-decaf-2026a100046l?ecd=mkm_ret_260220_mscpmrk-OUS_ICYMI_etid8114469&uac=48709HJ&impID=8114469

03/28/2026

♥️♥️♥️

03/25/2026

Dr. Annette will be there, will you?!
Dr. Annette is one of the main speakers at this year's Logan University Symposium. So register, come, learn from some brilliant minds in the world of chiropractic and functional wellness and get your CEs!

Have you registered for Symposium 2026 yet? Join Logan University on campus Friday, May 1, to Saturday, May 2, for an unforgettable continuing education experience. Join leading experts, expand your knowledge and connect with fellow professionals.

Learn more and register now: https://www.logan.edu/continuing-education-chiropractors/seminars/

03/19/2026

Simplify your life for 21 days and join us for the purification reset!!! And enjoy the video…it’s hilarious!!! ♥️

03/18/2026

Eat your beets!!! Better yet, take SP Red Food!

Menopause is often discussed in the context of bone health, but muscle health matters just as much: they go together as the musculoskeletal dynamic. Muscle quality and strength tend to decline during the postmenopausal years, influenced by hormonal changes, reduced nitric oxide signaling, and shifts in vascular and metabolic function. I sent out my weekly newsletter today on the topic of ensuring adequate hydration for muscles, and in addition to hydration, there are also nitrates to consider.

In a randomized, placebo-controlled trial, postmenopausal women who consumed nitrate-rich beetroot extract for 12 weeks showed improvements in muscle quality and rate of force development compared with placebo (nitrate-depleted beetroot extract). Dietary nitrates found in foods like beetroot can be converted in the body to nitric oxide, a signaling molecule that supports blood flow, mitochondrial function, and muscle performance.

It is another reminder that plant foods do more than provide vitamins and minerals. They also deliver bioactive compounds and phytochemicals that can support physiological resilience during the menopausal transition.

03/18/2026

Wondering what the 21 Day Reset includes and the cost? Click the link below to see a price break down for the 21 Day Reset and optional additions to help make this the best cleanse for you!
🌱✨
Ready to join us in April? Contact the office to sign up and get your kit and start with us on April 6!
endocrinewellness@gmail.com
217-370-5060 - IL office
417-590-2151 - MO office

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 sex-specific effects, absolute strength was higher in males (as expected), but relative improvements with Rhodiola were comparable across sexes. Moreover, the ergogenic and cognitive effects were not sex-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/