Your Statin Medication May be Increasing your Risk of Alzheimer's Dementia, Raising your Risk of Diabetes and may be making it harder to lose weight. Learn more....

Statins, GLP-1, and Metabolic Health: What Patients Should Know

GLP-1 Medicines are beneficial in many ways

If you take a statin to lower cholesterol, you’re in good company: statins are among the most widely prescribed medicines in the world. They reduce LDL (“bad cholesterol”) and convincingly lower the risk of heart attacks and strokes. That part is not in dispute.

What is being actively studied is how statins may influence blood-sugar control and a gut-derived hormone called GLP-1 (glucagon-like peptide-1), which helps regulate insulin release, appetite, and inflammation. Because GLP-1 also intersects with brain and blood-vessel health, patients often ask whether statins could nudge them toward diabetes or even affect cognition over time.

Below is a plain-spoken tour of the best evidence we have today, plus practical steps you can take with your clinician to protect both your heart and your metabolism.

GLP-1 in one minute

GLP-1 is a hormone released by intestinal L-cells after you eat. Think of it as a “meal messenger” that:

• Helps the pancreas release insulin when glucose rises

• Tamps down glucagon (reduces liver glucose output)

• Slows stomach emptying so glucose rises more gently

• Sends satiety signals to the brain

  
  

Boosting GLP-1 signaling—either by mimicking it (GLP-1 receptor agonists) or prolonging native GLP-1 (DPP-4 inhibitors)—improves glycemic control and reduces cardiometabolic risk in many patients. AHA Journals+1

A new twist: statins, the microbiome, bile acids… and lower GLP-1

GlP-1 influence many organs, including the liver, brain and stomach

In 2024, a high-quality translational study reported that statins can aggravate insulin resistance by reducing circulating active GLP-1 levels—and that the effect appears to be microbiome-dependent. Mechanistically, statins altered the bile-acid pool (notably lowering ursodeoxycholic acid, UDCA), which reduced signaling through the TGR5 receptor on intestinal cells, leading to less GLP-1 release. In the human arm of the study, active GLP-1 concentrations fell significantly within four weeks of atorvastatin therapy. Cell+1

Follow-up reviews summarize the idea this way: by shifting gut bacteria and bile acids, statins may unintentionally dial down your own GLP-1 signal—potentially nudging insulin resistance in the wrong direction, especially in those already at risk. Taylor & Francis Online

That is not the last word (one paper never is), but it’s a credible biologic pathway linking statins → bile acids/microbiome → GLP-1 → insulin resistance.

Do statins actually raise diabetes risk?

Insulin resistance may be worsened by statin medications

Short answer: yes, modestly—and the risk rises with higher-intensity dosing and in people already on the cusp of diabetes.

• An individual-participant meta-analysis of randomized trials (the most rigorous way to look) confirmed that statins increase the risk of new-onset diabetes, and clarified when and in whom it occurs. The Lancet+1

• Mechanistic and clinical studies show increased insulin resistance during statin therapy; for example, high-intensity atorvastatin over 10 weeks increased insulin resistance in non-diabetic adults. AHA Journals+1

• Observational and trial meta-analyses consistently estimate a ~9–13% average increase in diabetes risk across statins, with higher risks at intensive doses (e.g., atorvastatin 80 mg), and particularly in those with pre-diabetes. nmcd-journal.com+1

• A large cohort from Finland (METSIM) reported a higher, dose-responsive signal: 46% increased diabetes risk, tied to both decreased insulin sensitivity and insulin secretion. This is an outlier on the high end, but the design was careful and the pattern biologically plausible. PubMed+1

  
  

How might that tie back to GLP-1? The 2024 study suggests one pathway: if statins lower active GLP-1, the body’s post-meal insulin response and satiety signaling could be blunted, tending toward higher glucose and weight—especially in those with pre-existing insulin resistance. Cell

What if I already have pre-diabetes?

Pre-diabetes is a tipping-point condition. In several analyses, statin-associated dysglycemia is most evident in people who started close to that metabolic edge. High-intensity statins show the largest signal, and the effect appears dose-dependent. That’s not a reason to ignore your LDL or stop therapy abruptly; it is a reason to individualize choices, intensify lifestyle therapy, and monitor glucose and A1c more closely. ScienceDirect+1

In short, know the risk-benefit analysis. Statins need not be given to everybody. Often, it seems, they are prescribed to everybody, as we have so frequently been told, 'The lower the cholesterol, the better.' From an observational standpoint, as well as a personal experiential standpoint, is entirely wrong.

What about memory and dementia?

Here the evidence is mixed and, importantly, not aligned with a clear harm signal:

• The FDA added labeling in 2012 noting rare, generally reversible reports of memory loss or confusion with statins; they also noted small increases in blood sugar. This is real-world pharmacovigilance—signals to watch, not proof of ongoing injury. U.S. Food and Drug Administration+1

• Randomized evidence to date has not shown prevention of dementia by starting statins late in life; a Cochrane review concluded there was “good evidence” that statins do not prevent cognitive decline or dementia in that context. Cochrane Library+1

• Large observational syntheses are heterogeneous: some show neutral effects; others suggest protective associations (lower dementia risk among statin users). Observational results can be confounded (healthier users, better vascular care, etc.), so they don’t settle causality. Oxford Academic+1

  

  Diabetes and Statins may contribute to Alzheimer's disease

How do we square this with GLP-1? Chronically higher glucose and insulin resistance are linked to worse brain outcomes over time. If statins in some people nudge glucose up (possibly via lower GLP-1), that metabolic effect could, indirectly, be unfavorable for the brain. But head-to-head evidence that statins cause dementia is lacking, and several analyses point the other way. The most sensible stance: treat the vascular risk we know statins improve, while actively protecting metabolic and cognitive health with monitoring and targeted add-ons when needed. The Lancet+1

Practical counseling: how we minimize downside while keeping upside

1. Stratify your baseline risk.If your 10-year ASCVD risk is high, the cardiovascular benefits of statins are substantial. If your risk is moderate and you also have pre-diabetes, we weigh options more carefully (dose, molecule, or alternatives such as ezetimibe or bempedoic acid). Evidence of a small diabetes signal should be framed against the larger heart-attack/stroke risk reduction in higher-risk patients. The Lancet

2. Choose dose and molecule deliberately.Higher-intensity regimens carry a larger glycemic signal. Discuss whether a moderate-intensity statin plus ezetimibe (or bempedoic acid) can reach LDL goals with less metabolic friction. nmcd-journal.com

3. Track glucose proactively.Check fasting glucose, A1c, and—in those on the cusp—consider occasional post-meal checks or a short CGM trial to see what meals and medicines do in real life. Adjust diet (fiber, protein in early meals), activity (walks after meals), and timing. ScienceDirect

4. Reinforce GLP-1–friendly habits.Protein with breakfast, viscous fibers (oats, legumes), fermented foods, and resistance training can all improve incretin tone and insulin sensitivity. If weight, appetite, or post-meal spikes worsen after starting a statin, bring this up—don’t white-knuckle it.

5. Pharmacologic add-ons if needed.In people who develop hyperglycemia on statins—or who begin with pre-diabetes—consider therapies that enhance GLP-1 signaling (GLP-1 receptor agonists, DPP-4 inhibitors) or improve insulin sensitivity (metformin) while continuing evidence-based lipid lowering. Drug–drug interactions with GLP-1 RAs are generally minor (slower gastric emptying can lower peak levels of some oral drugs), and the benefits for cardiometabolic risk are well established. SpringerLink+1

6. Cognition: monitor, don’t panic.If you notice new brain-fog or short-term memory issues after a statin starts or a dose increases, tell your clinician. Many cases are reversible with dose adjustment or a switch in agent. Meanwhile, control of blood pressure, sleep apnea, glucose, exercise, and social/cognitive engagement are the heavy hitters for brain protection. U.S. Food and Drug Administration

   
   

Bottom line for patients

• Statins may save lives, by preventing heart attacks and strokes.

• A growing body of evidence indicates they can nudge glucose upward and increase diabetes risk, particularly at higher doses and in those with pre-diabetes. A mechanistic link—reduced active GLP-1 via microbiome/bile-acid changes—has now been demonstrated in humans. This, on the other hand, may cost lives. Cell

• Cognitive effects remain uncommon and typically reversible when they occur; large randomized data do not show dementia prevention from initiating statins late in life, and observational data on dementia risk are mixed. Cochrane Library+1

  
  

The best approach isn’t “statins good” or “statins bad.” It’s statins plus metabolic vigilance: choose the right intensity, monitor glucose, support GLP-1 biology with lifestyle (and, when appropriate, medication), and keep the heart-brain-metabolism picture in view.

There is a time and a place for statin medications, but using them without better consideration of the populations at risk, will result in increased incidence of diabetes, obesity and dementia.

1. Focus diagnosis and therapeutics on the inflammatory markers, as atherosclerosis starts as intravascular inflammation.

2. Reduce inflammation through a better understanding of the factors that lead to intravascular inflammation, and intervene according to the chemistry that is required.

3. Reduce the cholesterol value using natural and/or dietary approaches first.

4. Statins have a bad public reputation, for no other reason than they make a significant number of persons 'feel bad,' as they are taken.

References (15)

1. She J, et al. Statins aggravate insulin resistance through reduced blood glucagon-like peptide-1 levels in a microbiota-dependent manner. Cell Metab. 2024;36(2):408-421.e5. doi:10.1016/j.cmet.2023.12.027. [PubMed/Abstract] PubMed

2. She J, et al. A gut feeling of statin: How gut microbiota modulate the therapeutic and side effects of statins. Gut Microbes. 2024;16(1):e2291678. [Article] Taylor & Francis Online

3. Cholesterol Treatment Trialists’ Collaboration (Reith C, et al.). Effects of statin therapy on diagnoses of new-onset diabetes: individual participant data meta-analysis. Lancet Diabetes Endocrinol. 2024;12(6):xxx-xxx. [Article/Abstract] The Lancet+1

4. Abbasi F, et al. Statins are associated with increased insulin resistance and insulin secretion in adults without diabetes. Arterioscler Thromb Vasc Biol. 2021;41(11):e443-e455. [Article] AHA Journals

5. Laakso M. Statins and risk of type 2 diabetes: mechanism and clinical implications. Front Endocrinol. 2023;14:1239335. [PMC] PMC

6. Alvarez-Jimenez L, et al. Effects of statin therapy on glycemic control and insulin resistance: meta-analysis. Pharmacol Res. 2023;190:106695. [Abstract] ScienceDirect

7. Cederberg H, et al. Increased risk of diabetes with statin treatment is associated with impaired insulin sensitivity and insulin secretion: METSIM cohort. Diabetologia. 2015;58:1109-1117. [PubMed] PubMed

8. Crandall JP, et al. Statin use and risk of developing diabetes: Women’s Health Initiative. J Gen Intern Med. 2017;32(7):746-753. [PMC] PMC

9. Casula M, et al. Statin use and risk of new-onset diabetes: meta-analysis of observational studies. Nutr Metab Cardiovasc Dis. 2017;27(5):396-406. [Article] nmcd-journal.com

10. Navarese EP, et al. Impact of different statin types/doses on new-onset diabetes: meta-analysis. Am J Cardiol. 2013;111(8):1123-1130. [Abstract] ajconline.org

11. Barkas F, et al. High-intensity statin therapy and incident diabetes—greater risk in prediabetes. J Clin Lipidol. 2016;10(4):e-pub ahead of print. [Abstract] ScienceDirect

12. Dabhi KN, et al. Assessing the link between statins and insulin intolerance: systematic review. Cureus. 2023;15(6):e40112. [PMC] PMC

13. U.S. FDA. Drug Safety Communication: Safety label changes for statins (cognition and blood glucose). 2012. [FDA page] U.S. Food and Drug Administration

14. McGuinness B, et al. Statins for the prevention of dementia. Cochrane Database Syst Rev. 2016;CD003160. [Abstract] Cochrane Library

15. Olmastroni E, et al. Statin use and risk of dementia or Alzheimer’s disease: meta-analysis of observational studies. Eur J Prev Cardiol. 2022;29(5):804-814. [Article] Oxford Academic

A final word

If you’re on a statin (or considering one) and you also have pre-diabetes, diabetes, weight gain, or cognitive concerns, the right move is not to stop therapy on your own. It’s to personalize the plan: the right LDL goal, the right intensity, early glucose monitoring, GLP-1–supportive lifestyle (and medications if needed), and open communication about symptoms. That balanced strategy preserves the heart-protection statins offer while addressing the metabolic side of the ledger with equal seriousness.

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

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David S. Klein, MD Functional Medicine Physician

The Warburg Effect: Cancer Prevention & Understanding How We Can Starve Cancer Cells Naturally

The Warburg effect, decoded

Whatis the Warburg Effect?

Nearly a century ago, Otto Warburg observed that many tumors avidly ferment glucose to lactate even when oxygen is plentiful—so-called aerobic glycolysis. Rather than fully oxidizing glucose in mitochondria to squeeze out maximal ATP, cancer cells divert a large fraction of glucose carbon toward rapid ATP generation and biosynthesis (nucleotides, amino acids, lipids) needed for proliferation. Warburg originally argued this reflected “injured respiration”; modern work shows the reality is more nuanced: oncogenic signaling and the tumor microenvironment reprogram metabolism to favor glycolysis while mitochondria remain functional and essential for anabolism and redox balance. Understanding this principal is key to cancer prevention. refp.cohlife.orgPMCScience

In contemporary cancer biology, metabolic reprogramming is recognized as a hallmark of malignancy. This reprogramming is not simply about energy; it’s a control system that tunes redox state, epigenetic marks, and immune evasion. As Hanahan’s updated “Hallmarks of Cancer: New Dimensions” emphasizes, altered metabolism is intertwined with genomic instability, inflammation, and immune escape—features that collectively enable tumor progression. PubMed

Why glycolysis becomes an advantage

How understanding the Warburg Effect may improvie your longevity

Glycolysis is fast. When coupled to high glucose uptake and lactate export (via monocarboxylate transporters), it enables cells to grow under fluctuating oxygen and to sustain the pentose phosphate pathway and one-carbon metabolism. The acidified microenvironment created by lactate (pH ~6.3–6.9) promotes invasion, angiogenesis, and immune suppression. Lactate is not merely “waste”; it’s a signaling metabolite that shapes gene expression (including histone lactylation) and alters the behavior of stromal and immune cells. Clinically, our exploitation of this phenotype underpins FDG-PET, which images tumors because they often take up far more 18F-fluorodeoxyglucose than surrounding tissues. PMC+1Nature

Prevention: what the Warburg effect teaches us

It is crucial to avoid over-claiming: no diet or supplement “shuts off” the Warburg effect across cancers. That said, the phenotype highlights upstream levers—adiposity, insulin/IGF-1 signaling, and physical inactivity—that create a metabolic milieu favorable to glycolysis-dependent growth. Observational and mechanistic data connect chronic hyperinsulinemia and insulin resistance to higher risks of several cancers; insulin acts as a growth factor and can increase glucose uptake and glycolytic flux in susceptible tissues. PMC+1

Body weight and body composition. Excess adiposity fosters hyperinsulinemia, chronic inflammation, and altered adipokines—all of which tilt cells toward glycolytic programs and anabolic growth. Global consensus statements from the World Cancer Research Fund/AICR estimate that maintaining a healthy weight and limiting weight gain across adulthood lowers risk for multiple cancers. World Cancer Research Fund

Physical activity. Regular activity improves insulin sensitivity, reduces chronic inflammation, and enhances mitochondrial oxidative capacity—physiologic counterweights to the Warburg phenotype. Evidence syntheses and guidelines recommend 150–300 minutes/week of moderate or 75–150 minutes/week of vigorous activity, with more generally better; adherence is associated with lower incidence and mortality across several cancers. American Cancer SocietyPMC+1

Dietary pattern and carbohydrate quality. The Warburg frame sometimes inspires extreme carbohydrate restriction; evidence for universal cancer-prevention benefit of very low-carb or ketogenic diets remains limited. More solid is the signal that dietary patterns emphasizing fiber-rich, minimally processed foods (vegetables, fruits, legumes, whole grains) and minimizing refined starches and added sugars improve metabolic health and may lower risk of several cancers, notably colorectal. Meta-analytic and cohort data link higher glycemic load or poor carbohydrate quality to elevated colorectal cancer risk in some populations. PMC+1ScienceDirect

How clinicians already leverage the phenotype

The Warburg effect is not just a laboratory curiosity; it has diagnostic and therapeutic implications. FDG-PET/CT uses tumor glycolysis to localize disease and monitor response; in parallel, a wave of investigational strategies attempts to target metabolic nodes (glycolysis, lactate transport, redox recycling) or to recondition the microenvironment. While these approaches are still maturing clinically, they reflect a central point: tumor metabolism is plastic and intertwined with signaling, epigenetics, and immunity. Journal of Nuclear MedicineNature

Practical, evidence-anchored takeaways

1. Manage insulin exposure. Maintain a healthy waist circumference; prioritize dietary patterns that blunt post-prandial spikes (fiber-rich, minimally processed foods) and distribute carbohydrates with protein and healthy fats. For people with diabetes or prediabetes, evidence-based management (diet, exercise, medications as indicated) matters for cancer prevention as well as cardiometabolic health. PMC

2. Move more, most days. Accumulate at least the ACS-recommended activity minutes weekly, and reduce sedentary time. Even small increments improve insulin sensitivity and mitochondrial function, pushing cellular metabolism away from glycolysis-dominant states. American Cancer Society

3. Think in patterns, not magic bullets. No single food or supplement reliably “starves” cancer. Focus on patterns—weight control, fitness, high-quality carbohydrate, limited alcohol, and smoking cessation—that harmonize metabolism and reduce inflammatory tone long-term. World Cancer Research Fund

   
   

Bottom line

The Warburg effect captures a fundamental reprogramming that makes growth possible under stress; it also offers a lens for prevention. By improving insulin sensitivity, reducing chronic inflammation, and reinforcing mitochondrial health through diet and physical activity, we make it harder for premalignant cells to inhabit a glycolysis-favored niche. That’s not a guarantee—but it is a principled, evidence-based way to shift risk in our favor.

References (publication format with links)

1. Warburg O. On the Origin of Cancer Cells. Science. 1956;123(3191):309–314. https://www.science.org/doi/10.1126/science.123.3191.309 Science

2. DeBerardinis RJ, Chandel NS. Fundamentals of cancer metabolism. Sci Adv. 2016;2(5):e1600200. https://www.science.org/doi/10.1126/sciadv.1600200 Science

3. DeBerardinis RJ, Chandel NS. Fundamentals of cancer metabolism. Sci Adv. 2016;2(5):e1600200. (Open-access version) https://pmc.ncbi.nlm.nih.gov/articles/PMC4928883/ PMC

4. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646–674. https://pubmed.ncbi.nlm.nih.gov/21376230/ PubMed

5. Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discov. 2022;12(1):31–46. https://pubmed.ncbi.nlm.nih.gov/35022204/ PubMed

6. Faubert B, Solmonson A, DeBerardinis RJ. Metabolic reprogramming and cancer progression. Science. 2020;368(6487):eaaw5473. https://www.science.org/doi/10.1126/science.aaw5473 Science

7. Ippolito L, et al. Lactate: A Metabolic Driver in the Tumour Landscape. Trends Cell Biol. 2019;29(10):748–762. https://www.sciencedirect.com/science/article/abs/pii/S0968000418302275 ScienceDirect

8. Pérez-Tomás R, Pérez-Guillén I. Lactate in the Tumor Microenvironment: An Essential Molecule in Cancer Progression and Treatment Resistance. Cancers (Basel). 2020;12(11):3244. https://pmc.ncbi.nlm.nih.gov/articles/PMC7693872/ PMC

9. Chen J, et al. Lactate and lactylation in cancer. Signal Transduct Target Ther. 2025;10:??? (online). https://www.nature.com/articles/s41392-024-02082-x Nature

10. Kawada K, et al. Mechanisms underlying 18F-fluorodeoxyglucose accumulation in colorectal cancer. Int J Clin Oncol. 2016;21(5):898–906. https://pmc.ncbi.nlm.nih.gov/articles/PMC5120247/ PMC

11. Salas JR, et al. Signaling Pathways That Drive 18F-FDG Accumulation in Cancer. J Nucl Med. 2022;63(5):659–666. https://jnm.snmjournals.org/content/63/5/659 Journal of Nuclear Medicine

12. Perry RJ, et al. Mechanistic Links between Obesity, Insulin, and Cancer. Trends Endocrinol Metab. 2020;31(10):684–695. https://pmc.ncbi.nlm.nih.gov/articles/PMC7214048/ PMC

13. Jee SH, et al. Obesity, Insulin Resistance and Cancer Risk. Yonsei Med J. 2005;46(3):449–455. https://pmc.ncbi.nlm.nih.gov/articles/PMC2815827/ PMC

14. American Cancer Society. Guideline for Diet and Physical Activity for Cancer Prevention. Updated May 5, 2025. https://www.cancer.org/cancer/risk-prevention/diet-physical-activity/acs-guidelines-nutrition-physical-activity-cancer-prevention/guidelines.html American Cancer Society

15. World Cancer Research Fund/AICR. Diet, Nutrition, Physical Activity and Cancer: A Global Perspective (Third Expert Report). 2018. https://www.wcrf.org/wp-content/uploads/2024/11/Summary-of-Third-Expert-Report-2018.pdf World Cancer Research Fund

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

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Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

---

David S. Klein, MD Functional Medicine Physician

Insulin Level and the Risk of Cancer, Diabetes: Berberine may be the Answer by Lowering Insulin while Lowering Glucose.

Nutraceutical Approaches to Lowering Insulin and Supporting Diabetes Management & Weight

Elevated Insulin Puts You at High Risk for Diabetes

Berberine: An AMPK Activator with Insulin-Lowering Effects

Berberine, an isoquinoline alkaloid extracted from plants like Berberis vulgaris, is one of the most extensively studied natural compounds for metabolic health. Its primary mechanism involves the activation of AMP-activated protein kinase (AMPK), often described as a “metabolic master switch.” By activating AMPK, berberine enhances glucose uptake in skeletal muscle, reduces hepatic glucose production, and improves overall insulin sensitivity. Clinical trials demonstrate that berberine can lower fasting glucose, HbA1c, and fasting insulin to an extent comparable with first-line pharmaceuticals such as metformin. Additional benefits include improvement in lipid profiles and favorable modulation of gut microbiota, both of which reduce the systemic inflammation that contributes to insulin resistance. Berberine lowers insulin and blood sugar simultaneously.

Berberine 500 mg take 1 capsule twice to four times, daily

Chromium Picolinate and Vanadyl Sulfate: Trace Elements Influencing Insulin Action

Chromium, especially in the form of chromium picolinate, functions as a cofactor that enhances insulin receptor activity and improves intracellular signaling. Supplementation has been shown in human trials to improve glucose tolerance, lower fasting glucose, and reduce insulin resistance — though effects tend to be most pronounced in individuals with suboptimal chromium status. Vanadyl sulfate, a form of the trace mineral vanadium, mimics insulin at the receptor level and activates downstream pathways to promote glucose uptake while suppressing hepatic glucose output. Clinical studies show that vanadyl sulfate can lower blood glucose and improve insulin sensitivity in type 2 diabetes, but its long-term use is limited by safety concerns related to gastrointestinal tolerance and potential toxicity. Both agents highlight how micronutrients can intersect with cellular insulin signaling, but they should be used with medical oversight.

Diabet Stat II Take 1 capsule twice daily

Inositol: Restoring Second Messenger Function in Insulin Signaling

Inositol, particularly myo-inositol and D-chiro-inositol, serves as a critical second messenger in insulin signaling. When this pathway falters, tissues become less responsive to insulin, perpetuating hyperinsulinemia. Supplementation with inositol has been shown to restore proper signaling, improving insulin sensitivity and lowering both glucose and fasting insulin levels. Clinical studies in women with polycystic ovary syndrome (a condition tightly linked to insulin resistance) show improved ovulation, reduced androgen excess, and better metabolic profiles. In the broader population with metabolic syndrome or diabetes, inositol supplementation has demonstrated modest improvements in HOMA-IR, triglycerides, and HbA1c, supporting its role as a low-risk adjunct to diet and exercise.

Inositol 500 mg capsules Take 2 twice daily

Olive Leaf Extract: Harnessing Polyphenols for Metabolic Health

Olive leaf extract, derived from Olea europaea, contains powerful polyphenols such as oleuropein and hydroxytyrosol, compounds also abundant in extra-virgin olive oil. These molecules exert antioxidant and anti-inflammatory effects but also act directly on glucose metabolism. Mechanistically, olive leaf polyphenols enhance glucose uptake in peripheral tissues, increase GLUT4 translocation, and reduce oxidative stress that impairs insulin signaling. Human trials have shown that olive leaf supplementation can lower fasting glucose and HbA1c while improving lipid profiles and reducing inflammatory markers. Because of its cardiovascular benefits and general safety, olive leaf extract is emerging as a promising complementary intervention for those at risk of or living with type 2 diabetes.

References

Berberine

1. Yin J, Xing H, Ye J. Efficacy of berberine in patients with type 2 diabetes mellitus. Metabolism. 2008;57(5):712-717. PubMed

2. Zhang Y, Li X, Zou D, et al. Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine. J Clin Endocrinol Metab. 2008;93(7):2559-2565. PubMed

3. Dong H, Wang N, Zhao L, Lu F. Berberine in the treatment of type 2 diabetes mellitus: a systemic review and meta-analysis. Evid Based Complement Alternat Med. 2012;2012:591654. PubMed

4. Deng Y, Zhang Q, Li Y, et al. Berberine attenuates insulin resistance by enhancing insulin signaling and AMPK pathway in high-fat diet induced obese mice. Nutrients. 2020;12(9):2688. PubMed

5. Lan J, Zhao Y, Dong F, et al. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. J Ethnopharmacol. 2015;161:69-81. PubMed

   
   

Chromium Polynicotinate & Vanadyl Sulfate

6. Anderson RA, Bryden NA, Polansky MM, et al. Chromium supplementation of human subjects: effects on glucose, insulin, and lipids. Metabolism. 1997;46(8):1-10. PubMed

7. Balk EM, Tatsioni A, Lichtenstein AH, Lau J, Pittas AG. Effect of chromium supplementation on glucose metabolism and lipids: systematic review of RCTs. Diabetes Care. 2007;30(8):2154-2163. PubMed

8. Martin J, Vincent JB. Mineral-dependent insulin-mimetic compounds: vanadium, chromium, zinc, and selenium. J Trace Elem Med Biol. 2007;21(1):59-65. PubMed

9. Bal A, Singh AK. Effect of vanadium and its compounds on carbohydrate metabolism. Endocr Pract. 2008;14(7):886-889. PubMed

10. Waring MJ, Sanders JA. Tolerance of diabetics to oral vanadyl sulfate. Diabetes Res Clin Pract. 1995;28(1):57-60. PubMed

    
    

Inositol & Olive Leaf Extract

11. Pintaudi B, Di Vieste G, Bonomo M. Myo-inositol may improve insulin resistance and metabolic syndrome in type 2 diabetes patients. Int J Endocrinol. 2016;2016:9132054. PubMed

12. Nestler JE, Jakubowicz DJ. Decreases in ovarian cytochrome P450c17α activity and serum free testosterone after reduction of insulin secretion in PCOS with D-chiro-inositol. N Engl J Med. 1999;340(17):1314-1320. PubMed

13. Konstantinidou V, et al. In vivo nutrigenomic effects of virgin olive oil polyphenols within the frame of the Mediterranean diet: modulation of inflammation and oxidative stress in humans. BMC Genomics. 2010;11:253. PubMed

14. Wainstein J, Ganz T, Boaz M, et al. Olive leaf extract improves insulin sensitivity in humans. J Med Food. 2012;15(7):605-610. PubMed

15. Lockyer S, Rowland I, Spencer JP, et al. Impact of phenolic-rich olive leaf extract on blood pressure, plasma lipids and inflammatory markers: randomized controlled trial. Eur J Nutr. 2017;56(4):1421-1432. PubMed

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

---

David S. Klein, MD Functional Medicine Physician