Supporting Cardiovascular Health and Recovery: What the Evidence Actually Shows

When I first wrote about recovering from a cardiovascular injury in 2022, many readers were searching for practical ways to support recovery from cardiovascular and vascular injury associated with COVID-19 infection and vaccination. The question people kept asking was simple:

“What can I do to help my body heal from CVD or cardiac injury or to improve cardiac health?”

Four years later, the foundational answer remains largely unchanged. There is still no magic pill. There is still no government-funded Manhattan Project focused on helping people recover from long-term cardiovascular injury. And there are still remarkably few large clinical trials evaluating inexpensive, unpatentable nutritional interventions, despite the scale of need.

Cardiovascular disease remains the leading cause of death in the United States, claiming nearly one million lives each year, and NIH spending specifically targeted toward heart and vascular disease research is about $2.1 billion annually. That may sound like a large number until one considers the scale of the problem: roughly one American dies from cardiovascular disease every 34 seconds.

We spend billions studying heart disease, yet devote comparatively little effort to implementing many low-cost interventions for which substantial evidence already exists.

Despite the government’s limited interest in rigorously evaluating many inexpensive approaches that could reduce the burden of cardiovascular disease, the evidence supporting several of the supplements discussed below has continued to accumulate. Looking back four years later, I am more confident in many of these recommendations than when I first wrote them. The data are stronger, the biological rationale is clearer, and the need for practical prevention has only become more apparent.

I have also expanded this essay beyond the specific context of COVID-related cardiovascular injury, because the underlying biology is not unique to that insult. Endothelial dysfunction, coagulation dysregulation, mitochondrial stress, and chronic inflammation are common pathways in cardiovascular disease broadly defined, whether the triggering event was a viral infection, a vaccination-associated adverse event, metabolic syndrome, or simply decades of aging under suboptimal conditions.

The core supplements remain: Vitamin K2-MK7 for vascular health and calcium regulation; magnesium for endothelial function, blood pressure, and metabolic resilience; and taurine, which has emerged as an increasingly important nutrient for cardiovascular function, glucose regulation, mitochondrial health, and healthy aging.

In this updated version, I add several additional agents whose evidence base has matured sufficiently to warrant serious discussion.

Why the Evidence Looks Different

Before proceeding, it is important to understand a structural problem in cardiovascular research. Many of the compounds discussed below will never be evaluated in the kind of massive, multi-center, randomized clinical trials that dominate modern medical evidence. The reason is not scientific. It is economic. These compounds cannot be patented. There is no realistic opportunity to generate the financial return required to justify spending hundreds of millions of dollars on a Phase III clinical trial of magnesium, taurine, vitamin D, or berberine.

That does not mean the evidence is weak. It means the evidence comes from a different place. Instead of a handful of blockbuster clinical trials, it is assembled from smaller randomized studies, epidemiologic observations, laboratory research, physiological understanding, and decades of clinical experience. None of these sources of evidence are perfect. Neither are large clinical trials, for that matter. Each has strengths and limitations.

The absence of a funded Phase III trial does not mean the absence of evidence. It means we must examine the available data carefully, weigh the totality of the evidence, and remain honest about the limits of our knowledge. Throughout this review, I will try to distinguish between what is well supported, what appears promising, and what remains genuinely uncertain.

For more than four years, one of the most common questions I have received has been simple:

“What can I do to help my body heal?”

It is a reasonable question. Millions of people have experienced cardiovascular and vascular problems associated with aging, metabolic disease, COVID-19, or mRNA COVID-19 vaccine injury. Yet remarkably little effort has been devoted to studying inexpensive interventions that might support recovery.

The discussion below is not based on pharmaceutical marketing, government guidance, or internet folklore. It is based on a careful review of the scientific literature, clinical experience, and years of conversations with physicians and researchers grappling with these issues.

No pharmaceutical company sponsored this work. No government grant paid for the hours spent reviewing the evidence. Independent scientific analysis only exists because readers choose to support it.

In the full article below, I review what has held up over the last four years, what has not, and which supplements have accumulated the strongest evidence for supporting cardiovascular and vascular health.

The Vascular Foundation:

Vitamin K2-MK7

Vitamin K2 in the MK7 form remains one of the most compelling supplements for supporting vascular health. Its primary mechanism is the activation of matrix Gla protein (MGP), the most potent known inhibitor of vascular calcification. In the absence of sufficient K2, MGP remains undercarboxylated and inactive, and calcium that should deposit in bone instead accumulates in arterial walls.

Arterial calcification is not merely a marker of cardiovascular disease; it is a direct contributor to arterial stiffness, reduced vascular compliance, and elevated systolic blood pressure. The Rotterdam Study, one of the largest prospective cohort studies examining dietary K2 intake, found that higher K2 consumption was associated with significantly reduced cardiovascular mortality and aortic calcification, associations that were not observed for K1.

The MK7 form is preferred over MK4 due to its substantially longer half-life, which provides more stable tissue saturation with once-daily dosing. Typical supplemental doses range from 90 to 200 micrograms daily. Individuals on vitamin K antagonist anticoagulants (warfarin) should not supplement without close physician supervision.

In the context of cardiovascular disease, K2 addresses one of the most underappreciated contributors to long-term vascular aging: the slow, progressive mineralization of arterial tissue that accelerates after midlife and is dramatically worsened by K2 insufficiency.

Magnesium

Magnesium deficiency is among the most common nutritional insufficiencies in industrialized populations, with surveys consistently suggesting that 50% or more of adults fail to meet recommended intakes. The cardiovascular consequences are substantial.

Magnesium deficiency has become remarkably common in the United States. The causes are multiple. Modern agricultural practices have gradually depleted magnesium from many soils, food processing removes much of the magnesium naturally present in grains and other foods, and Americans consume far fewer magnesium-rich foods such as leafy greens, legumes, nuts, and seeds than previous generations. At the same time, chronic stress, alcohol consumption, certain medications, high sugar intake, diabetes, and aging all increase magnesium requirements or losses.

This matters because magnesium participates in more than 300 enzymatic reactions throughout the body. It influences blood pressure regulation, glucose metabolism, cardiac rhythm, vascular function, inflammation, and even the activation and utilization of vitamin D. Yet magnesium status is rarely assessed in routine medical care, and standard serum magnesium measurements often fail to detect deficiencies within tissues. In many respects, magnesium may be one of the most overlooked nutrients in cardiovascular health.

Magnesium functions as a physiological calcium antagonist. It is required for proper endothelial function, vascular smooth muscle relaxation, cardiac rhythm stability, glucose metabolism, and the activity of hundreds of enzymatic reactions. Epidemiological data consistently associate lower magnesium status with higher rates of hypertension, coronary artery disease, cardiac arrhythmia, and metabolic syndrome.

Intervention studies have shown that magnesium supplementation can meaningfully lower blood pressure, improve insulin sensitivity, reduce inflammatory markers, and support a healthy heart rhythm, particularly in individuals who are deficient to begin with.

For supplementation, form matters. Magnesium oxide, the cheapest and most commonly sold form, is poorly absorbed. Better-tolerated and better-absorbed options include magnesium glycinate, malate, threonate (which has particular affinity for neural tissue), and citrate. Typical therapeutic doses range from 200 to 400 mg elemental magnesium daily. Individuals with kidney disease should consult their physician before supplementing.

Magnesium should be considered in combination with vitamin K2, A, and vitamin D, as these three nutrients interact closely in calcium metabolism and vascular physiology.

Taurine

Taurine has moved considerably toward the mainstream since I first wrote about it in 2022. A landmark 2023 study published in Science found that taurine levels decline significantly with aging in multiple species, and that taurine supplementation extended healthy lifespan and improved multiple markers of metabolic and physiological function in animal models. While we must always be cautious in extrapolating from animal data, the biological plausibility in humans is substantial.

In the cardiovascular system specifically, taurine supports endothelial function, reduces oxidative stress in cardiac tissue, moderates blood pressure through effects on the renin-angiotensin system, and appears to improve glucose regulation and mitochondrial efficiency. It is particularly concentrated in cardiac muscle, where it plays structural roles in membrane stabilization.

Taurine is conditionally essential. The body synthesizes it, but synthesis may be insufficient under conditions of metabolic stress, aging, or illness. It is found primarily in animal-derived foods; vegetarians and vegans are at greater risk of insufficiency. Supplemental doses of 1 to 3 grams daily are generally well tolerated with an excellent safety profile.

Energy and Metabolic Support

Coenzyme Q10 (CoQ10)

CoQ10 is a naturally occurring molecule found in every cell, where it plays a central role in the mitochondrial electron transport chain, the process by which cells generate ATP, the fundamental currency of cellular energy. The heart is among the most metabolically demanding organs in the body and contains some of the highest concentrations of CoQ10 in human tissue.

Two factors make CoQ10 clinically relevant for a broad population: aging and statin therapy. CoQ10 levels decline substantially with age. Statin medications, among the most widely prescribed drugs in the world, inhibit the same mevalonate pathway used to synthesize CoQ10, a biochemical consequence that is often underappreciated in clinical practice.

The strongest evidence for CoQ10 supplementation comes from heart failure, where the Q-SYMBIO randomized trial demonstrated that CoQ10 at 300 mg daily significantly reduced major adverse cardiac events compared to placebo over two years. Evidence also supports its use in statin-associated myopathy, mitochondrial disorders, and as an antioxidant in settings of elevated oxidative stress.

CoQ10 comes in two forms: ubiquinone (oxidized) and ubiquinol (reduced, the active antioxidant form). Ubiquinol may be better absorbed, particularly in older individuals whose capacity to convert ubiquinone is diminished. Typical doses range from 100 to 300 mg daily; CoQ10 is fat-soluble and should be taken with a meal containing fat.

For patients on statins, individuals with established heart failure or cardiomyopathy, and those experiencing unexplained fatigue or muscle symptoms, CoQ10 is one of the more biologically plausible and evidence-supported supplements in this category.

Berberine

Berberine is an alkaloid found in several botanical species that has attracted growing attention for its effects on metabolic health. Cardiovascular disease and metabolic disease are intimately linked. Elevated blood glucose, insulin resistance, dyslipidemia, and chronic low-grade inflammation all contribute to endothelial damage and accelerate atherosclerosis. Interventions that address metabolic dysfunction are therefore relevant to cardiovascular risk.

Berberine appears to act primarily through activation of AMP-activated protein kinase (AMPK), a master regulator of cellular energy metabolism. Through this and related mechanisms, berberine has demonstrated the ability to improve insulin sensitivity, lower fasting glucose and hemoglobin A1c, reduce LDL cholesterol, and lower triglycerides in multiple randomized trials, several of which showed effect sizes comparable to metformin or low-dose statins.

A note of caution is warranted, however. Berberine inhibits certain cytochrome P450 enzymes and drug transporters, creating the potential for clinically meaningful interactions with medications including cyclosporine, some statins, and anticoagulants. Anyone on prescription medications should review potential interactions before initiating berberine.

Berberine is not a substitute for dietary improvement, regular physical activity, or weight loss, which remain the most powerful interventions for metabolic syndrome. It may, however, provide meaningful adjunctive support for individuals struggling to achieve adequate metabolic control through lifestyle means alone. Typical doses range from 500 mg two to three times daily with meals.

Newer formulations, such as dihydroberberine, have also been developed to improve absorption and bioavailability.

Targeting Coagulation and Fibrinolysis

Nattokinase and Serrapeptase

These two enzymes have attracted particular interest in the context of post-COVID vascular injury, where microthrombi, fibrin deposition, and impaired fibrinolysis have been implicated in persistent symptoms including fatigue, dyspnea, cognitive impairment, and exercise intolerance.

Nattokinase is a serine protease derived from natto, a traditional Japanese fermented soybean preparation. It has demonstrated fibrinolytic activity, specifically the capacity to degrade fibrin clots, in both in vitro and animal studies, with more limited but suggestive human data showing reductions in fibrinogen and blood viscosity. It appears to work through direct fibrin degradation as well as stimulation of endogenous tissue plasminogen activator (tPA).

Serrapeptase is a proteolytic enzyme originally derived from the gut of Bombyx mori silkworms and now produced through bacterial fermentation. It has demonstrated anti-inflammatory and fibrinolytic properties in animal models and some human studies, with potential effects on biofilm degradation and reduction of abnormal protein deposits.

The limitations of the evidence are that well-designed, adequately powered randomized controlled trials in humans are sparse. Much of the enthusiasm for these agents in post-COVID contexts rests on mechanistic plausibility, case reports, and small observational series rather than rigorous clinical trial data. That said, the biological rationale, supporting normal fibrinolytic activity in individuals with evidence of hypercoagulability, is coherent, and the safety profile of both agents appears acceptable in otherwise healthy individuals at standard doses.

Important practical considerations: both agents carry theoretical bleeding risk and should not be combined with anticoagulants or antiplatelet drugs without physician oversight. Nattokinase supplements should not contain vitamin K2 if coagulation monitoring is a concern, as the two have opposing effects on clotting pathways. Both should be taken on an empty stomach for optimal absorption.

As an aside, I recently restarted nattokinase on the advice of my personal physician, the logic being that my body continues to produce a high circulating blood titer of anti-spike antibodies. This might be the consequence of the continued production of the spike protein. I do not take any other form of blood thinners. I developed a substantial local hematoma (blood in tissue) after bonking my shin with a big block of wood. Then I noticed that a razor nick kept bleeding for a long time, and nothing seemed to stop the (minor, annoying) bleeding. I stopped the nattokinase, and my blood clotting returned to normal. So, this is not an “academic” issue. Oral nattokinase should be treated like any other type of anticoagulant or antiplatelet medication and used under medical supervision.

Anti-Inflammatory and Antioxidant Support

Omega-3 Fatty Acids

The evidence base for omega-3 fatty acids in cardiovascular disease has matured considerably over the past decade, and the picture is more nuanced than the early enthusiasm suggested.

High-dose prescription omega-3 preparations, specifically icosapentaenoic acid (EPA) in pure form, have demonstrated significant reductions in cardiovascular events in high-risk patients with elevated triglycerides, as shown in the REDUCE-IT trial. This benefit appears to be specific to high-dose pure EPA; the STRENGTH trial, which used a combined EPA/DHA formulation, did not replicate these findings, suggesting that the cardiovascular benefit may be dose-dependent, formulation-dependent, or related to specific mechanisms of EPA that are not shared by DHA.

For general use, omega-3 supplementation reliably lowers triglycerides in a dose-dependent fashion and has anti-inflammatory effects that are biologically plausible in the context of vascular injury. The evidence for reduction in hard cardiovascular endpoints with standard consumer supplement doses (1 to 2 grams daily) is less robust.

When supplementing, quality matters: fish oil is prone to oxidation, which may attenuate or reverse its benefits. Choose products with third-party testing for oxidation markers (TOTOX values), store them in the refrigerator, and discontinue use if the product smells rancid.

Omega-3s at higher doses have mild antiplatelet effects; this is generally not a clinical concern at standard supplement doses but warrants awareness in individuals on anticoagulation therapy.

Resveratrol and Polyphenols

Resveratrol became a subject of enormous scientific interest in the mid-2000s following discoveries that it activates sirtuins, longevity-associated proteins, and mimics some effects of caloric restriction in animal models. Human clinical trials have been considerably more sobering.

The bioavailability of resveratrol is poor; it is rapidly metabolized after absorption, limiting sustained systemic exposure. Clinical trials in humans have produced mixed results, with some showing modest improvements in metabolic markers, blood pressure, or inflammatory indices, and others showing no significant benefit. A major methodological issue is that effective doses in animal models translate to impractically large quantities in humans.

The more compelling story may lie not in resveratrol specifically but in dietary polyphenols broadly. Epidemiological evidence consistently associates high dietary polyphenol intake, from vegetables, fruits, olive oil, green tea, dark chocolate, and red wine in moderation, with reduced cardiovascular risk. Whether this reflects the direct actions of specific polyphenols, their effects on the gut microbiome, or simply the overall dietary pattern in which polyphenol-rich foods tend to appear is difficult to disentangle.

Pterostilbene, a methylated analog of resveratrol found in blueberries, has better bioavailability and has shown promise in preclinical and small human studies for blood pressure and lipid effects. It merits watching as the evidence matures.

My practical recommendation: prioritize polyphenol-rich whole foods over supplements. If supplementing, maintain realistic expectations; the evidence does not support dramatic cardiovascular effects from resveratrol supplementation at currently available doses. The strongest signal remains dietary.

Dietary Fiber

This recommendation does not sell supplement bottles, but it is supported by as strong an evidence base as anything else in this essay.

Adequate dietary fiber intake consistently improves metabolic health, glucose regulation, cholesterol metabolism, and gut microbial diversity. Soluble fiber in particular, from sources such as psyllium husk, oats, legumes, and many vegetables and fruits, has repeatedly demonstrated favorable effects on LDL cholesterol, blood pressure, insulin sensitivity, and inflammatory markers.

Meta-analyses of psyllium supplementation show LDL reductions comparable to low-dose statin therapy in some populations. The evidence is not obscure; it is simply not profitable, so it receives little attention relative to proprietary supplement blends with far weaker evidentiary backing.

For individuals whose dietary fiber intake falls short of the recommended 25 to 38 grams daily, which describes the majority of adults in Western populations, addressing this deficit is likely to provide measurable cardiovascular benefit.

Vitamin D: A Prerequisite, Not a Therapy

Some readers may wonder why vitamin D does not appear more prominently in this essay. The answer is simple: I consider vitamin D to be foundational. It is not merely another supplement on a list. Vitamin D functions more like a hormone than a traditional vitamin and plays critical roles in immune regulation, vascular biology, muscle function, calcium metabolism, and metabolic health.

Critics often point to large clinical trials such as VITAL and D-HEALTH, which failed to demonstrate dramatic reductions in cardiovascular events from routine vitamin D supplementation. But these studies share a fundamental limitation. Most administered a fixed dose of vitamin D without targeting a specific blood level, and many enrolled participants who were not substantially deficient to begin with. That is analogous to studying blood pressure treatment without measuring blood pressure, or evaluating statins without measuring cholesterol. If vitamin D status is what matters biologically, then supplement dose is only a crude surrogate.

After decades of research, it is difficult to ignore another uncomfortable observation. Many of the largest and most influential vitamin D trials were designed around doses that many experts would now consider insufficient to achieve optimal blood levels in a substantial portion of participants. This approach has repeatedly generated studies that are well suited to demonstrate a lack of effect while leaving the central biological question unresolved.

My view remains that maintaining a 25-hydroxyvitamin D level in the range of approximately 50-70 ng/mL is one of the fundamental pillars of long-term health. Vitamin D should not be viewed primarily as a drug directed at a single disease endpoint. It is a nutrient-hormone that influences a broad range of biological processes, including immune function, inflammation, calcium regulation, skeletal integrity, metabolic health, and cardiovascular physiology. For that reason, I view optimization of vitamin D status not as a targeted cardiovascular intervention, but as a prerequisite for many other preventive and therapeutic strategies to function optimally.

Vitamin D should always be considered alongside magnesium, vitamin K2, vitamin A, and zinc. Magnesium is required for vitamin D metabolism and activation. Vitamin K2 helps ensure that calcium absorbed under the influence of vitamin D is directed to the tissues where it belongs. Vitamin A and zinc participate in many of the same cellular signaling and gene regulatory pathways through which vitamin D exerts its effects. These nutrients function as an integrated system. Focusing on vitamin D alone while ignoring the others risks missing the broader biological context in which it operates.

Practical Synthesis

None of these supplements substitutes for the interventions with the strongest evidence in cardiovascular medicine. The foundation remains a whole-food diet emphasizing nutrient density, adequate protein, fiber, healthy fats, minimal refined carbohydrates, and minimal ultra-processed foods, combined with regular physical activity, adequate sleep, avoidance of smoking, moderation of alcohol consumption, and management of chronic stress. No supplement can compensate for the metabolic consequences of getting these fundamentals wrong.

A reasonable foundation for most adults concerned about cardiovascular and metabolic health begins with maintaining adequate vitamin D status, ideally confirmed by periodic measurement of serum 25-hydroxyvitamin D levels, with a target of 50 to 70 ng/mL.

• Vitamin D3 should be considered alongside magnesium, vitamin K2, zinc, and vitamin A, which participate in overlapping physiological pathways.

• Magnesium glycinate, malate, or taurate in the range of 200–400 mg daily is a practical starting point for many adults.

• Vitamin K2-MK7 at 100–200 mcg daily may help support appropriate calcium distribution, while zinc at 15–30 mg daily supports immune, metabolic, and vascular health.

• Taurine at 1–2 grams daily has a growing evidence base for supporting cardiovascular function.

• High-quality omega-3 fatty acids are most useful when regular consumption of fatty fish is low. CoQ10 becomes particularly relevant for individuals taking statins or those with established cardiovascular disease.

• Berberine is best targeted toward individuals with insulin resistance, metabolic syndrome, or impaired glucose regulation.

• Nattokinase at appropriate dosages may have a role in supporting fibrinolytic balance, particularly in selected individuals with post-COVID sequelae, although clinical evidence remains incomplete.

As always: these decisions should be made in conversation with a knowledgeable physician, particularly if you are taking prescription medications or have significant medical comorbidities. Some of these agents carry real interaction risks that are not trivial.

The absence of a funded clinical trial does not mean the absence of evidence. It means we must examine the available data carefully, draw reasonable conclusions from biology and physiology where clinical trials are lacking, and remain appropriately humble about what we know, what we suspect, and what remains uncertain.

That standard has not changed since 2022. And it remains the right one.

References

Vitamin K2 and Vascular Health

1. Geleijnse, Johanna M., Cees Vermeer, Diederick E. Grobbee, Leon J. Schurgers, Marjo H. J. Knapen, Irene M. van der Meer, Albert Hofman, and Jacqueline C. M. Witteman. “Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study.” Journal of Nutrition 134, no. 11 (2004): 3100–3105.

2. Schurgers, Leon J., Henri M. H. Spronk, Birgit A. M. Soute, Paul M. Schiffers, Jo G. R. De Mey, and Cees Vermeer. “Regression of Warfarin-Induced Medial Elastocalcinosis by High Intake of Vitamin K in Rats.” Blood 109, no. 7 (2007): 2823–2831.

3. Knapen, Marjo H. J., Narrow Braam, Leon J. Schurgers, and Cees Vermeer. “Vitamin K2 Supplementation Improves Hip Bone Geometry and Bone Strength Indices in Postmenopausal Women.” Osteoporosis International 18, no. 7 (2007): 963–972.

Magnesium

4. Rosanoff, Andrea, Connie M. Weaver, and Robert K. Rude. “Suboptimal Magnesium Status in the United States: Are the Health Consequences Underestimated?” Nutrition Reviews 70, no. 3 (2012): 153–164.

5. Qu, Xuan, Fan Jin, Ye Hao, Hao Li, Tingting Tang, Huiwu Li, and Kerong Dai. “Magnesium and the Risk of Cardiovascular Events: A Meta-Analysis of Prospective Cohort Studies.” PLOS ONE 8, no. 3 (2013): e57720.

6. Razzaque, Mohammed S. “Magnesium: Are We Consuming Enough?” Nutrients 10, no. 12 (2018): 1863.

Taurine

7. Singh, Parminder, Kishore Gollapalli, Stefano Mangiola, Arne Schranner, Mohit A. Bhanu Bhanu, Mani Mohapatra, Shankar Prabu, et al. “Taurine Deficiency as a Driver of Aging.” Science 380, no. 6649 (2023): eabn9257.

8. Militante, Joan D., and John B. Lombardini. “Treatment of Hypertension with Oral Taurine: Experimental and Clinical Studies.” Amino Acids 23, no. 4 (2002): 381–393.

Coenzyme Q10

9. Mortensen, Svend Aage, Franklin Rosenfeldt, Adarsh Kumar, Peter Dolliner, Attilio J. Filipiak, Daniel Pella, Umberto Alehagen, Gian-Paolo Littarru, and Guy D. Folkers. “The Effect of Coenzyme Q10 on Morbidity and Mortality in Chronic Heart Failure: Results From Q-SYMBIO.” JACC: Heart Failure 2, no. 6 (2014): 641–649.

10. Littarru, Gian Paolo, and Luca Tiano. “Bioenergetic and Antioxidant Properties of Coenzyme Q10: Recent Developments.” Molecular Biotechnology 37, no. 1 (2007): 31–37.

11. Caso, Graziamaria, Paul Kelly, Mark A. McNurlan, and Wayne E. Lawson. “Effect of Coenzyme Q10 on Myopathic Symptoms in Patients Treated with Statins.” American Journal of Cardiology 99, no. 10 (2007): 1409–1412.

Berberine

12. Yin, Jun, Huili Xing, and Jianping Ye. “Efficacy of Berberine in Patients with Type 2 Diabetes Mellitus.” Metabolism 57, no. 5 (2008): 712–717.

13. Zhang, Yifei, Xiaoying Li, Dajin Zou, Wei Liu, Jialin Yang, Na Zhu, Li Huo, et al. “Treatment of Type 2 Diabetes and Dyslipidemia with the Natural Plant Alkaloid Berberine.” Journal of Clinical Endocrinology and Metabolism 93, no. 7 (2008): 2559–2565.

14. Lan, Jiong, Yanyun Zhao, Fenfen Dong, Zhiyong Shi, Jianwei Zheng, Jing Fan, and Guofang Sun. “Meta-Analysis of the Effect and Safety of Berberine in the Treatment of Type 2 Diabetes Mellitus, Hyperlipemia and Hypertension.” Journal of Ethnopharmacology 161 (2015): 69–81.

Nattokinase and Serrapeptase

15. Kurosawa, Yutaka, Takeshi Nirengi, Takayuki Homma, Kazuki Esaki, Mayumi Ohta, Tatsuro Jo, and Toshiharu Takamatsu. “A Single-Dose of Oral Nattokinase Potentiates Thrombolysis and Anti-Coagulation Profiles.” Scientific Reports 5 (2015): 11601.

16. Ero, M. P., M. K. Ng, C. A. Mihailovski, N. R. Harvey, and B. H. Alexander. “A Pilot Study of the Serolytic Activities of Serrapeptase, Nattokinase and the Seaprose-S.” Asian Pacific Journal of Tropical Biomedicine 3, no. 3 (2013): 209–213.

Omega-3 Fatty Acids

17. Bhatt, Deepak L., P. Gabriel Steg, Michael Miller, Eliot A. Brinton, Terry A. Jacobson, Steven B. Ketchum, Ralph T. Doyle, Jr., et al. “Cardiovascular Risk Reduction with Icosapentaenoic Acid for Hypertriglyceridemia.” New England Journal of Medicine 380, no. 1 (2019): 11–22.

18. Nicholls, Stephen J., Ariel Lincoff, Michelle Garcia, Deepak Bhatt, Neal Baran, Christie Ballantyne, M. John Chapman, et al. “Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk: The STRENGTH Randomized Clinical Trial.” JAMA 324, no. 22 (2020): 2268–2280.

Resveratrol and Polyphenols

19. Baur, Joseph A., and David A. Sinclair. “Therapeutic Potential of Resveratrol: The In Vivo Evidence.” Nature Reviews Drug Discovery 5, no. 6 (2006): 493–506.

20. Chachay, Veronique S., George A. Macdonald, Jennifer H. Martin, Jonathan P. Whitehead, Terrence J. O’Moore-Sullivan, Philip Lee, Matthew Franklin, et al. “Resveratrol Does Not Benefit Patients with Nonalcoholic Fatty Liver Disease.” Clinical Gastroenterology and Hepatology 12, no. 12 (2014): 2092–2103.

21. Zamora-Ros, Raul, Augustin Scalbert, Nadia Slimani, Aurelie Knaze, Vanessa Romieu, Isabelle Romieu, Heinz Freisling, et al. “Like-for-Like Comparison of Urinary Biomarkers of Polyphenol Exposure and Estimated Dietary Polyphenol Intake in 8-Hour Spot versus 24-Hour Collected Urine Samples.” European Journal of Nutrition 55, no. 3 (2016): 1179–1189.

Dietary Fiber

22. Giacco, Rosalba, Gabriella Costabile, and Angela A. Rivellese. “Dietary Fibre in Treatment of Diabetes: From Hypothesis to Facts.” Diabetologia 58, no. 7 (2015): 1478–1483.

23. Wei, Z. H., H. Wang, X. Y. Chen, B. S. Wang, Z. X. Rong, B. S. Wang, B. H. Su, and H. Chen. “Time- and Dose-Dependent Effect of Psyllium on Serum Lipids in Mild-to-Moderate Hypercholesterolemia: A Meta-Analysis of Controlled Clinical Trials.” European Journal of Clinical Nutrition 63, no. 7 (2009): 821–827.

Vitamin D

24. Manson, JoAnn E., Nancy R. Cook, I-Min Lee, William Christen, Shari S. Bassuk, Stephanie Mora, Heike Gibson, et al. “Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease.” New England Journal of Medicine 380, no. 1 (2019): 33–44.

25. Scragg, Robert, Mason Kaufman, Carlos A. Camargo, Jr., Rachael L. Morton, Ian R. Reid, Carlene M. M. Lawes, Andrew Grey, et al. “Effect of Monthly High-Dose Vitamin D Supplementation on Cardiovascular Disease in the D-HEALTH Trial: A Randomised Controlled Trial.” Lancet Diabetes and Endocrinology 9, no. 12 (2021): 764–773.