Dr. Vliet’s Health Tip: Healthy Blood Vessels: Protect Your Pipes Before They Burst!

© by Elizabeth Lee Vliet MD and Kathy Kresnik

Damage to blood vessels is a seriously escalating, but tragically hidden, problem not really addressed in most primary care and cardiology practices.  Small vessel damage silently progresses and leads to heart attacks, strokes, kidney trouble, gut dysfunction, and brain damage including memory loss and more serious cognitive decline, including dementia.

Vascular damage and dysfunction, primarily to the lining of the blood vessels (endothelium) has many causes but has skyrocketed since 2021 due specifically to the COVID injections and their ongoing spike protein production, as well as the COVID illness syndromes to a lesser extent.  There are many additional causes often not addressed in medical settings today:

• environmental chemicals (endocrine disrupters, microplastics, glyphosate, pesticides, herbicides)
• dietary toxins and highly processed foods high in seed oils, trans fats, sugars, and synthetic additives
• lifestyle factors with lack of exercise, sunlight and sleep
• decline in testicular and ovarian hormones (due to above combined adverse effects) adds to endothelium damage and fragility of the blood vessel walls.

Reproductive hormone damage affects every aspect of our health, but most doctors never even think about this factor, and certainly rarely ever check ovarian or testicular hormone levels unless someone is undergoing treatment for infertility.  That’s why I continue to emphasize the overlooked hormone connections in our Faith Over Fear programs and Health Tips.  As a physician in active medical practice, I think identifying risk factors and then taking active steps to protect your blood vessels is one of the most important steps you can take for optimal health and resilience to recover from illness or surgery, and for improved longevity.

Damage to blood vessels is a core driver of heart attacks, strokes, kidney disease, and other major illnesses, making vascular health one of the most important determinants of overall health today.

REALITY: The data shows devastating damage:

• Cardiovascular diseases (CVD)—disorders of the heart and blood vessels—are the leading cause of death worldwide, responsible for about 17.9–19 million deaths per year This translates to roughly one in three global deaths due to CVD.
• Recent global burden reports confirm that CVD remains the top cause of disability‑adjusted life years (DALYs), with hundreds of millions of years of disability attributed to CVD in 2023.
• In the U.S., heart disease and stroke remain the leading causes of death, exceeding all combined deaths from cancers and accidents!

Vascular dysfunction plays a KEY ROLE in Disease:

• Endothelial and vascular dysfunction are central mechanisms that dominate the CVD category: atherosclerosis, hypertension, ischemic heart disease, stroke (also vascular types of dementia from cumulative mini-strokes).
• Chronic kidney disease (CKD) and cardiometabolic disease meta-analyses reviews emphasize that endothelial dysfunction (impaired regulation of tone, inflammation, coagulation, and vascular remodeling) is an independent predictor of cardiovascular events, organ failure, and death.
• Vascular dysfunction also contributes to complications in other systems—loss of muscle (leading to loss of strength and exercise tolerance), gut disorders, kidney disease, and brain damage/cognitive decline—further supporting its role as a major driver of disease.

WARNING: The choices YOU make each day can help you avoid being a victim of this silent disease!

Seven Major Action Steps YOU Can Choose to BEGIN NOW:

These core strategies are well supported by world-wide outcomes data for many years.  I teach my patients these steps to protect blood vessels to decrease overall cardiovascular risk:

1. Don’t smoke or vape

• Smoking/vaping directly, plus exposure to secondhand smoke, both damage the lining of arteries, promote clotting, and increase blood pressure and heart rate.
• Quitting smoking can make a difference at any age. Quitting rapidly lowers heart attack and stroke risk compared with those who continue to smoke.

2. Move your body daily!

• Regular physical movement—even simple walking—improves endothelial function, lowers blood pressure, improves cholesterol and blood sugar, improves cellular oxygenation (reduces oxidate stress from being sedentary),  and reduces inflammation.
• Count your steps with a wrist tracker and aim for 5000 to 10, 000 steps most days of the week, even if you aren’t in shape for more aerobic activity.
• As strength and exercise tolerance improves, aim for at least about 150 minutes per week of moderate activity (like brisk walking, cycling, swimming, QiGong, Tai Chi, Pilates).  Then add in resistance training 2-3 times a week for added vascular benefit.

3. Eat a blood vessel-friendly diet

• A Mediterranean-style pattern rich in vegetables, fruits, whole grains, nuts, beans, olive oil, fish, grass-fed lamb/beef or venison all work together to improve endothelial function and the health of blood vessels, which results in lower blood pressure, reductions in LDL, glucose, insulin excess, and oxidative stress.
• If you want to reduce damage to blood vessels with plaque buildup and improve your long-term health and vitality, you simply must eliminate or markedly reduce your intake of ultra-processed foods loaded with chemical additives, artificial flavors and colors, added sugars, trans fats, excess saturated fats.

4. Maintain healthy weight, sleep habits, and stress management

• Healthy body weight, good quality and adequate duration of sleep, and limiting excessive alcohol all work together to improve blood pressure, insulin sensitivity, and lipid profiles, all of which in turn combine to have protective effects on blood vessel walls.
• Stress management techniques (relaxation exercise, prayer/meditation, biofeedback, visualization exercises, social support) PLUS quality and optimal duration of sleep comine to reduce cardiovascular risk by many mechanisms, including reduction harmful effects of stress hormones: cortisol and catecholamine excess for example.

5. Take a Natural Approach: Top Nutraceuticals that Promote Vascular Health

There are a number of nutraceutical supplements that have evidence for supporting vascular health overall, and we have addressed those in previous articles.  But there are two powerful tools for specifically improving the health of both the microvascular blood vessels and our larger blood vessels, and I have included these products in our Truth for Health store. But – KEEP IN MIND! Supplements are “add‑ons” to—not substitutes for—lifestyle and risk‑factor control steps I already listed above IN Steps 1-4. I always recommend a comprehensive, integrated approach to maximize success in improving your health and preventing disease.

Polyphenols and Flavanols

• Cocoa flavanols improve flow‑mediated dilation, lower blood pressure slightly, and reduce markers of endothelial injury in healthy and older adults.  Pro-tip: Add a teaspoon of raw cacao to your morning coffee or to a cup of warm milk with a teaspoon of raw, unfiltered honey for an evening treat.
• Broader polyphenol‑rich extracts (grape seed, green tea, mixed botanical blends, citrus flavonoids) can enhance nitric oxide availability, reduce inflammation and oxidative stress, and reduce arterial stiffness in small trials and a recent multi‑compound nutraceutical study.

These polyphenols and flavanols can be found in two of our most popular supplements:  Endocalyx Pro™ and TruMicroVascular™. Interestingly, these products are similar but uniquely different in their role and mechanism in protecting the vascular system – and that is why I elected to carry both in our store. These two products work on different aspects of the vascular system and complement each other, so it is hard to pick a favorite!

However, it has created some confusion. I am frequently asked “What is the difference between Endocalyx Pro™  and TruMicroVascular™? “Which is better?”  “Can I take both?” That’s one of the big reasons I wanted to provide this article describing both, in a side-by-side comparison, and answer these questions.  After I discuss Step 6 next,  I discuss these two products in more detail, including the side-by-side comparison, plus we have resources at end for additional information and background on the science.

6. Maintain and optimize sex hormones

I. Estradiol (E2) l for women – Estradiol, the primary active form of estrogen prior to menopause—E2 is NOT the same as estrone (E3) dominant post-menopausal estrogen, Estriol (E3) primarily made by placenta during pregnancy, or Estetrol (E4) made only by the fetal lliver during pregnancy).  E2 crucial beneficial effects prior to menopause (and lost at menopause) include many that support endothelial health through several complementary mechanisms that enhance nitric oxide bioavailability, reduce inflammation, and limit atherogenesis:

• Estradiol (E2) rapidly activates endothelial nitric oxide synthase (eNOS) via membrane estrogen receptor‑α, PI3K–Akt, MAPK and calcium‑dependent pathways, increasing nitric oxide (NO) production within minutes which promotes vasodilation.
• E2 increases eNOS expression at the transcriptional level and stabilizes eNOS mRNA, sustaining higher baseline NO output over time.
• AMPK activation by estradiol enhances eNOS catalytic activity and its association with HSP90, further boosting NO bioavailability independent of changes in eNOS phosphorylation.
• ·E2 improves flow‑mediated dilation and reduces vasoconstrictor tone by increasing endothelial NO and improving NO signaling, which is central to endothelial health.

Estradiol additional anti‑atherosclerotic and vascular structural effects:

• Experimental and animal models consistently show that 17β‑estradiol reduces atherosclerotic plaque formation and progression, partly via enhanced NO, reduced oxidative stress, and favorable lipid and vascular wall benefits.
• Estradiol attenuates vascular smooth muscle cell proliferation and migration after injury, a key mechanism in limiting blood vessel intima hyperplasia and new stenosis (narrowing) of blood vessels.
• E2 modulates matrix remodeling and endothelial repair, supporting maintenance of an intact, endothelial surface that is less likely to trigger formation of blood clots (thromboses).
• 17β‑estradiol studies show more robust improvement in endothelial function and greater inhibition of plaque development than seen with any with other estrogens: equilin (one of the horse estrogens in Premarin), generic conjugated (equine) estrogens, or estrone, estriol.
• Inflammation, immune signaling, and thrombosis: Estradiol down‑regulates key endothelial inflammatory pathways, reducing expression of adhesion molecules and lowering cytokines such as TNF‑α and IL‑1β in younger vessels, thereby decreasing leukocyte adhesion and vascular inflammation.
  • These anti‑inflammatory effects appear age‑ and timing‑dependent: vessels from older, long‑term estrogen‑deficient animals and post-menopausal women years after natural or surgical menopause without hormone therapy, show a shift over time where too much added estrogen doesn’t have these many benefits or could even become neutral or even pro‑inflammatory.
  • Oral estrogen can potentially increase coagulation risk, and increase liver production of CRP and fibrinogen.  Transdermal patch, gel or vaginal delivery of physiologic 17-beta estradiol has the opposite effect: helps reduce risk of blood clots buy maintaining normal platelet function, lowering fibrinogen and C-reactive protein markers, improving nitric oxide release.

·        Disease prevention: why biology and trials diverge: Observational data suggested that postmenopausal women who chose hormone therapy had lower rates of cardiovascular events, consistent with estradiol’s vascular biology.

• But the largest randomized trials such as WHI and HERS did not confirm those CV benefits because of serious flaws in study designs:

1. They started hormone therapy in older women too many years past menopause, missing the critical window of time to prevent vascular damage.
2. They used ONLY ORAL estrogen derived from horse urine, NOT the 17-beta estradiol identical to the human ovary hormone, and oral estrogens increase risk of blood clots, while transdermal estradiol lowers blood clot risk.
3. They used high doses of conjugated equine estrogens with high dose of MPA, a synthetic potent progestin which has unique characteristics that negate estrogen benefits and add to risk of cardiovascular events, venous thromboembolism, and ischemic stroke.

• Estradiol is a preserver of healthy tissue, but doesn’t repair damaged tissue as well. Contemporary analyses emphasize a hormone therapy “timing hypothesis.”  The data show the best heart and blood vessel protective effects occur when E2 is started right at menopause in women whose arteries have not suffered years of damage due to loss of estradiol.  Starting estrogen therapy years after menopause, when damage to blood vessels has already happened, cannot achieve same benefits as starting earlier, although we still see many positive effects.
• Route, dose, and formulation matter: preclinical and biomarker studies suggest that physiological‑dose 17β‑estradiol delivered by non-oral patch, gel, or vaginal forms, has significantly more favorable endothelial effects and less hepatic stimulation of clotting factors than oral equine estrogens used in older trials.   You can think of estradiol as restoring a more youthful endothelial phenotype (higher NO, lower inflammatory tone, better repair capacity), but clinical outcomes hinge on timing, vascular substrate, and competing thrombotic risks.
• For my menopause patients for the last thirty-five years I have primarily used non-oral bioidentical 17-beta estradiol with FDA-approved products we have had in the US since 1975! These include transdermal patches, sustained delivery gels, vaginal rings/tablets/creams, occasionally injectable forms for someone with skin sensitivity to patch adhesive or gel components. I track hormone levels, lipids, metabolic and inflammatory/clotting/immune markers, bone density scans, and other measures.  We can see demonstrable improvement over time in lipids, insulin sensitivity, glucose regulation, bone density, reduction in inflammatory and blood clot markers, improvement in sleep, mood, cognitive and immune function, reduction in UTIs and inflammatory gut problems as the health of microvascular vessels is maintained and improved.  My patients are emphatic that the benefits they experience far outweigh reported risks and I monitor them closely catch such risks before problems arise.

II. Testosterone for men – Aging men—and younger men with testicular damage from environmental chemicals, smoking (pot or tobacco), drug use, COVID shots, many Rx medicines that decrease testosterone—also  have similar adverse vascular changes from losing optimal levels of testosterone, much like we see in menopausal women losing critical estradiol that helps maintain vascular health.

Data over the last 40 years from world-wide multi-center, multi-ethnic group studies clearly show that physiologic non-oral testosterone therapy lowers overall CVD risk, lowers blood pressure, reduces risk of diabetes and metabolic syndrome (major vascular damage risk factors), improves blood vessels structure, function, and supports endothelial health via many mechanisms, including maintaining nitric‑oxide–dependent vasodilation, endothelial repair capacity, and a favorable cardiometabolic profile.  I have explained all these in my four-part Faith Over Fear series on Testosterone for men, archived under Faith Over Fear seminars on our Truth for Health.org website.  Testosterone deficiency in men of any age is consistently linked with endothelial dysfunction and higher cardiovascular risk in men.

Summary of major vascular health benefits of Testosterone:

Direct endothelial and Nitric Oxide (NO) effects:

• Low testosterone is associated with reduced endothelial NO production, via down‑regulation of endothelial NO synthase (eNOS), higher asymmetric dimethylarginine (ADMA), and impaired NO–cGMP signaling.
• Testosterone replacement in hypogonadal men can improve NO bioavailability, increase eNOS activity, and enhance downstream cGMP signaling, improving vasodilation in vascular and penile tissue.
• Testosterone modulates phosphodiesterase‑5 (PDE5) expression, so normalization of levels can enhance responsiveness to endogenous NO and to PDE5 inhibitors in erectile tissue, which is a clinically visible readout of endothelial function.

Endothelial repair and vascular structure:

• Testosterone influences endothelial progenitor cells (EPCs), with deficiency linked to lower EPC number and impaired proliferation and migration, which limits endothelial repair after injury.
• Testosterone replacement to achieve physiologic levels improves EPC function, supporting better maintenance of an intact, anti‑thrombotic endothelial surface.
• Various sources of data show that chronic low testosterone contributes to atherosclerotic risk through endothelial dysfunction, increased oxidative stress, adverse vascular remodeling, adverse metabolic effects on lipids, glucose-insulin pathways, and fat metabolism.
• Physiologic non-oral replacement can reverse these abnormalities in hypogonadal men, as shown for many years in world-wide multi-center studies.

Cardiometabolic and disease‑risk associations:

• In my years of working with hormone issues in men, I have carefully reviewed world-wide scientific and clinical data that show low testosterone is a marker and contributor to increased cardiovascular disability and death in men, especially when deficiency is persistent and accompanied by metabolic diseases like diabetes and metabolic syndrome.
• Low endogenous testosterone is strongly correlated with increasing blood pressure, middle body (visceral) obesity, metabolic syndrome, insulin resistance, type 2 diabetes, and atherogenic changes in lipids and triglycerides, dyslipidemia. All of these adverse changes combine to increase cardiovascular disease risk and endothelial injury.
• In low T, hypogonadal men, physiologic testosterone therapy improves body composition (more lean mass, less fat), insulin sensitivity, and several lipid parameters, indirectly reducing endothelial stressors. Multi-center international studies (NOT the US VA study that was seriously flawed) have shown reductions in cardiac events, death from MI and strokes, as well as lower risk of diabetes, and improvement in diabetes control in established diabetic patients.

Practical implications for men’s vascular health:

• In men with normal testosterone levels, it helps to maintain optimal  natural physiologic testosterone production via weight management, aerobic exercise, resistance training, maintaining good sleep habits, managing stress, and reducing/eliminating opioids and excess alcohol. These combined strategies help preserve endothelial NO signaling and reduce long‑term vascular risk, even without adding any testosterone Rx medicines.
• In men with confirmed low T/hypogonadism, plus cardiometabolic risk, carefully monitored nonoral, physiologic testosterone replacement therapy can improve endothelial function markers, erectile function, and metabolic parameters, but best practices will also combine T therapy with proper BP management, nutrition to improve lipids, glucose and insulin.

BOTTOM LINE: Physiologic optimal testosterone levels help maintain healthier endothelial lining in blood vessels (adequate NO, better repair, lower metabolic burden).

• Testosterone deficiency tilts the system toward dysfunction and disease.
• T replacement is best viewed as maintaining and helping to restore normal cardiovascular function, integrity, function and signaling rather than as a primary or sole strategy to reduce heart disease.
• As in everything we teach, it takes an integrated, comprehensive approach tailored to the individual person following a careful evaluation of individual risk factors.

7. Check Your Medications:  Hidden saboteurs of vascular health can come in Rx Bottles!
Several different medicines can injure or inflame blood vessels, but they do so in different ways and with very different levels of risk. Always check with your physician to discuss overall health needs and consider vascular risk vs. the potential benefits of Rx medicines you are given. If you find yourself needing to take any of these medications, it is even more important to incorporate the above lifestyle and nutritional support strategies I outlined in Steps #1-#5
.

• Drugs that can cause vasculitis (direct vessel wall inflammation):
  • Propylthiouracil and other antithyroid drugs (e.g., methimazole, carbimazole)
  • Hydralazine (antihypertensive)
  • Minocycline and some other antibiotics (penicillins, cephalosporins, sulfonamides, quinolones, cefaclor)
  • Allopurinol
  • D‑penicillamine, sulfasalazine
  • Pharmacovigilance databases show association between several forms of vasculitis and biologic/immunomodulating anti‑TNF drugs, such as infliximab, adalimumab; alemtuzumab, rituximab
• Recreational/illicit drugs with strong vascular toxicity:
  • Cocaine and methamphetamine can cause intense vasospasm, endothelial dysfunction, inflammation, accelerated atherosclerosis, myocardial infarction, stroke, aortic dissection, pulmonary hypertension, and blood–brain barrier damage.
  • Smoking/vaping tobacco/nicotine products, as well as smoking marijuana, can cause endothelial dysfunction and is a primary driver of vascular damage in cardiovascular disease.
• Some chemotherapy and targeted anticancer drugs:
  Multiple cytotoxic and targeted agents have documented endothelial toxicity and vascular complications (e.g., hypertension, thrombosis, ischemia) through direct injury to vascular endothelium. This is why oncologists also monitor heart and other organs and refer cancer patients to specialists and for imaging as needed.
• Other medications linked to higher risk of aneurysmal subarachnoid hemorrhage:
  • Warfarin anticoagulant
  • Venlafaxine antidepressant
  • Certain analgesic combinations

Further Exploration of Endocalyx Pro™ and TruMicroVascular™

So back to the questions I have been hearing from my patients – What is the difference between Endocalyx Pro™ and TruMicroVascular?™ Is one better than the other? Can I take both?

KEY POINT: Endocalyx Pro™ and TruMicroVascular are working at very different “levels” of the vascular tree: Endocalyx Pro is a glycocalyx‑targeted, multi‑ingredient formula aimed at microvascular surface structure, while TruMicroVascular™ is essentially micronized diosmin/hesperidin aimed at venous tone, capillary leakage, and lymphatic drainage.

Core purpose for each:

• Endocalyx Pro™ is designed specifically to restore, regenerate, and protect the vascular endothelial glycocalyx, a thin, sugar‑rich coating on the inner surface of blood vessels that acts as a protective barrier. When the glycocalyx is damaged or sheds, it causes significant increase in vascular permeability, inflammation, and atherosclerotic and blood clot (thrombotic) risk all. Endocalyx Pro™ is a targeted glycocalyx therapy with downstream effects on endothelial function and microvascular perfusion.
• TruMicroVascular™ is a combination of two citrus bioflavonoids, Diosmin and Hesperidin, that is formulated to support veins, capillaries, lymphatic drainage, and microcirculation via direct effects on veins effects of these two citrus bioflavonoids.  The combination improves venous hemodynamics and capillary permeability, but does not directly target “rebuilding” the glycocalyx as does Endocalyx Pro.™ TruMicroVascular™ specifically supports the function, tone, or structural integrity of veins to help protect against edema and inflammation by improving venous tone, and reducing capillary permeability.