Why we avoid Animal Products: Science and Success Behind Bethsaida Hospital’s Whole-Food Plant-Based Cardiac Program

Cardiovascular disease remains the leading cause of morbidity and mortality globally, with atherosclerosis and restenosis as critical pathological contributors. Accumulating evidence suggests that diets high in animal products—including red meat, eggs, and dairy—are significant contributors to these conditions through mechanisms such as oxidative stress, inflammation, Nitric Oxide (NO) depletion, insulin resistance, mitochondrial dysfunction, and disruption of the gut microbiota. This review presents a comprehensive synthesis of the molecular and physiological pathways by which animal-based diets contribute to vascular disease, while highlighting the protective and therapeutic potential of Whole Food Plant-Based Diets (WFPBDs). Central to this discussion is the pioneering implementation of WFPBD at Bethsaida Hospital in Tangerang, Indonesia—the first in the country to integrate WFPBD into standard cardiac care under the leadership of Prof. Dasaad Mulijono (DM). Clinical outcomes from Bethsaida demonstrate remarkable reversal or stabilization of hypertension, Type 2 Diabetes (T2D), dyslipidaemia, Chronic Kidney Disease (CKD), and Coronary Artery Disease (CAD), including a strikingly low restenosis rate of 2% in patients undergoing Drug-Coated Balloon (DCB) therapy.

Bethsaida’s experience provides a compelling, real-world testament to the transformative power of nutritional intervention in cardiovascular medicine, underscoring the urgency of repositioning nutrition as a central therapeutic strategy.

Cardiovascular Disease (CVD) continues to be the leading cause of death globally, with atherosclerosis and restenosis remaining significant clinical challenges [1,2]. Atherosclerosis, a chronic inflammatory condition of the arterial wall, and restenosis, the pathological vascular healing response following angioplasty, are significantly influenced by dietary patterns [3-10]. Traditional approaches to cardiovascular nutrition have primarily emphasized the reduction of dietary cholesterol and saturated fat. However, emerging research reveals a far more complex and multifaceted landscape. Diets rich in animal products have been shown to contribute to vascular injury through mechanisms including Nitric Oxide (NO) depletion, oxidative stress, elevated Trimethylamine N-oxide (TMAO) levels, mitochondrial dysfunction, and chronic systemic inflammation. Additionally, specific components inherent to animal-derived foods—such as heme iron, Advanced Glycation End-Products (AGEs), insulin-like growth factor 1 (IGF-1), Branched-Chain Amino Acids (BCAAs), and N-glycolylneuraminic acid (Neu5Gc)—further exacerbate these deleterious processes.

Accordingly, one of the principal therapeutic advantages of our WFPBD program at Bethsaida Hospital is that it avoids animal products altogether. This deliberate exclusion eliminates multiple pro-atherogenic and pro-restenotic factors, thereby supporting vascular healing, disease reversal, and improved clinical outcomes.

In contrast, WFPBDs—rich in vegetables, fruits, legumes, whole grains, nuts, and seeds—have been shown to restore endothelial function, enhance NO bioavailability, reduce oxidative stress, improve gut microbiota composition, protect mitochondria, and prevent telomere shortening [3-10].

Despite strong evidence supporting WFPBDs, most healthcare systems struggle to integrate nutrition into mainstream cardiovascular care. However, Bethsaida Hospital in Indonesia has pioneered the formal incorporation of WFPBD into its standard cardiac practice. The hospital’s impressive outcomes—including near-universal medication reductions and markedly low restenosis rates—highlight the urgent need to reframe nutritional intervention as a cornerstone of cardiovascular treatment.

Saturated fats and cholesterol: The cholesterol burden

Animal-derived foods, particularly red meats, dairy products, and eggs, are rich in saturated fats and dietary cholesterol [11,12]. These components increase plasma Low-Density Lipoprotein (LDL) cholesterol, a well-established risk factor for atherosclerotic cardiovascular disease. LDL particles penetrate the endothelium and undergo oxidation, initiating an inflammatory cascade that leads to foam cell formation and plaque buildup. Despite the availability of statins that lower LDL and reduce cardiovascular events, primary prevention through dietary reduction of saturated fats remains underutilized.

Obesity, hypertension, and cardiometabolic burden

Diets high in animal products are often calorically dense and low in fibre, promoting weight gain and obesity. Excess adipose tissue, particularly visceral fat, functions as an endocrine organ, releasing cytokines such as TNF-alpha and IL-6, which exacerbate insulin resistance and systemic inflammation. This metabolic dysfunction is a major contributor to endothelial damage, atherosclerosis, hypertension, and the development of restenosis following vascular interventions [13-16].

Fibre deficiency and gut Dysbiosis

Animal-based diets lack dietary fibre, which is essential for producing Short-Chain Fatty Acids (SCFAs) such as butyrate, propionate, and acetate. These SCFAs play critical roles in maintaining colonic mucosal integrity, modulating immune responses, and suppressing inflammatory signalling. Fiber scarcity also alters gut microbiota composition, favouring pro-inflammatory species and increasing gut permeability—factors that enhance systemic inflammation and vascular injury [17-20].

Antioxidant deficiency and oxidative stress

Animal products contain negligible amounts of antioxidants, including vitamins C and E, carotenoids, and polyphenols. The absence of these molecules permits unchecked reactive oxygen species (ROS) activity, leading to oxidative modification of lipids and proteins in the vasculature. Oxidative stress contributes to endothelial dysfunction, foam cell formation, and plaque instability—key events in atherosclerosis progression and restenosis [21-23].

NO deficiency

NO is a vasoprotective molecule that endothelial NO synthase (eNOS) produces. It regulates vascular tone, inhibits platelet aggregation, and reduces leukocyte adhesion [24,25]. Diets devoid of nitrate-rich vegetables impair NO synthesis. Additionally, oxidative stress from animal-based diets inactivates NO, further compromising endothelial function and facilitating restenosis after vascular [26-28].

TMAO: A novel biomarker and mediator

TMAO is generated in the liver from Trimethylamine (TMA), a metabolite produced by gut bacteria from carnitine and choline found abundantly in red meat, eggs, and dairy. Elevated plasma TMAO levels are associated with increased platelet hyperreactivity, endothelial dysfunction, and enhanced cholesterol accumulation in arterial walls. TMAO is now recognized as an independent predictor of major adverse cardiovascular events, including restenosis [29-33].

ROS amplification

Thermal processing of animal proteins, such as grilling or frying, leads to the formation of ROS-inducing compounds, including AGEs and heterocyclic amines. These compounds promote oxidative stress, damage endothelial cells, and stimulate inflammatory pathways, accelerating atherogenesis and restenotic processes [34-37].

Hyperinsulinemia and insulin resistance

Animal foods, especially those with high saturated fat content, impair insulin receptor function and glucose transport, leading to hyperinsulinemia and insulin resistance [38-43]. Insulin resistance is central to the pathophysiology of metabolic syndrome, which includes hypertension, dyslipidaemia, and pro-thrombotic states—all conducive to vascular damage and restenosis.

Inflammatory amino acid profiles

Animal proteins are rich in BCAAs and methionine. Excessive intake of these amino acids is associated with increased mTOR activation, inflammation, and oxidative stress. Elevated BCAAs also impair insulin sensitivity, compounding metabolic derangements and promoting endothelial injury [44-50].

Elevated IGF-1

IGF-1, primarily elevated through consumption of dairy products, stimulates cellular proliferation and inhibits apoptosis. Elevated IGF-1 levels are linked to increased risk of neointimal hyperplasia and restenosis following angioplasty, through its mitogenic and pro-inflammatory effects on vascular smooth muscle cells [51-53].

AGEs and endothelial damage

AGEs are formed during high-temperature cooking of animal products and are potent activators of the receptor for AGEs (RAGE). The engagement of RAGE triggers oxidative stress and NF-κB activation, leading to chronic vascular inflammation and structural vessel changes consistent with atherosclerosis and restenosis [54-60].

Gut microbiota disruption by antibiotics

The widespread use of antibiotics in animal agriculture alters the microbiota of livestock; residues persist in animal-derived foods. These residues can affect the human gut microbiome, reducing microbial diversity and promoting dysbiosis, which has been implicated in inflammatory and metabolic disorders contributing to vascular disease [61-64].

Heme iron and free radical formation

Heme iron, abundant in red meat, participates in the Fenton reaction to generate highly reactive hydroxyl radicals. This catalyses lipid peroxidation, endothelial injury, and DNA damage. In contrast, non-heme iron from plant sources is regulated more efficiently and generates less oxidative stress [65-72].

suPAR and chronic inflammation

suPAR is an inflammatory biomarker linked to immune activation and poor cardiovascular outcomes. Diets high in animal protein are associated with elevated suPAR levels, indicating persistent low-grade inflammation that impairs vascular repair mechanisms and increases the risk of restenosis [73-77].

Neu5Gc-induced inflammation

Neu5Gc is a non-human sialic acid incorporated into human tissues from red meat and dairy consumption. The immune response to Neu5Gc-containing tissues leads to chronic inflammation, vascular injury, and enhanced risk of atherosclerosis and restenosis [78-81].

Persistent organic pollutants (POPs)

POPs, including dioxins and Polychlorinated Biphenyls (PCBs), accumulate in the adipose tissue of animals and are ingested through meat and dairy. These environmental toxins disrupt endocrine function and provoke oxidative and inflammatory responses in vascular tissues, contributing to arterial damage [82-85].

Nitrates, nitrites, and carcinogenicity

Processed meats often contain nitrates and nitrites as preservatives, which, when heated to high temperatures, convert to nitrosamines—known carcinogens. These compounds also exert pro-inflammatory and endothelial-disruptive effects, increasing the susceptibility to vascular injury and plaque instability [86-92].

Mitochondrial dysfunction

Animal-based diets may impair mitochondrial biogenesis and function, leading to reduced ATP production, increased ROS generation, and accelerated cellular senescence. Mitochondrial dysfunction impairs the reparative capacity of endothelial cells and smooth muscle regulation, thereby exacerbating restenosis [93-95].

Telomere shortening and aging

Telomeres protect chromosomal ends from deterioration; their shortening is a marker of cellular aging. Diets high in animal fats and low in antioxidants accelerate telomere attrition, predisposing individuals to the early onset of cardiovascular diseases, including restenosis [96-100].

Systemic acidosis and vascular dysfunction

High-protein animal diets create an acidogenic load that the body buffers via skeletal calcium mobilization and renal ammonia genesis. Chronic metabolic acidosis induces endothelial dysfunction, vascular calcification, and systemic inflammation—key drivers of atherosclerosis, vascular calcification, and restenosis [101-103].

We are pleased to share the remarkable outcomes achieved at the Cardiology Centre of Bethsaida Hospital in Tangerang, Indonesia. We have implemented a WFPBD for nearly seven years and strictly limited animal products as part of our standard cardiac care. This initiative represents the first in Indonesia—a pioneering effort to integrate evidence-based nutritional therapy into cardiovascular practice, led by Prof. DM.

The transformational impact of WFPBD on our patients’ health has been undeniable. In the following sections, we present real-world testimonies and clinical data that highlight the profound benefits of this lifestyle intervention in reversing or stabilizing chronic diseases. We aim to contribute meaningful, experience-driven insight to the global discussion on nutrition and cardiovascular care, and to inspire broader adoption of this life-saving approach.

• Hypertension reversal Without Medications:  Numerous patients have achieved normotensive readings without antihypertensive medications. By adopting a WFPBD rich in potassium, magnesium, and NO-boosting greens while avoiding sodium-laden animal products, blood pressure normalization was observed within weeks to months.
• Diabetes management without insulin:  Many T2D patients have successfully discontinued insulin while maintaining glycaemic control with minimal or no oral antidiabetic medications. HbA1c values have improved significantly, and patients report increased energy and enhanced quality of life.
• LDL reduction without Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) Inhibitors: Patients receiving high-intensity statins and ezetimibe with a WFPBD have experienced profound reductions in LDL-C, eliminating the need for PCSK9 inhibitors. The diet’s high fiber content and absence of saturated fats contribute significantly to lipid regulation.
• Sustainable weight loss: Overweight and obese individuals who adopt the WFPBD consistently reach an ideal body mass index (BMI) of 20–22 without calorie restriction. Plant foods’ high satiety index and nutrient density encourage natural portion control.
• Renal function restoration: Patients with mild to moderate CKD have shown significant improvement or normalization of serum creatinine and glomerular filtration rate (GFR), enabling them to avoid dialysis and stabilize their kidney function.
• Improved heart failure outcomes: In patients with heart failure with reduced ejection fraction (HFrEF), we have observed a substantial improvement in symptoms and left ventricular ejection fraction when a WFPBD was incorporated alongside standard heart failure therapy.
• CAD regression and exceptional restenosis rates:  Our CAD patients often demonstrate angiographic regression of plaques, supported by lifestyle modification and optimal pharmacotherapy. Our DCB restenosis rate is just 2%, starkly contrasting with the 10–20% observed in other centres.
• Other chronic inflammatory conditions:  Patients with autoimmune diseases, psoriasis, and other chronic inflammatory conditions report symptom improvement and disease modulation under a plant-based regimen. Some patients with early-stage cancers have achieved disease stabilization or regression.

This review consolidates an extensive and growing body of literature that links animal-based diets to atherosclerosis and restenosis through multifaceted mechanisms. Beyond cholesterol and saturated fat, the roles of gut dysbiosis, oxidative stress, mitochondrial impairment, and inflammatory amino acid profiles, as well as novel biomarkers such as TMAO, suPAR, and Neu5Gc, reveal the systemic burden induced by the consumption of animal products.

Bethsaida Hospital’s real-world application of WFPBD offers robust clinical validation of these mechanistic insights. Under the leadership of Prof. DM, Bethsaida has demonstrated that WFPBD can reverse hypertension, eliminate insulin dependence in T2D, improve renal function, and drastically reduce restenosis rates in patients undergoing PCI with DCB. These findings echo and expand upon controlled trial data by demonstrating what is possible in routine clinical practice when nutritional intervention is prioritized.

Moreover, Bethsaida’s outcomes underscore the practicality, sustainability, and therapeutic efficacy of WFPBDs, even in resource-constrained settings. The hospital’s approach exemplifies the shift from reactive pharmacologic management to proactive lifestyle-based prevention and disease reversal.

The evidence presented in this review—both mechanistic and clinical—makes a compelling case for adopting plant-based dietary strategies to prevent and treat cardiovascular disease. Animal products exacerbate vascular injury through multiple pathways, hindering the body’s innate capacity to heal and regenerate.

Bethsaida Hospital’s experience confirms that WFPBD is a scientifically sound and clinically transformative approach. With demonstrable benefits in reversing chronic diseases and improving procedural outcomes, WFPBD should be embraced as a foundational tool in modern cardiology.

As global health systems grapple with the burden of chronic disease, incorporating evidence-based dietary interventions such as WFPBD represents a paradigm shift with the potential to save lives, reduce costs, and restore human health at scale.

D.M.; Conceptualization, writing, review, and editing.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Data are contained within the article.

Conflict of Interest

The authors declare no conflict of interest.

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