Search Results (1,945)

Background/Objectives: The incidence of metabolic-dysfunction-associated steatotic liver disease (MASLD) is on the rise worldwide. The purpose of this paper is to review the current and emerging trends in the management and treatment of this condition. Methods: A comprehensive literature review was conducted using PubMed and GoogleScholar, focusing on articles published within the last ten years. Results: As the incidence of MASLD rises worldwide, it is becoming ever more important to call attention to disease prevention and progression. Although weight loss, diet, and exercise play a major role, certain therapies including GLP-1 receptor agonists, resmetirom, lanifibranor, and FGF-3 analogs are showing promise when treating patients with MASLD. As more drugs become available, it will be important to note how these medications change the global outlook of this disease. Conclusions: Overall, the treatment landscape of MASLD is rapidly changing. Several phase 3 trials have revealed promising data when it comes to improving liver fibrosis and histology. This shift in treatment will provide new hope for patients and clinicians when treating this challenging disease. Full article

Background: Enteropathy-associated T-cell lymphoma (EATL) is a rare subtype of mature T-cell lymphoma, accounting for fewer than 5% of peripheral T-cell lymphomas, with an aggressive course and poor prognosis. There are two types of this disease based on morphology and immunophenotype: type I, which is often, but not always, associated with celiac disease (classic EATL), and type 2, monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL). Risk factors for classic EATL are poor adherence to a gluten-free diet, advanced age, male sex, and HLA-DQ2 homozygosity. The treatment options include surgery and various chemotherapy regimens with autologous stem cell transplantation, but the outcomes are discouraging, and clinical trials with targeted and biologic therapies are needed. Case Presentation: We report three cases of type 1 EATL, all with lethal outcomes, with one patient dying during initial treatment, one dying following several surgical interventions and without waiting to start chemotherapy, and one dying following a good treatment response but with severe infection. Full article

Olive oil, a cornerstone of the Mediterranean diet, is increasingly recognized not only for its cardiovascular benefits but also for its potential role in cancer prevention and therapy. Among its bioactive constituents, several phenolic compounds—tyrosol, hydroxytyrosol, oleuropein, oleacein, and oleocanthal—have demonstrated promising anticancer activities in various experimental models. These compounds act synergistically through diverse mechanisms, including antioxidant, anti-inflammatory, and immunomodulatory effects, as well as modulation of cell proliferation, apoptosis, angiogenesis, and metastasis. Notably, oleocanthal selectively induces cancer cell death via lysosomal membrane permeabilization, while hydroxytyrosol and oleuropein exhibit potent radical-scavenging and anti-proliferative properties. This review synthesizes findings from in vitro, in vivo, and clinical studies on the anticancer potential of these polyphenols, with emphasis on their mechanisms of action and possible applications in cancer prevention and adjunctive therapy. Given the established link between obesity and cancer development, clinical studies examining the metabolic, anti-inflammatory, and immunomodulatory effects of olive polyphenols in populations with obesity or prediabetes provide valuable insights into their potential to influence cancer-related pathways indirectly. However, direct clinical evidence in cancer patients remains limited and preliminary, underscoring the need for focused, well-controlled trials with cancer-specific endpoints. Furthermore, it critically evaluates the translational relevance of these findings, highlighting gaps in clinical research and future directions. Literature was retrieved from Google Scholar, PubMed, and ScienceDirect using keywords such as cancer, immunomodulatory, anti-inflammatory, olive, tyrosol, hydroxytyrosol, oleuropein, oleacein, and oleocanthal. Given the rising global cancer burden and the favorable safety profiles of these natural molecules, elucidating their molecular actions may support the development of novel integrative therapeutic strategies. Full article

Introduction: Recent guidelines developed by the European Association for the Study of Obesity (EASO) and the European Federation of the Associations of Dietitians (EFAD) focused on the dietetic management of obesity in adults. The present study aimed to explore the perspectives of healthcare professionals regarding these guidelines. Methods: In total, 85 registered dietitians/nutritionists from Greece, the Netherlands, the Republic of Ireland, and the United Kingdom completed an online survey, and 10 were interviewed, in February–March 2023. Demographic data were also collected. Results: Awareness of the EASO-EFAD guidelines among registered dietitians/nutritionists was moderate (57.6%), but only 20% had read them in full. Dietitians with higher education and relevant experience were more likely to have read the guidelines. Less than half reported that key evidence-based recommendations, such as individualized medical nutrition therapy and intensive behavioral interventions, are already included in national guidance. Recommendations like portfolio or DASH diets, partial meal replacements, and calorie restriction were less commonly part of national guidance/usual practice. A small percentage of participants described their adoption of several nutritional approaches novel to them. These included the portfolio dietary pattern, partial meal replacements, and intermittent fasting or continuous calorie restriction. For some Irish dietitians, prioritizing weight as the main outcome conflicted with their emphasis on overall health and individualized nutrition therapy. Other barriers of recommendation implementation included exclusive availability in English, rapid changes in obesity management, staffing shortages, limited multidisciplinary collaboration, and inconsistent knowledge among healthcare providers. Conclusions: The present study identified gaps in the adoption of the EASO-EFAD guidelines into dietetic/clinical practice. EFAD will develop strategies to disseminate these guidelines at different levels of stakeholders (national/local authorities, dietitians/nutritionists, and patients). Full article

This review aims to provide a comprehensive overview of how oxidative stress drives inflammation, structural remodeling, and clinical expression of childhood asthma, while critically appraising emerging redox-sensitive biomarkers and antioxidant-focused preventive and therapeutic strategies. Oxidative stress arises when reactive oxygen species (ROS) and reactive nitrogen species (RNS) outpace airway defenses. This surplus provokes airway inflammation: ROS/RNS activate nuclear factor kappa-B (NF-κB) and activator protein-1 (AP-1), recruit eosinophils and neutrophils, and amplify type-2 cytokines. Normally, an antioxidant network—glutathione (GSH), enzymes such as catalase (CAT) and superoxide dismutase (SOD), and nuclear factor erythroid 2-related factor 2 (Nrf2)—maintains redox balance. Prenatal and early exposure to fine particulate matter <2.5 micrometers (µm) (PM_2.5), aeroallergens, and tobacco smoke, together with polymorphisms in glutathione S-transferase P1 (GSTP1) and CAT, overwhelm these defenses, driving epithelial damage, airway remodeling, and corticosteroid resistance—the core of childhood asthma pathogenesis. Clinically, biomarkers such as exhaled 8-isoprostane, hydrogen peroxide (H₂O₂), and fractional exhaled nitric oxide (FeNO) surge during exacerbations and predict relapses. Therapeutic avenues include Mediterranean-style diet, regular aerobic exercise, pharmacological Nrf2 activators, GSH precursors, and mitochondria-targeted antioxidants; early trials report improved lung function and fewer attacks. Ongoing translational research remains imperative to substantiate these approaches and to enable the personalization of therapy through individual redox status and genetic susceptibility, ultimately transforming the care and prognosis of pediatric asthma. Full article

Background: Purple loosestrife (Lythrum salicaria L.) is a medicinal plant native to the spontaneous Romanian flora. The aim of this study was to investigate the phenolic profile, total phenolic content (TPC), and antioxidant capacity (AC) of two L. salicaria L. extracts, a hydro-methanolic extract (LSmet-1) and a hydro-ethanolic extract (LSeth-2), and their putative toxicity, as well as the effect on eye pigment content in the case of Drosophila melanogaster of an extract derived from LSmet-1 (LSmet-3). To the best of our knowledge, this is the first study to evaluate the influence of L. salicaria L. extracts on cytotoxicity and the expression of genes as determined by eye pigment levels, using a D. melanogaster-based model system. Methods: High-performance liquid chromatography was carried out to investigate the chemical composition of the extracts. Spectrophotometric methods were used to estimate their TPC and AC. Cytotoxicity was evaluated using an in vivo D. melanogaster diet-dependent viability assay and eye pigments of w^m4h males, suitable for position-effect variegation studies, which were quantified by a spectrophotometric method. Results: The results indicated that the main phenolic compounds were gallic acid, resveratrol, and rutin in LSmet-1, whereas in LSeth-2, gallic acid and quercetin were the most relevant. LSmet-1 had a higher TPC compared to LSeth-2. Both extracts exhibited notable efficacy in the applied in vitro antioxidant tests. The viability of flies on normal media increased in a concentration-dependent manner at lower concentrations, with the extract being toxic at higher concentrations. On a high-sugar diet, even lower concentrations were toxic. All tested concentrations influenced the eye pigment content. Conclusions: Our study brings new findings on L. salicaria L. extracts, suggesting the need for further investigation before introducing them in therapy. Full article

Background/Objectives: Hypercholesterolemia remains a major risk factor for cardiovascular disease and a leading cause of global mortality. Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes degradation of low-density lipoprotein receptors (LDLR), thereby reducing LDL-cholesterol (LDL-C) clearance. While monoclonal antibodies (mAbs) targeting PCSK9 are effective, their short half-life requires frequent dosing and incurs high treatment costs. This study evaluates a novel peptide-based Anti-PCSK9 product aimed at providing sustained LDL-C reduction. Methods: A novel PCSK9 based-peptide conjugated to diphtheria toxoid (DT) was evaluated in various preclinical models: high-fat diet-fed C57BL/6 mice, APOB100/hCETP transgenic mice, BALB/c mice and normocholesterolemic non-human primates. Immunogenicity (Anti-PCSK9 antibody titers, binding affinity by SPR), pharmacodynamics (LDL-C levels, inhibition of PCSK9-LDLR interaction) and safety were assessed. Toxicity was evaluated in rodents, rabbits and dogs through clinical monitoring, histopathology, organ function and safety pharmacology studies. Results: The Anti-PCSK9 product induced robust and long-lasting immune response in all models antibody titers in BALB/c mice peaked by week 6 and persisted for 12 months. LDL-C reductions of 44% in APOB100/hCETP mice and 37% in C57BL/6 mice correlated with high antibody titers and strong PCSK9-binding affinities (85 and 49 RU), leading to 59% and 58% inhibition of PCSK9-LDLR interaction, respectively. Non-human primates showed sustained responses. No systemic toxicity was observed; injection-site reactions were mild and reversible. No adverse effects were detected on cardiovascular, neurological, or respiratory systems. Conclusions: This peptide-based Anti-PCSK9 therapy offers sustained efficacy and safety, representing a promising long-acting alternative for managing hypercholesterolemia. Full article

Chaya leaf has long been used in folk medicine and is gaining scientific interest for its potential role in diabetes management. Recent research indicates that chaya leaf may help to regulate glucose, enhance insulin secretion, and reduce related complications, primarily due to the presence of bioactive compounds such as polyphenols and flavonoids. These compounds are believed to enhance insulin sensitivity and offer protection against oxidative stress, a key contributor to diabetes-related complications. Chaya extracts, particularly methanolic and aqueous forms, have shown anti-diabetic effects in animal models, lowering blood glucose, cholesterol, and triglycerides and reducing inflammation; their bioactive compounds, like quercetin, rutin, and ferulic acid, may enhance the insulin response, reduce inflammation, and improve antioxidant activity. Some studies warn of potential interactions with metformin. This review compiles findings from the past five years, drawing from databases such as PubMed, SciELO, ScienceDirect, Dialnet, Web of Science, and Google Scholar. It highlights chaya’s phytochemical profile, explores proposed anti-diabetic mechanisms, and summarizes evidence from in vivo, in vitro, and clinical studies. The results indicate that adding chaya leaf to the diet may help people with diabetes as a complementary therapy to conventional treatment; nonetheless, further clinical studies are required to comprehend the exact mechanisms and define specific usage instructions. Further investigation into the specific types of compounds present in chaya, their effective dosages, and their safety in human populations is essential to support its integration into medical practice. Full article

UDP-Gal-β-1,4 galactosyltransferase-V (GalT-V) is a member of a large family of galactosyltransferases whose function is to transfer galactose from the nucleotide sugar UDP-galactose to a glycosphingolipid glucosylceramide, to generate lactosylceramide (LacCer). It also causes the N and O glycosylation of proteins in the Trans Golgi area. LacCer is a bioactive lipid second messenger that activates an “oxidative stress pathway”, leading to critical phenotypes, e.g., cell proliferation, migration angiogenesis, autophagy, and apoptosis. It also activates an “inflammatory pathway” that contributes to the progression of disease pathology. β-1,4-GalT-V gene expression is regulated by the binding of the transcription factor Sp-1, one of the most O-GlcNAcylated nuclear factors. This review elaborates the role of the Sp-1/GalT-V axis in disease phenotypes and therapeutic approaches targeting not only Sp-1 but also Notch-1, Wnt-1 frizzled, hedgehog, and β-catenin. Recent evidence suggests that β-1,4GalT-V may glycosylate Notch-1 and, thus, regulate a VEGF-independent angiogenic pathway, promoting glioma-like stem cell differentiation into endothelial cells, thus contributing to angiogenesis. These findings have significant implications for cancer and cardiovascular disease, as tumor vascularization often resumes aggressively following anti-VEGF therapy. Moreover, LacCer can induce angiogenesis independent of VEGF and its level are reported to be high in tumor tissues. Thus, targeting both VEGF-dependent and VEGF-independent pathways may offer novel therapeutic strategies. This review also presents an up-to-date therapeutic approach targeting the β-1,4-GalT-V interactome. In summary, the β-1,4-GalT-V interactome orchestrates a broad network of signaling pathways essential for maintaining cellular homeostasis. Conversely, its dysregulation can promote unchecked proliferation, angiogenesis, and inflammation, contributing to the initiation and progression of multiple diseases. Environmental factors and smoking can influence β-1,4-GalT-V expression and its interactome, whereas elevated β-1,4-GalT-V expression may serve as a diagnostic biomarker of colorectal cancer, inflammation—exacerbated by factors that may worsen pre-existing cancer malignancies, such as smoking and a Western diet—and atherosclerosis, amplifying disease progression. Increased β-1,4-GalT-V expression is frequently associated with tumor aggressiveness and chronic inflammation, underscoring its potential as both a biomarker and therapeutic target in colorectal and other β-1,4-GalT-V-driven cancers, as well as in cardiovascular and inflammatory diseases. Full article

Type 2 diabetes (T2D) is a complex metabolic disease characterized by chronic hyperglycemia due to insulin resistance and inadequate insulin secretion. Beyond the classically implicated organs, emerging evidence highlights the gut as a central player in T2D pathophysiology through its interactions with metabolic organs. The gut hosts trillions of microbes and enteroendocrine cells that influence inflammation, energy homeostasis, and hormone regulation. Disruptions in gut homeostasis (dysbiosis and increased permeability) have been linked to obesity, insulin resistance, and β-cell dysfunction, suggesting multifaceted “Gut-X axes” contribute to T2D development. We aimed to comprehensively review the evidence for gut-mediated crosstalk with the pancreas, endocrine system, liver, and kidneys in T2D. Key molecular mechanisms (incretins, bile acids, short-chain fatty acids, endotoxins, etc.) were examined to construct an integrated model of how gut-derived signals modulate metabolic and inflammatory pathways across organs. We also discuss clinical implications of targeting Gut-X axes and identify knowledge gaps and future research directions. A literature search (2015–2025) was conducted in PubMed, Scopus, and Web of Science, following PRISMA guidelines (Preferred Reporting Items for Systematic Reviews). Over 150 high-impact publications (original research and review articles from Nature, Cell, Gut, Diabetologia, Lancet Diabetes & Endocrinology, etc.) were screened. Data on gut microbiota, enteroendocrine hormones, inflammatory mediators, and organ-specific outcomes in T2D were extracted. The GRADE framework was used informally to prioritize high-quality evidence (e.g., human trials and meta-analyses) in formulating conclusions. T2D involves perturbations in multiple Gut-X axes. This review first outlines gut homeostasis and T2D pathogenesis, then dissects each axis: (1) Gut–Pancreas Axis: how incretin hormones (GLP-1 and GIP) and microbial metabolites affect insulin/glucagon secretion and β-cell health; (2) Gut–Endocrine Axis: enteroendocrine signals (e.g., PYY and ghrelin) and neural pathways that link the gut with appetite regulation, adipose tissue, and systemic metabolism; (3) Gut–Liver Axis: the role of microbiota-modified bile acids (FXR/TGR5 pathways) and bacterial endotoxins in non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance; (4) Gut–Kidney Axis: how gut-derived toxins and nutrient handling intersect with diabetic kidney disease and how incretin-based and SGLT2 inhibitor therapies leverage gut–kidney communication. Shared mechanisms (microbial SCFAs improving insulin sensitivity, LPS driving inflammation via TLR4, and aryl hydrocarbon receptor ligands modulating immunity) are synthesized into a unified model. An integrated understanding of Gut-X axes reveals new opportunities for treating and preventing T2D. Modulating the gut microbiome and its metabolites (through diet, pharmaceuticals, or microbiota therapies) can improve glycemic control and ameliorate complications by simultaneously influencing pancreatic islet function, hepatic metabolism, and systemic inflammation. However, translating these insights into clinical practice requires addressing gaps with robust human studies. This review provides a state-of-the-art synthesis for researchers and clinicians, underlining the gut as a nexus for multi-organ metabolic regulation in T2D and a fertile target for next-generation therapies. Full article

This review focuses specifically on pediatric patients with cystic fibrosis. Cystic fibrosis (CF) is a serious inherited disease that affects the respiratory and gastrointestinal systems in children and adolescents, causing chronic inflammation, infections, and impaired nutrient absorption. A key component of patient care is monitoring nutritional status, particularly based on BMI, which correlates with lung function and life expectancy. This paper presents the latest guidelines for dietary therapy, including a high-calorie and fat-rich diet supported by pancreatic enzymes, as well as the importance of vitamin and mineral supplementation in the context of CF pathophysiology. The role of modern therapies that modulate CFTR function to improve patients’ quality of life and support antimicrobial therapy is discussed. Particular attention is paid to the role of the gut microbiota and the potential for its modulation by probiotics, highlighting their potential to alleviate inflammation and support the immune system. The conclusions underscore the need for a comprehensive, individualized approach to diagnosis and therapy, which is crucial for improving the quality of life and health prognosis of children with CF. New visual tools and a clinical case study enhance the practical applicability of current recommendations, while emerging areas such as microbiome-targeted interventions and treatment inequalities are also addressed. Full article

Type 2 diabetes (T2D), a growing global health concern, is closely linked to obesity and sedentary behavior. Central to its development are insulin resistance and impaired glucose metabolism in peripheral tissues, particularly skeletal muscle, which plays a key role in energy expenditure, glucose uptake, and insulin sensitivity. Notably, increased accumulation of lipid metabolites in skeletal muscle is observed both in endurance exercise—associated with improved insulin sensitivity—and in high-fat diets that induce insulin resistance. The review examines the contrasting metabolic adaptations of skeletal muscle to these opposing conditions and highlights the key signaling molecules involved. The focus then shifts to the role of the stress kinase p38α mitogen-activated protein kinase (MAPK) in skeletal muscle adaptation to overnutrition and endurance exercise. p38α enhances mitochondrial oxidative capacity and regulates nutrient utilization, both critical for maintaining metabolic homeostasis. During exercise, it cooperates with AMP-activated protein kinase (AMPK) to boost glucose uptake and fatty acid oxidation, key mechanisms for improving insulin sensitivity. The co-activation of p38α and AMPK in skeletal muscle emerges as a promising therapeutic avenue to combat insulin resistance and T2D. The review explores strategies for selectively enhancing p38α activity in skeletal muscle. In conclusion, it advocates a comprehensive approach to T2D prevention and treatment, combining established caloric intake-reducing therapies, such as GLP-1 receptor agonists, with interventions aimed at increasing energy expenditure via activation of p38α and AMPK signaling pathways. Full article

Background/Objectives: Individuals with posttraumatic stress disorder (PTSD) tend to show patterns of elevated cardiovascular disease (CVD) risk earlier in life than the general population. The need for effective interventions for CVD risk-reduction in PTSD is increasingly evident. In this paper we present preliminary results from a longitudinal study of a health behavior intervention, as an adjunct to standard trauma therapy in PTSD. The health behavior intervention addresses CVD-related heath behaviors (physical activity, nutrition, sleep, and stress) in a 12-week program delivered individually in 90-min sessions. Behavior change recommendations included: increased aerobic activity; establishing a balanced diet, enhancing consumption of fruits and vegetables and reducing sugars and fat/saturated fat; incorporating strategies to enhance sleep and lower PTSD-related disruptions (e.g., nightmares); and relaxation and cognitive coping skills to reduce general stress. Methods: Participants were randomized to the health behavior intervention plus standard trauma therapy experimental condition or a standard trauma therapy control group. Outcomes were measured at baseline and after the 12-week intervention phase. Sleep efficiency was measured from actigraphy watches. Physical activity was assessed by self-report and blood pressure was measured using an automated device. The preliminary outcomes are for 29 participants to date who have pre-post data. Results: Sleep efficiency was improved in the intervention group compared to controls (p < 0.05). The intervention group also evidenced significant pre-post increases in moderate physical activity compared to the control group (p < 0.05). Changes in vigorous physical activity did not reach statistical significance in this preliminary sample but the pattern of results are similar to those for moderate activity. Trends toward significance were also observed for pre-post changes in systolic (p = 0.06) and diastolic blood pressure (p = 0.07), with small reductions for the intervention group and increases for the control group. Conclusions: These findings provide preliminary information about the effectiveness of the health behavior intervention on multiple parameters for adults with PTSD. The findings suggest that focusing on health behavior change in multidisciplinary treatments for PTSD may enhance outcomes such as sleep and physical activity and potentially result in greater quality of life. However, the small preliminary sample size reported here should be considered when interpreting the outcomes. Further research may also determine how improvements in health parameters impact other indices of long-term cardiovascular health. Full article

Type 2 diabetes mellitus (T2DM) is a multifactorial disorder defined by insulin resistance, β-cell dysfunction, and chronic hyperglycemia. Although peripheral mechanisms have been extensively studied, increasing evidence implicates the gastrointestinal tract in disease onset. Insights from bariatric surgery, gut hormone signaling, and incretin-based therapies suggest that the gut contributes actively beyond nutrient absorption. Yet, a cohesive framework integrating these observations remains absent, leaving a critical gap in our understanding of T2DM’s upstream pathophysiology. This work builds upon the anti-incretin theory, which posits that nutrient-stimulated neurohormonal signals—termed “anti-incretins”—arise from the proximal intestine to counteract incretin effects and regulate glycemic homeostasis. The excess of anti-incretin signals, perhaps stimulated by macronutrient composition or chemical additives of modern diets, disrupts this balance and may cause insulin resistance and β-cell depletion, leading to T2D. We hypothesize that the neuroendocrine signals produced by cholecystokinin (CCK)-I and secretin-S cells, both located in the proximal intestine, function as endogenous anti-incretins. In this context, we hypothesize a novel model centered on the chronic overstimulation of I and S cells by high-fat, high glycemic index modern diets. This drives what we term “amplified digestion”—a state marked by heightened vagal and hormonal stimulation of biliary and pancreatic secretions, increased enzymatic and bile acid activity, and alterations in bile acid composition. This condition leads to an extended breakdown of carbohydrates, lipids, and proteins into absorbable units, thereby promoting excessive nutrient absorption and ultimately contributing to insulin resistance and progressive β-cell failure. Multiple lines of clinical, surgical, and experimental evidence converge to support our model, rooted in the physiology of digestion and absorption. Western dietary patterns appear to induce an over-digestive adaptation—marked by excessive vagal and hormonal stimulation of biliary and pancreatic secretion—which amplifies digestive signaling. This heightened state correlates with increased nutrient absorption, insulin resistance, and β-cell dysfunction. Interventions that disrupt this maladaptive signaling—such as truncal vagotomy combined with duodenal bypass—may offer novel, physiology-based strategies for T2DM treatment. This hypothesis outlines a potential upstream contributor to insulin resistance and T2DM, grounded in digestive tract-derived neurohormonal dysregulation. This gut-centered model may provide insight into early, potentially reversible stages of the disease and identify a conceptual therapeutic target. Nonetheless, both the hypothesis and the accompanying surgical strategy—truncal vagotomy combined with proximal intestinal bypass—remain highly exploratory and require systematic validation through mechanistic and clinical studies. Further investigation is warranted to clarify the molecular regulation of I and S enteroendocrine cells, including the genetic and epigenetic factors that may drive hypersecretion. While speculative, interventions—surgical or pharmacologic—designed to modulate these digestive signals could represent a future avenue for research into T2DM prevention or remission, pending rigorous evidence. Full article

Background/Objectives: In hypertension (HTN), lifestyle modification is important for controlling blood pressure (BP) and lipidemic profile. The HINTreat trial showed that an anti-inflammatory diet was associated with improved endothelial function, after six months of intensive nutritional treatment. Methods: This post hoc analysis of the HINTreat trial examined how adherence to various nutritional patterns like the Mediterranean Diet (MedDiet), the Dietary Approaches to Stop Hypertension (DASH) diet, and anti-inflammatory diet, had impact on the blood lipids profile and the CVD risk. Patients with stage 1 HTN, allocated either on intensive lifestyle treatment (ILT) or usual care (UC) standard treatment, participated in the analysis. From the original sample size of the HINTreat trial, all patients that were prescribed lipid lowering medication at any time of the study period were excluded from the total analysis; thus, the intervention and the control groups consisted of 33 and 28 patients, respectively. Nutritional intakes were assessed with repeated 24 h recalls from the previous day, and dietary indexes and scores were calculated as follows: MedDiet score, DASH index, and Dietary Inflammatory Index (DII). After six months of intervention, changes in the nutritional indexes and their effect on the lipidemic profile and CVD risk were analyzed. Results: In the ILT group, reductions were noted in Ambulatory Blood Pressure Monitoring (ABPM) for day systolic BP (SBP) (−12.7 mmHg) and diastolic BP (DBP) (−8.4 mmHg), total cholesterol (TC) (−35.4 mg/dL), triglycerides (TG) (−21.4 mg/dL), LDL cholesterol (LDL-C) (−27.5 mg/dL) concentrations, and CVD risk score (−1.5%), p < 0.001 for all. Multiple regression analysis showed that dietary quality indices independently influenced improvements in blood lipid profile and cardiovascular disease (CVD) risk among patients receiving ILT. Specifically, a higher Mediterranean Diet (MedDiet) score was significantly associated with reductions in TC (B = −7.238, p < 0.001), TG (B = −4.103, p = 0.035), and LDL-C (B = −6.431, p = 0.004). The DASH index was positively associated with TG levels (B = 9.913, p = 0.010), suggesting a more complex relationship that may require further investigation. In addition, DII was positively associated with increased CVD risk (B = 0.973, p < 0.001). Conclusions: The findings suggest that ILT can improve BP levels, target blood lipids concentrations, and reduce CVD risk in patients with stage 1 HTN. Full article