Familial hypercholesterolemia is a genetic lipid disorder characterized by elevated levels of low-density lipoprotein cholesterol and an increased risk of premature atherosclerotic cardiovascular disease. Traditionally considered a monogenic disorder caused by mutations in genes involved in low-density lipoprotein metabolism, advances in molecular genetics have revealed more complex genetic architectures, including oligogenic and polygenic forms. Oligogenic familial hypercholesterolemia results from the interaction of multiple rare variants across genes involved in lipid metabolism, while polygenic hypercholesterolemia is caused by the cumulative effect of numerous common genetic variants that modestly increase low-density lipoprotein cholesterol levels. These genetic patterns influence disease severity, clinical diagnosis, and therapeutic approaches. This review discusses the epidemiology, genetic mechanisms, clinical manifestations, diagnostic strategies, and treatment options for oligogenic and polygenic familial hypercholesterolemia, emphasizing the importance of early detection and aggressive lipid-lowering therapy to prevent cardiovascular complications.

Cardiovascular-kidney-metabolic syndrome integrates obesity, insulin resistance, type 2 diabetes mellitus, chronic kidney disease, and cardiovascular disease into a unified pathophysiological continuum. Within this framework, chronic kidney disease is both a consequence of metabolic dysfunction and an important driver of cardiovascular risk. This narrative review summarizes kidney-specific recommendations from the 2026 American Heart Association/American College of Cardiology/American Diabetes Association/American Society of Nephrology Cardiovascular-Kidney-Metabolic Guideline and the 2024 Kidney Disease: Improving Global Outcomes Chronic Kidney Disease Guideline. Kidney-related staging criteria, screening recommendations, pharmacologic therapies, monitoring strategies, and key kidney outcome trials referenced by the guideline were reviewed. Chronic kidney disease is defined by abnormalities of kidney structure or function, including an estimated glomerular filtration rate below 60 mL/min/1.73 m² or a urine albumin-to-creatinine ratio of at least 30 mg/g persisting for three months or longer. Within the cardiovascular-kidney-metabolic framework, the presence of chronic kidney disease places an individual at a minimum of stage 2 disease. Annual assessment of kidney function and albuminuria is recommended for individuals with cardiovascular-kidney-metabolic risk factors. Early initiation of renin-angiotensin system inhibitors and sodium-glucose cotransporter 2 inhibitors, followed by the addition of finerenone and glucagon-like peptide-1 receptor agonists when appropriate, forms the foundation of kidney-protective therapy. Lifestyle interventions, risk-factor modification, and risk stratification using the Kidney Disease: Improving Global Outcomes heat map remain central to management. The 2026 Cardiovascular-Kidney-Metabolic Guideline repositions chronic kidney disease from a late complication to a central determinant of cardiovascular-kidney-metabolic risk. Earlier detection and implementation of evidence-based kidney-protective therapies may substantially slow disease progression, reduce cardiovascular events, and delay the need for kidney replacement therapy.

Diabetes mellitus is diagnosed by HbA1c ≥ 6.5%, fasting plasma glucose ≥ 126 mg/dL, 2-hour oral glucose tolerance test glucose ≥ 200 mg/dL, or random plasma glucose ≥ 200 mg/dL with symptoms. Prediabetes is defined by HbA1c 5.7–6.4%, fasting glucose 100–125 mg/dL, or 2-hour oral glucose tolerance test glucose 140–199 mg/dL. Glycemic targets generally aim for HbA1c < 7%, with individualized goals based on age, comorbidities, and hypoglycemia risk. Recommended glucose targets include fasting levels of 80-130 mg/dL and postprandial levels < 180 mg/dL. Lifestyle management emphasizes at least 150 minutes of weekly physical activity, 5-10% weight loss, healthy dietary patterns, adequate sleep, and stress control. Metformin remains first-line therapy for type 2 diabetes, with Sodium-Glucose Cotransporter 2 inhibitors or glucagon-like peptide-1 receptor agonists preferred in patients with cardiovascular disease, heart failure, chronic kidney disease, or weight-loss goals. Insulin is indicated for severe hyperglycemia or treatment failure. Comprehensive care includes blood pressure control (<130/80 mmHg), statin therapy based on cardiovascular risk, routine screening for kidney disease, retinopathy, neuropathy, and foot complications, and adherence to adult vaccination schedules. Continuous glucose monitoring is increasingly recommended, and special populations such as pregnancy and type 1 diabetes require tailored glycemic targets and insulin-based management.

The analytical technique in the psychotic part of the personality faces challenges in the interpretation-construction of the primitive material, requiring more sensorial approaches, such as metaphors and myths. Interpretation should consider analogy, symmetry and polyvalence, helping the patient to reconstruct his way of thinking. Bion explains that through sounds and associations, internal conflicts about rivalry and envy are revealed. The psychoanalytic technique does not refer only to psychotics, but also to neurotics who manifest metonymic language and symbolic codes. The analyst must balance empathy and objectivity, avoiding memories and preconceptions, allowing for more authentic interpretations. The analyst's role includes containing fragmentations of the self, decoding symbolic messages, and dealing with neurotic and psychotic defenses. Bion's concept of "not knowing" highlights the importance of renouncing partial vision in order to achieve deeper understanding, comparable to the mythical wisdom of Tiresias. Finally, the psychoanalyst must be attentive to unconscious thought, which operates in a symbolic and non-logical way. The psychoanalysis of psychoses requires humility, telepathy and understanding of primitive psychic functioning, allowing the patient to differentiate the self from the object and reconstruct his psychic identity.

Renal patients face profound psychological distress arising from financial strain, disease burden, and social stigma, often reshaping their self-concept and quality of life through adaptive coping strategies. Qualitative studies reveal how patients re-evaluate personal meaning and priorities, identifying key themes like control, acceptance, and doctor-patient relationships. Quantitative data confirm high rates of psychological distress, fatigue, irritability, and sleep problems, with social support strongly linked to self-esteem. Treatment demands-dietary restrictions, medication side effects, and the physical limitations of dialysis-further disrupt daily life and personal autonomy. Meta-syntheses describe hemodialysis as both a physical and emotional “shackle,” while peritoneal dialysis may offer greater independence and a sense of control. Studies consistently highlight the heavy emotional, social, and existential toll of end-stage renal disease, emphasizing the need for holistic care that extends beyond biomedical management. Adaptation occurs through resilience, social support, and redefined identity, progressing from restriction toward regained control and optimism. However, financial hardship and limited access to psychosocial resources-especially in developing countries-exacerbate distress and hinder coping. Across this research, the central finding is clear: renal disease profoundly affects all dimensions of life, yet patients exhibit remarkable psychological flexibility and resilience. Comprehensive, multidisciplinary interventions that integrate psychological, social, and informational support-rather than focusing solely on clinical outcomes-are essential to promote adjustment, improve well-being, and enhance treatment satisfaction in this vulnerable population.

During pregnancy, significant physiological changes occur in lipid metabolism, which are fundamental for fetal development, but which may pose risks when associated with maternal dyslipidemias. Elevation of lipids such as LDL-cholesterol and triglycerides is common and physiological, but in women with genetic dyslipidemias, such as heterozygous or homozygous familial hypercholesterolemia, levels can reach pathological values. Despite this, most of these pregnant women do not present an increase in maternal-fetal risk, as long as they are adequately monitored. Severe dyslipidemias, such as hypertriglyceridemias (> 1,000 mg/dL), are associated with complications such as pancreatitis and preeclampsia. Lipoprotein (a), another risk factor, rises during pregnancy and may be linked to thrombotic events and preterm births. Lipid screening in pregnancy is recommended especially for women with a history of dyslipidemia. Preconception cardiovascular evaluation is ideal in cases of severe hypercholesterolemia. Treatment includes a balanced diet and, in specific cases, medications. Statins, although traditionally contraindicated, have been reevaluated: recent studies indicate relative safety, especially for women at high cardiovascular risk. Pravastatin has the best safety profile. Other therapeutic options include exchange resins (allowed), lipoprotein apheresis (indicated for severe cases), and omega-3 (effective in hypertriglyceridemias). Ezetimibe, PCSK9 inhibitors, ANGPTL3, bempedoic acid, lomitapide, and fibrates should be avoided or used with caution, depending on the severity and individualized risk-benefit. The therapeutic decision during pregnancy should be shared between physician and patient, balancing fetal risks and maternal benefits, always based on the most current evidence.

The kidney plays a central role in lipoprotein(a) catabolism, acting as a “cemetery for lipoprotein(a)” through uptake, fragmentation, and excretion. Direct human evidence comes from Kronenberg et al., who found significant arteriovenous differences in lipoprotein(a) levels between the aorta and renal vein, demonstrating active renal uptake. Clinical evidence from renal replacement therapy further supports this role: lipoprotein(a) levels decrease rapidly after kidney transplantation but remain unchanged with hemodialysis, indicating that functioning renal tissue, not filtration, drives lipoprotein(a) metabolism. Animal studies by Reblin et al. provided mechanistic insights, showing rapid clearance of injected human lipoprotein(a) in rats, with apolipoprotein(a) localized in proximal tubular cells and fragments detected in urine. This supports the idea that the kidney fragments lipoprotein(a) before excretion. Kostner & Kostner proposed a model where circulating lipoprotein(a) undergoes proteolytic cleavage in the kidney, producing apolipoprotein(a) fragments that may themselves be biologically active and contribute to lipoprotein(a)’s atherogenicity. Clinical observations confirm that chronic kidney disease alters lipoprotein(a) metabolism. Patients with proteinuria or amyloidosis show elevated lipoprotein(a), often correlating with urinary albumin excretion, highlighting the kidney’s regulatory role. The mechanism of elevation varies by disease: in proteinuria and peritoneal dialysis, hepatic synthesis is upregulated, while in hemodialysis, impaired catabolism predominates. These abnormalities likely amplify the already high cardiovascular risk in chronic kidney disease, particularly in individuals with genetically determined small apolipoprotein(a) isoforms. Despite advances, the precise site and mechanisms of lipoprotein(a) clearance remain unclear. However, the consensus is that reduced clearance, not increased production, drives lipoprotein(a) accumulation in kidney disease. Understanding renal processing of lipoprotein(a) may provide therapeutic opportunities, with future strategies aiming to inhibit lipoprotein(a) assembly or enhance apolipoprotein(a) fragmentation to mitigate cardiovascular risk.

Persistent chylomicronemia is a rare but serious metabolic disorder characterized by extremely high triglyceride levels - often surpassing 1,000 mg/dL - and the abnormal presence of fasting chylomicrons. This results from severely impaired clearance of chylomicrons, leading to their continuous accumulation and posing a major risk for recurrent, potentially fatal acute pancreatitis. Its etiology includes monogenic and polygenic forms. The monogenic form, known as familial chylomicronemia syndrome, is extremely rare and caused by biallelic mutations in genes essential for lipoprotein lipase function, such as lipoprotein lipase, APOC2, APOA5, GPIHBP1, and LMF1. In contrast, the polygenic/multifactorial form is far more common and results from the combined effect of multiple genetic variants together with secondary factors such as uncontrolled diabetes, obesity, hypothyroidism, alcohol intake, nephrotic syndrome, and certain medications. Clinically, the most severe consequence is acute pancreatitis, triggered by capillary obstruction and toxic free fatty acid release within the pancreas. Other manifestations include eruptive xanthomas, lipemia retinalis, hepatosplenomegaly, and neurological symptoms linked to hyperviscosity. Diagnosis involves identifying markedly elevated triglycerides (typically >885 mg/dL) and fasting chylomicrons, sometimes evident as lactescent plasma. Genetic testing is useful when familial chylomicronemia syndrome is suspected. Management requires lifelong intervention, with strict dietary fat restriction (10-15% of daily calories), avoidance of simple sugars and alcohol, and lifestyle measures such as weight loss and smoking cessation. Traditional triglyceride-lowering drugs - fibrates, omega-3 fatty acids, and niacin—are often ineffective in familial chylomicronemia syndrome due to absent lipoprotein lipase activity. Emerging therapies focus on lipoprotein lipase - independent pathways. APOC-III inhibitors, including volanesorsen, olezarsen, and plozasiran, produce substantial triglyceride reductions across various forms of chylomicronemia. Patients with residual lipoprotein lipase activity may also benefit from ANGPTL3 inhibitors. Improved recognition, education, and personalized treatment based on clinical phenotype - not solely genetics - are essential to reduce complications and mortality.

Atherosclerosis begins in childhood and can be aggravated by dyslipidemias, such as hypercholesterolemia and hypertriglyceridemia, especially in the presence of obesity and metabolic syndrome. The infant lipid profile should be assessed with a fast of 8 to 9 hours. Primary dyslipidemias, usually genetic, include heterozygous familial hypercholesterolemia and homozygous hypercholesterolemia, with diagnosis based on LDL-c levels and family history. Treatment involves diet, physical activity, and statins, and may include ezetimibe and PCSK9 inhibitors in more severe cases. Hypertriglyceridemia’s can be mild to severe, with primary causes (such as familial chylomicronemia syndrome) or secondary causes (related to diet, endocrine disease, and medications). Combined dyslipidemia is common in children with obesity and insulin resistance. Treatment is based on lifestyle changes and, in more severe cases, the use of statins, fibrates, or omega-3s. Secondary dyslipidemias are associated with diseases such as diabetes, hypothyroidism, and lupus. Treating the underlying cause can normalize lipids, but medications may be indicated in cases of moderate or high risk. Early screening is essential and should be done universally between 9-11 and 17-21 years, and selectively between 2-8 and 12-16 years for children with risk factors. Early identification and management of these conditions are key to reducing cardiovascular risk in adulthood.

The aim of this study was to evaluate clinical and laboratory results found in the database of an institution for the prevention, promotion and recovery of health. Clinical and laboratory parameters were observed during the examination of 458 medical records of patients who underwent a clinical program of acute lifestyle intervention, and what changes were produced by this treatment. The clinical parameters evaluated were body weight and waist circumference. In the statistical analysis, with statistical significance (p<0.05), there was an improvement in the biochemical indices studied in both groups, especially in the group with longer permanence, improvement in body weight, and there was also a significant improvement (p<0.05) in those with metabolic syndrome, among whom approximately 36% no longer had this condition. Acute lifestyle intervention reduced or reversed risk factors for coronary artery disease and the presence of metabolic syndrome.

Severe hypertriglyceridemia and familial chylomicronemia syndrome are lipid disorders associated with significant cardiovascular and metabolic risks. The American Congress of Cardiology 2024 highlighted transformative developments in understanding and managing these conditions. Novel therapeutic strategies, particularly targeting genetic and molecular pathways, have emerged, offering hope for improved patient outcomes. This article emphasizes the advancements in pharmacological treatments, diagnostic technologies, and multidisciplinary care approaches. Additionally, the article explores the interplay of genetic, environmental, and secondary factors in hypertriglyceridemia, integrating insights into the clinical differentiation and management of familial chylomicronemia syndrome and multifactorial severe hypertriglyceridemia.

Evidence from the China Health and Retirement Longitudinal Study (CHARLS) highlights the intertwined roles of kidney decline and cardiometabolic-renal syndrome in shaping health risks among middle-aged and older adults in China. Reduced kidney function, defined by an estimated glomerular filtration rate below 60 ml/min/1.73m², is strongly associated with higher risks of cancer, hearing loss, and falls, emphasizing chronic kidney disease as a systemic driver of poor health rather than a condition limited to renal outcomes. CHARLS findings identify multiple risk factors for chronic kidney disease, including frailty, sarcopenia, circadian syndrome, social isolation, adverse early-life health and unfavorable social determinants, particularly in men. Conversely, regular physical activity of over 300 minutes per week consistently reduces chronic kidney disease risk by approximately 40%, underscoring its protective role. Cardiometabolic-renal syndrome, which integrates cardiovascular, metabolic, and renal dysfunction, is highly prevalent, with baseline rates ranging from 6.3% to 46.3% depending on classification. Disease progression is substantial, with nearly 30% worsening over four years. Chronic kidney disease incidence is particularly elevated in individuals with cardiovascular disease and metabolic syndrome. Determinants of cardiometabolic-renal progression include metabolic dysfunction, cardiovascular comorbidities, systemic inflammation (e.g., high C-reactive protein), visceral obesity, advanced age, male sex, and depression. Once again, physical activity emerges as a protective factor. Population disparities are evident: men tend to experience greater deterioration, lower socioeconomic groups face higher disability risks, and regional variations influence disease prevalence and staging. Overall, CHARLS studies reveal overlapping biological and social pathways linking kidney decline and cardiometabolicrenal syndrome, involving inflammation, frailty, and socioeconomic disadvantage. Physical activity consistently mitigates these risks, highlighting the importance of targeted interventions, particularly for older men, disadvantaged populations, and individuals with metabolic or cardiovascular vulnerabilities

This review explores how spirituality and religion influence healthcare at the patient, provider, and system levels, shaping decisions, processes, and outcomes. Evidence highlights two main strands: the impact of religious beliefs and practices on care trajectories, and the effects of structured spiritual interventions. At the provider level, clinicians’ religious affiliation strongly influences end-of-life decisions. For example, Jewish, Greek Orthodox, and Muslim physicians are more inclined to withhold treatment, while Catholic, Protestant, and non-affiliated providers more often withdraw life-sustaining measures. These differences reflect divergent moral frameworks regarding death and permissible interventions. Patients’ religiosity and affiliation also affect care, often leading to more aggressive treatment near the end of life. However, chaplain involvement tends to moderate this, fostering clearer communication and value-concordant care. In mental health, intrinsic religiosity, supportive communities, and positive religious coping; seeking spiritual support, benevolent reframing are linked to better adjustment and faster recovery, while negative coping predicts poorer outcomes. Structured interventions-such as chaplaincy, spiritual group therapy, meditation, and retreats-demonstrate benefits including reduced psychological distress, improved quality of life, and greater satisfaction for patients and families across diverse settings. Importantly, these effects depend on timing, cultural tailoring, and alignment between patients and providers. Methodological challenges remain, including heterogeneous measures and limited randomized studies. Future research should clarify mechanisms, assess early integration of spiritual care, and evaluate provider training. Overall, the evidence suggests that respectful, patient-centered attention to spiritual needs can enhance psychological adjustment, improve care alignment, and support well-being, particularly in serious illness and end-of-life contexts.

There are many biochemical elements implicated with the inflammation mediators and markers and this review show their identities and their atherosclerotic effects. Cytokines identified as participants in the mechanisms of atherogenesis were first discovered as involved in the process of natural (or innate) and specific (or acquired) immunity, responsible for defending against foreign organisms such as viral or bacterial agents. They are protein hormones produced mainly by mononuclear phagocytes (monocins) in direct response to microbes, or originated from T lymphocytes (lymphocins) when stimulated by antigen, as part of specific immunity. T lymphocytes produce several cytokines that primarily serve to regulate the activation, growth and differentiation of the various lymphocyte populations. Other cytokines derived from the T lymphocyte work primarily in the activation and regulation of inflammatory cells, such as mononuclear phagocytes, neutrophils and eosinophils. Thus, cytokines derived from T lymphocyte are effector molecules of cell-mediated immunity, and are also responsible for communications between the cells of the immune and inflammatory systems.

It has long been known that the most common lipoprotein alteration among diabetic patients is hypertriglyceridemia. Plasma triglyceride elevation is directly related to decreased lipoprotein lipase activity. Mixed dyslipidemias are also common in diabetic individuals. It is worth calling attention to the abnormalities related to low-density lipoprotein cholesterol (LDL-c) particles. The treatment of dyslipidemia in diabetic individuals begins with measures aimed at adequate control of the underlying disease. Normalization of glycemic levels is often sufficient to correct Iipid changes. Diabetes control involves some non-pharmacological measures that are common to the treatment of dyslipidemias: diet and physical exercise (both related to the improvement in insulin resistance). Dietary guidance aims to adjust the daily caloric intake, so that the individual reaches and/or maintains adequate weight, and changes in the distribution of carbohydrates, proteins and fats in the diet, in order to provide satisfactory control of glycemic and lipid levels. Therefore, the introduction or adjustment of previous doses of oral hypoglycemic agents or insulin is necessary. If lipid levels remain high after adequate glycemic control and adherence to the proposed lifestyle modifications (diet, regular physical exercise...), we must rule out other causes of secondary dyslipidemia before indicating lipid-lowering drugs. The most commonly used medications in diabetic individuals are HMG[1]CoA reductase inhibitors and fibric acid derivatives.

There are many biochemical elements implicated with the inflammation mediators and markers and this review show their identities and their atherosclerotic effects. Cytokines identified as participants in the mechanisms of atherogenesis were first discovered as involved in the process of natural (or innate) and specific (or acquired) immunity, responsible for defending against foreign organisms such as viral or bacterial agents. They are protein hormones produced mainly by mononuclear phagocytes (monocins) in direct response to microbes, or originated from T lymphocytes (lymphocins) when stimulated by antigen, as part of specific immunity. T lymphocytes produce several cytokines that primarily serve to regulate the activation, growth and differentiation of the various lymphocyte populations. Other cytokines derived from the T lymphocyte work primarily in the activation and regulation of inflammatory cells, such as mononuclear phagocytes, neutrophils and eosinophils. Thus, cytokines derived from T lymphocyte are effector molecules of cell-mediated immunity, and are also responsible for communications between the cells of the immune and inflammatory systems.

There is a close relationship between emotional tensions and respiratory function, which makes it likely that many diseases of this apparatus have aetiology or are compromised by psychogenic factors, which occurs, for example, in allergic diseases such as rhinitis and asthma, as well as in certain inflammatory diseases. Asthma is diagnosed by the sensation of oppression in the chest, dyspnea that can evolve to cyanosis, discrepancy between the combined action of the diaphragm and the levator muscles of the ribs, which remove air through the narrowed bronchioles, and the weak exhalation force, which depends on the elasticity of the lungs, making breathing difficult and leading to emphysema during paroxysm. In the initial stages there may be simple cough; later, the expectoration of a thick, foamy phlegm begins. The temperature is normal and the pulse is tachycardic. Auscultation reveals crackling rales and wheezing. Asthmatics can improve with the various types of psychotherapy: supportive, cognitive behavioral techniques, counseling, relaxation techniques and mainly psychoanalytic therapy, either individual or in group. In conclusion, the treatment of asthma and allergic rhinitis, should be done by two specialists, the allergist and the psychotherapist.

C-reactive protein is a crucial biomarker for inflammation and widely used in assessing cardiovascular disease risk. Produced by the liver in response to inflammatory stimuli like infection or injury, C-reactive protein levels rise significantly during acute and chronic inflammation. High-sensitivity C-reactive protein testing detects even low-grade inflammation, providing greater accuracy in identifying cardiovascular risk. C-reactive protein relevance in cardiovascular health stems from its association with atherosclerosis, an inflammatory process that leads to plaque buildup in arteries. Elevated C-reactive protein levels are linked to higher risks of heart attacks, strokes, and heart failure. The JUPITER study demonstrated that using high-sensitivity C-reactive protein to guide statin therapy in high-risk individuals significantly reduced cardiovascular disease events and mortality. Beyond being a marker, C-reactive protein actively contributes to atherothrombosis by impairing endothelial function and promoting a pro-thrombotic environment. Genetic and environmental factors, such as smoking, diet, and seasonal variations, also influence C-reactive protein levels. Additionally, C-reactive protein is a strong predictor of adverse outcomes following acute coronary syndrome. Studies show that both high-sensitivity C-reactive protein and B-type natriuretic peptide, when measured 30 days after acute coronary syndrome, independently predict heart failure and cardiovascular death. In conclusion, C-reactive protein, particularly through high-sensitivity C-reactive protein testing, is a vital tool in evaluating inflammation and predicting cardiovascular risk. Its role in personalized medicine continues to grow, as ongoing research explores the genetic and environmental factors influencing C-reactive protein and its potential as a therapeutic target in inflammatory diseases. As research progresses, C-reactive protein remains a cornerstone in cardiovascular risk management.