Niacin (Vitamin B3) for Cholesterol Management and Heart Health Niacin, also known as Vitamin B3, is an essential nutrient belonging to the family of B vitamins that play a critical role in maintaining overall health.1 This water-soluble vitamin is vital for energy metabolism, aiding the body in converting food, including carbohydrates, fats, and proteins, into glucose, which serves as the primary source of energy.1 Beyond its role in energy production, niacin is crucial for the proper functioning of the nervous system, digestive system, and skin.2 Notably, the human body can also synthesize a limited amount of niacin from the amino acid tryptophan, which is obtained from dietary protein sources.5 The diverse physiological functions of niacin suggest that its influence on heart health may extend beyond simply modifying lipid levels, potentially involving a range of metabolic pathways and cellular processes. The term "niacin" encompasses a group of related compounds known as vitamers, which include nicotinic acid (also commonly referred to as niacin), nicotinamide (also known as niacinamide), and nicotinamide riboside.1 While all three forms can be converted within the body to nicotinamide adenine dinucleotide (NAD) and possess vitamin activity, they exhibit distinct pharmacological effects and side effect profiles, particularly in relation to lipid modification and the occurrence of skin flushing.9 Nicotinic acid is the primary form recognized for its ability to alter lipid profiles, making it relevant for managing cholesterol levels.1 In contrast, nicotinamide typically does not lower cholesterol levels or cause flushing and is often utilized in skincare formulations.1 Nicotinamide riboside is a more recently identified form of vitamin B3 that is being investigated for various potential health benefits, including its capacity to boost NAD+ levels, although its effects on lipid profiles are less pronounced compared to nicotinic acid.9 The specific focus of inquiries regarding cholesterol lowering and heart health necessitates a primary emphasis on nicotinic acid due to its established lipid-modifying properties. Following absorption, all forms of niacin are converted by bodily tissues into its principal metabolically active form, the coenzyme nicotinamide adenine dinucleotide (NAD).18 NAD serves as an essential cofactor for over 400 enzymes involved in a wide array of metabolic processes critical for cellular function, including energy transfer, DNA repair, and cell signaling.7 NAD is also converted to nicotinamide adenine dinucleotide phosphate (NADP), another active coenzyme that plays a significant role in anabolic reactions, such as the synthesis of cholesterol and fatty acids, as well as in maintaining cellular antioxidant function.18 The body possesses the ability to synthesize NAD from both dietary niacin and the amino acid tryptophan through distinct biochemical pathways.12 This fundamental involvement of niacin in numerous cellular processes suggests that its impact on cardiovascular health could extend beyond direct alterations in lipid metabolism to encompass influences on cellular functions within the cardiovascular system itself. Prescription-strength nicotinic acid has demonstrated a modest ability to lower low-density lipoprotein (LDL) cholesterol, often referred to as "bad" cholesterol.1 Typical daily dosages ranging from 1000 to 4000 mg have been shown to reduce LDL cholesterol levels by approximately 10 to 25%.23 However, it is important to note that the LDL-lowering effect of niacin may be less pronounced when compared to other commonly prescribed medications such as statins.4 While niacin does contribute to lowering LDL cholesterol, the extent of this reduction and its clinical significance in the context of contemporary cholesterol management strategies warrant careful consideration. Niacin is well-recognized for its capacity to significantly elevate high-density lipoprotein (HDL) cholesterol, often referred to as "good" cholesterol.2 Daily dosages in the range of 1000 to 4000 mg can lead to increases in HDL cholesterol levels of 10 to 30%, and in some cases, even greater than 30%.23 Despite this notable ability to raise HDL cholesterol, recent research indicates that niacin therapy may not consistently result in lower rates of death, heart attack, or stroke in most individuals.4 Some studies have even suggested that niacin might increase the levels of certain atherogenic proteins associated with HDL, potentially counteracting the anticipated benefits of elevated HDL-C levels.40 This observation, often referred to as the "niacin paradox," highlights the complexity of HDL's role in cardiovascular protection and suggests that simply increasing HDL-C numbers may not be the primary determinant of reduced cardiovascular risk. Further investigation into the functional aspects of HDL and the broader lipoprotein profile appears necessary to fully understand these findings. Niacin has demonstrated effectiveness in lowering triglyceride levels, another type of fat found in the blood.1 Daily dosages ranging from 1000 to 4000 mg can lead to reductions in triglyceride levels of 20 to 50%.23 This triglyceride-lowering effect of niacin may be particularly beneficial for individuals with very high triglyceride levels who face an increased risk of pancreatitis.4 The consistent reduction in triglycerides observed with niacin treatment suggests that this might be one of its more reliable benefits, especially in specific patient populations where elevated triglycerides are a primary concern. Niacin exerts its effects on lipid profiles through several key mechanisms. It reduces the liver's production of very low-density lipoprotein (VLDL), which serves as a precursor to LDL, thereby leading to lower levels of both LDL and triglycerides in the bloodstream.20 This reduction in VLDL production is partly attributed to niacin's inhibition of diacylglycerol O-acyltransferase 2 (DGAT2), a crucial enzyme involved in the synthesis of triglycerides within the liver.24 Furthermore, niacin has been observed to increase the size and buoyancy of LDL particles, which may have implications for their atherogenic potential.31 The precise mechanism by which niacin increases HDL cholesterol is not entirely elucidated but appears to involve the inhibition of apolipoprotein A1 breakdown, a key protein component of HDL, as well as the suppression of cholesterol ester transfer protein (CETP) production, which plays a role in HDL metabolism.24 Additionally, niacin activates specific G protein-coupled receptors, including hydroxycarboxylic acid receptor 2 (HCA2) and HCA3, predominantly expressed in adipose tissue. Activation of these receptors leads to a reduction in the release of free fatty acids from fat cells, consequently reducing the availability of these fatty acids to the liver for the synthesis of triglycerides and other lipoproteins.16 The multifaceted impact of niacin on various aspects of lipoprotein metabolism underscores its broad influence on the overall lipid profile. Beyond its effects on cholesterol levels, niacin has been observed to influence other factors relevant to overall heart health. It has been shown to improve blood circulation 1 and possesses vasodilatory properties, causing blood vessels to widen, which can manifest as flushing, particularly in the face and upper body.4 Research suggests a potential link between dietary niacin intake and a decrease in blood pressure, especially in individuals with newly diagnosed hypertension.2 However, it is also important to note that niacin can cause low blood pressure in some individuals.1 The effects of niacin on blood vessels are therefore complex, presenting both potential benefits in terms of circulation and blood pressure regulation in certain contexts, as well as risks such as flushing and hypotension in others. Niacin has demonstrated the ability to suppress inflammation.1 Studies indicate that it can inhibit inflammatory pathways by interacting with its receptor GPR109A, which is found on adipocytes and certain types of white blood cells.27 Research also suggests that niacin can modulate the secretion of pro-inflammatory cytokines, potentially contributing to its anti-atherosclerotic effects.47 However, more recent investigations have revealed a more complex picture. Excess niacin can be metabolized into byproducts, such as 2PY and 4PY, which have been implicated in increasing inflammation and potentially contributing to cardiovascular risk.22 Specifically, 4PY has been shown to directly promote inflammation within blood vessels.22 This dual nature of niacin's inflammatory effects, exhibiting both anti- and pro-inflammatory properties depending on its metabolism, may help explain some of the inconsistent findings observed in clinical trials. Some research suggests that niacin might play a role in slowing the progression of certain types of heart disease 1 and has been explored for its potential in preventing memory loss and dementia.2 Its role in improving NAD metabolism might also confer broader benefits for cellular health and longevity.37 However, it is crucial to consider that niacin has also been associated with an increased risk of developing diabetes and can negatively affect blood sugar levels, which is a significant risk factor for cardiovascular disease.1 Therefore, while niacin may offer some benefits beyond cholesterol reduction, its potential to adversely impact glucose metabolism necessitates careful consideration, particularly in individuals who have or are at risk of developing diabetes. When used for managing cholesterol levels, prescription niacin is typically administered at higher doses, generally ranging from 1000 to 3000 mg per day.2 Treatment often begins with a lower dose, such as 250-500 mg taken at bedtime, which is then gradually increased over several weeks to enhance tolerance and minimize side effects like flushing.17 Extended-release formulations of niacin are available and may lead to less flushing; however, some evidence suggests a potential for increased risk of liver damage with prolonged use.1 The maximum recommended daily dosage for extended-release niacin is often 2000 mg.41 Immediate-release formulations are generally less expensive and have more extensive data supporting their role in reducing cardiovascular events and mortality, but they are more likely to cause flushing.23 The maximum daily dose for immediate-release niacin can be as high as 6000 mg.21 The choice between immediate-release and extended-release niacin involves a consideration of the trade-offs between flushing and the potential for liver toxicity, underscoring the importance of medical guidance in selecting the appropriate formulation. Niacin is also available as an over-the-counter (OTC) supplement; however, it is important to recognize that these supplements are not subject to the same regulatory oversight as prescription medications, and the quality and effects of different products can vary.4 Using OTC niacin to treat high cholesterol without consulting a healthcare professional is not recommended due to the potential for serious side effects at the high doses required for lipid management.2 The recommended daily allowance (RDA) for niacin as a nutrient is significantly lower (14-16 mg for adults) than the dosages used for cholesterol management 4, and the upper tolerable limit (UL) for niacin from supplements is 35 mg per day.5 This substantial difference between nutritional requirements and pharmacological dosages highlights the need to distinguish between supplementation for general health and the use of niacin as a medication for specific medical conditions. The selection of a niacin formulation, whether immediate-release or extended-release, should be tailored to the individual's needs and tolerance, ideally in consultation with a healthcare provider. Timed-release or extended-release niacin formulations may be associated with fewer flushing episodes compared to regular niacin.1 However, long-term use of these formulations has been linked to an increased risk of liver damage in some instances.1 Immediate-release niacin is absorbed more rapidly and is generally less expensive but tends to cause more pronounced flushing.23 A common recommendation is to take extended-release niacin at bedtime after consuming a low-fat snack.29 Ultimately, the decision regarding the most suitable formulation should involve a discussion with a healthcare professional who can assess the patient's specific risk factors for side effects, the presence of any liver conditions, and the overall goals of lipid management, while also considering the cost of the medication. One of the most common side effects associated with niacin supplementation, particularly at higher doses, is flushing, characterized by a sensation of warmth, redness, itching, or tingling of the skin, primarily affecting the face and neck.1 This reaction, which can occur in up to 70% of individuals taking niacin, is caused by the dilation of blood vessels and is largely mediated by the release of prostaglandin D2.44 Gastrointestinal issues are also frequently reported, including upset stomach, nausea, vomiting, diarrhea, and abdominal pain.1 Other common side effects may include headache, dizziness, and itching.1 The high incidence of flushing can be a significant deterrent to adherence with niacin therapy, making strategies to manage this side effect particularly important. While common side effects like flushing are often manageable, higher doses and prolonged use of niacin, especially extended-release formulations, can lead to more serious adverse effects. Liver damage is a significant concern, ranging from mild elevations in liver enzymes to more severe conditions such as hepatitis and liver failure.1 Regular monitoring of liver function through blood tests is essential for individuals undergoing high-dose niacin therapy.1 Niacin has also been shown to increase blood sugar levels and may elevate the risk of developing diabetes in individuals without diabetes or worsen blood glucose control in those already diagnosed with the condition.1 Careful monitoring of blood glucose levels is therefore necessary in diabetic patients taking niacin.1 Paradoxically, despite its beneficial effects on lipid profiles, recent research has linked high levels of niacin metabolites, such as 4PY, to an increased risk of cardiovascular events, including heart attack and stroke, possibly due to the promotion of vascular inflammation.2 Other serious side effects that can occur include gout, low blood pressure, muscle pain or weakness (rhabdomyolysis, particularly when combined with statins), and disturbances in heart rhythm.1 The potential for these serious adverse events has significantly influenced the current clinical recommendations regarding the use of niacin. Several strategies can be employed to manage and mitigate the side effects of niacin. Initiating treatment with low doses and gradually increasing them can help to reduce the incidence and severity of flushing.2 Taking niacin after a meal and ensuring adequate fluid intake may help alleviate gastrointestinal upset.17 Avoiding the consumption of alcohol, hot beverages, and spicy foods around the time of niacin administration can also help minimize flushing.2 In some cases, taking a non-enteric coated aspirin (325 mg) or ibuprofen approximately 30 minutes before taking niacin may help to reduce flushing, but this should only be done under the guidance of a healthcare professional.1 While extended-release formulations may offer some reduction in flushing, their potential for liver toxicity needs to be carefully considered.1 Despite these management strategies for common side effects like flushing, the more serious risks associated with niacin often necessitate careful medical monitoring and may limit its long-term use in many patients. Niacin can interact with several classes of medications, potentially affecting their efficacy or increasing the risk of side effects. When used in combination with other cholesterol-lowering medications, particularly statins, niacin may increase the risk of side effects such as muscle inflammation or liver damage.1 Due to these concerns, the Food and Drug Administration (FDA) has withdrawn its approval for the use of extended-release niacin in combination with statins, as large clinical trials have not demonstrated that the benefits of this combination outweigh the risks.55 Niacin can also interfere with the absorption of bile acid sequestrants, such as cholestyramine, colestipol, and colesevelam, potentially reducing their effectiveness. Therefore, it is recommended that niacin be taken at least 4 to 6 hours after these medications.1 Combining niacin with gemfibrozil, another lipid-lowering drug, may increase the risk of muscle damage.65 The interaction profile of niacin with other cholesterol-lowering drugs, especially statins, suggests that caution is warranted when considering their combined use. Niacin can also interact with medications used to manage blood pressure and diabetes. It may enhance the effects of blood pressure medications, potentially leading to excessively low blood pressure (hypotension).1 Furthermore, niacin can increase blood sugar levels, which may reduce the effectiveness of diabetes medications, necessitating adjustments in dosage and careful monitoring of blood glucose.1 The risk of bleeding may be increased when niacin is taken concurrently with anticoagulant and antiplatelet medications, as well as certain herbs and supplements that have similar effects.1 Alcohol consumption can elevate the risk of liver damage and exacerbate niacin-related side effects such as flushing and itching.2 Niacin should not be taken at the same time as the antibiotic tetracycline, as it can interfere with the antibiotic's absorption.1 Additionally, taking niacin with zinc supplements might worsen flushing and itching.4 Niacin can also interact with medications used to treat gout, such as allopurinol and probenecid, potentially worsening gout and reducing the effectiveness of these medications.4 There is also a possibility that niacin might decrease the effectiveness of thyroid hormone replacement therapy 65, and the use of nicotine patches with niacin may increase the risk of flushing and dizziness.1 Certain medications, including phenytoin and valproic acid, may lead to niacin deficiency, while niacin might increase the levels of other drugs like carbamazepine and primidone.1 This extensive list of potential drug interactions underscores the critical importance of a comprehensive review of a patient's current medication regimen before initiating niacin therapy. Niacin is contraindicated in individuals with certain pre-existing medical conditions. These include active liver disease or unexplained persistent elevations in liver enzymes 4, active peptic ulcer disease or a history of stomach ulcers 2, and arterial bleeding.36 Individuals with a known hypersensitivity to niacin or any of its components should also avoid its use.36 Niacin should be used with caution in patients with a history of jaundice, hepatobiliary disease, gout, diabetes, low blood pressure, coronary artery disease, unstable angina, gallbladder conditions, and thyroid disorders.1 Furthermore, prescription niacin is generally not recommended for pregnant women who have high cholesterol.2 These numerous contraindications and conditions requiring cautious use highlight that niacin is not an appropriate treatment for all individuals and necessitates a thorough medical evaluation to assess the potential risks and benefits. Early scientific studies provided initial insights into the efficacy of niacin in managing lipid profiles. The Coronary Drug Project (conducted between 1969 and 1975) demonstrated that niacin therapy was associated with a reduction in the incidence of nonfatal myocardial infarction compared to placebo.23 A longer-term follow-up of this study, extending to 15 years, revealed an 11% lower overall mortality rate in the group that received niacin.27 The HDL-Atherosclerosis Treatment Study (HATS) showed that the combination of niacin with low-dose simvastatin led to a regression of coronary artery narrowing and a significant decrease in cardiovascular events in patients with established coronary artery disease and low levels of HDL cholesterol.27 The Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) studies suggested that niacin, whether used alone or in conjunction with a statin, could slow down or even reverse the progression of atherosclerosis, as measured by the thickness of the carotid artery wall.27 These initial studies offered promising evidence for the use of niacin in reducing cardiovascular events, particularly when used as a standalone treatment or in combination with other lipid-lowering agents. However, more recent large-scale randomized controlled trials have yielded less encouraging results regarding the benefits of adding niacin to standard statin therapy. Studies such as AIM-HIGH and HPS2-THRIVE failed to demonstrate a significant reduction in cardiovascular events or mortality with the addition of niacin to statin treatment, despite observing improvements in HDL cholesterol and triglyceride levels.4 In fact, the AIM-HIGH trial was terminated prematurely due to a lack of demonstrated efficacy.64 A meta-analysis of earlier clinical trials suggested that niacin use was associated with a reduction in the composite endpoints of any cardiovascular event and major coronary heart disease events, but not with a significant decrease in stroke incidence. Notably, the extent of the increase in HDL cholesterol achieved with niacin treatment did not appear to be significantly correlated with the magnitude of its effect on cardiovascular outcomes.31 The failure of more recent trials to replicate the earlier positive findings, especially in the context of widespread statin use, has prompted a re-evaluation of the role of niacin in cardiovascular prevention.4 The discrepancies between the outcomes of earlier and more recent clinical trials investigating niacin's efficacy may be attributed to several factors. These include variations in study design, the characteristics of the patient populations enrolled (particularly the increased prevalence of statin use in more recent trials), and the evolving understanding of HDL cholesterol as a therapeutic target, with some questioning whether simply raising HDL-C levels translates to improved cardiovascular outcomes.22 The discovery of niacin metabolites, such as 4PY, that can promote inflammation offers a potential explanation for the "niacin paradox," where improvements in lipid profiles do not consistently result in a reduction in cardiovascular events.22 Current clinical practice guidelines generally do not recommend the routine addition of niacin to statin therapy for the purpose of reducing cardiovascular risk.4 However, niacin might still be considered in specific clinical scenarios, such as in patients who exhibit very high triglyceride levels and low HDL cholesterol and who are unable to tolerate statins, provided they are under close medical supervision.4 The evolving body of evidence underscores the importance of continuous research and the need to interpret findings within the context of current treatment strategies and available therapeutic options. When comparing niacin to other pharmacological treatments for high cholesterol, statins stand out as the primary therapy for lowering LDL cholesterol and reducing the risk of cardiovascular events, supported by a robust body of evidence.4 Other medications available for managing cholesterol include ezetimibe, PCSK9 inhibitors, and bile acid sequestrants, each targeting different aspects of lipid metabolism.1 Fibrates represent another class of drugs primarily used to lower triglyceride levels and raise HDL cholesterol.16 In comparison to statins, niacin's ability to lower LDL cholesterol is generally less potent, and its effectiveness in reducing cardiovascular events, particularly when added to statins, has not been consistently demonstrated in recent clinical trials.4 While niacin does impact multiple lipid parameters, the availability of more effective and better-tolerated LDL-lowering drugs like statins has led to a more limited role for niacin as a first-line treatment for high cholesterol in many patients. Lifestyle modifications, encompassing a heart-healthy diet, regular physical activity, weight management, and cessation of smoking, are fundamental to the management of high cholesterol and the promotion of heart health.4 These modifications can contribute to improvements in cholesterol levels, including lowering LDL and triglycerides and raising HDL, as well as reducing other significant cardiovascular risk factors.22 In some individuals, lifestyle changes alone may be sufficient to achieve and maintain healthy cholesterol levels, while in others, they serve as a crucial adjunct to pharmacological interventions.4 Therefore, lifestyle modifications should always form the cornerstone of any strategy aimed at managing high cholesterol and promoting cardiovascular well-being, and the potential role of niacin, if any, should be considered within this broader context. Despite the limitations highlighted by recent research, niacin might still be considered a suitable treatment option in specific situations. For instance, it may be considered for patients who present with high triglyceride levels and low HDL cholesterol, particularly if they are unable to tolerate statin medications.4 Niacin could also be an option for individuals who cannot take statins due to intolerable side effects and who require LDL lowering, although other alternatives with stronger evidence for cardiovascular risk reduction might be preferred based on current guidelines.4 In certain cases, niacin might be used in combination with other lipid-lowering therapies under close medical supervision, although the evidence supporting additional benefit in reducing cardiovascular events in such combinations is currently limited.2 The decision to use niacin should be based on a thorough assessment of the individual patient's lipid profile, overall cardiovascular risk factors, tolerance to other medications, and the most current evidence derived from clinical trials, always under the guidance of a healthcare professional. Table 1: Different Forms of Niacin (Vitamin B3)FormOther NamesPrimary Effects on LipidsCommon Side EffectsTypical UsesNicotinic AcidNiacinLowers LDL, Lowers Triglycerides, Raises HDLFlushing, Gastrointestinal upset, HeadacheCholesterol management, treatment of niacin deficiencyNicotinamideNiacinamideMinimal effect on lipidsGenerally well-tolerated at typical dosesTreatment of niacin deficiency, often used in skincare productsNicotinamide RibosideNRLess pronounced lipid-modifying effects compared to nicotinic acidWell-tolerated at typical dosesInvestigated for NAD+ boosting and other potential health benefits Table 2: Niacin Dosage Guidelines for Hyperlipidemia (Adults)FormulationStarting DosageMaintenance DosageMaximum DosageKey ConsiderationsImmediate-Release250 mg orally once daily with the evening meal1 to 2 g orally 2 to 3 times a day6 g/day in 2 to 3 divided dosesTake with food to reduce GI upset, higher risk of flushing, inexpensiveExtended-Release500 mg orally at bedtime1 to 2 g orally once daily at bedtime2 g/dayMay cause less flushing, potentially higher risk of liver damage with long-term use, take after a low-fat snack Table 3: Key Drug Interactions with NiacinDrug Category/Specific DrugPotential InteractionClinical SignificanceStatinsIncreased risk of muscle damage (myopathy, rhabdomyolysis) and liver damageUse with caution, monitor for side effects, FDA no longer supports co-administration of extended-release niacin with statins for cardiovascular risk reduction in statin-treated patientsBile Acid SequestrantsReduced absorption and effectiveness of both niacin and the sequestrantTake niacin 4-6 hours after the bile acid sequestrantBlood Pressure MedicationsEnhanced hypotensive effects, potentially leading to low blood pressureMonitor blood pressure closely, dosage adjustments of blood pressure medication may be necessaryDiabetes MedicationsIncreased blood sugar levels, potentially reducing the effectiveness of diabetes drugsMonitor blood glucose closely, dosage adjustments of diabetes medication may be necessaryAnticoagulants/AntiplateletsIncreased risk of bleedingUse with caution, monitor for signs of bleedingAlcoholIncreased risk of liver damage and worsening of niacin side effects (flushing, itching)Avoid or limit alcohol consumption, especially around the time of niacin intake Table 4: Summary of Key Clinical Trials Investigating Niacin for Cardiovascular HealthStudy Name (Year)Patient PopulationIntervention (Niacin Dosage)Key Outcomes Related to Lipid Levels and Cardiovascular EventsOverall ConclusionCoronary Drug Project (1969-1975)Patients with previous myocardial infarction3 g/day nicotinic acidReduced nonfatal myocardial infarction, trend towards lower mortalityNiacin showed benefit in secondary prevention as monotherapyHATS (1992)Patients with coronary artery disease and low HDL-CNiacin and colestipol vs. placeboIncreased HDL-C, regression of coronary stenosis, reduced cardiovascular eventsCombination therapy showed benefit in reducing events and atherosclerosis progressionAIM-HIGH (2011)Patients with established CVD and atherogenic dyslipidemia on statin therapyExtended-release niacin 1.5-2 g/day vs. placeboIncreased HDL-C, lowered triglycerides, no reduction in cardiovascular events, increased risk of ischemic stroke (non-significant)Adding niacin to statin therapy did not reduce cardiovascular eventsHPS2-THRIVE (2014)Patients with established vascular diseaseExtended-release niacin 2 g/day + laropiprant vs. placeboIncreased HDL-C, lowered triglycerides, no significant reduction in major vascular events, increased risk of serious adverse eventsAdding niacin to statin-based therapy did not significantly reduce cardiovascular events and was associated with more adverse events In conclusion, while niacin (specifically nicotinic acid) has been shown to favorably alter lipid profiles by lowering LDL cholesterol and triglycerides and raising HDL cholesterol, its role in improving overall heart health has become increasingly complex and less certain with the results of recent large-scale clinical trials. The earlier promise of niacin in reducing cardiovascular events, particularly as a monotherapy, has not been consistently replicated when added to contemporary standard treatments like statins. Furthermore, the potential for significant side effects, including liver damage, new-onset diabetes, and the paradoxical association of high niacin metabolite levels with increased cardiovascular risk, necessitates a cautious approach to its use. Lifestyle modifications remain the cornerstone of managing high cholesterol and promoting heart health. While niacin might still have a role in specific clinical scenarios, such as in patients with significant hypertriglyceridemia or those intolerant to statins, its use should be carefully considered under close medical supervision, taking into account the individual patient's risk factors, potential drug interactions, and the latest available evidence.