What Causes High Triglycerides With Normal Cholesterol Key Factors

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High triglycerides accompanied by normal cholesterol levels present a metabolic paradox often overlooked in clinical assessments. While elevated triglycerides independently increase cardiovascular risk, their dissociation from LDL cholesterol complicates diagnostic and therapeutic approaches. This condition arises from a confluence of dietary excesses, insulin resistance, and endocrine disruptions that selectively amplify hepatic triglyceride synthesis without proportionally affecting LDL metabolism. Understanding these mechanisms is critical, as interventions targeting triglycerides alone may fail to address the root causes—ranging from fructose-driven lipogenesis to genetic mutations in lipoprotein metabolism.

The interplay between macronutrient ratios, hormonal imbalances, and physical activity further obscures the distinction between isolated triglyceride elevation and broader dyslipidemia. For instance, metabolic syndrome and polycystic ovary syndrome frequently manifest with elevated triglycerides yet stable LDL, driven by hyperinsulinemia and cortisol excess. Meanwhile, genetic predispositions such as APOA5 deficiencies disrupt triglyceride clearance without impairing LDL receptor function. Deciphering these pathways enables precision in patient management, from dietary modifications to targeted pharmacotherapies that restore lipid homeostasis.

what causes high triglycerides but normal cholesterol

Biological and Metabolic Causes of High Triglycerides with Normal LDL Cholesterol

The discrepancy between elevated triglycerides and normal low-density lipoprotein (LDL) cholesterol levels arises from distinct metabolic pathways governing triglyceride synthesis, clearance, and lipoprotein assembly. Unlike LDL, which primarily reflects dietary cholesterol absorption and hepatic LDL receptor activity, triglycerides are dynamically influenced by carbohydrate metabolism, insulin signaling, and genetic predispositions that selectively impair triglyceride-rich lipoprotein (TRL) processing. This imbalance is particularly evident in metabolic disorders where insulin resistance and overnutrition drive hepatic lipogenesis without proportionate increases in LDL production.
Key Biochemical Distinction:
Triglycerides originate from de novo lipogenesis (DNL) in the liver, whereas LDL cholesterol is derived from dietary cholesterol or hepatic synthesis via the HMG-CoA reductase pathway. Insulin resistance disrupts this balance by enhancing DNL while sparing LDL receptor-mediated clearance.

Excess Dietary Carbohydrates and De Novo Lipogenesis

High intake of fructose and refined carbohydrates (e.g., sucrose, high-fructose corn syrup) directly elevates hepatic triglyceride synthesis through de novo lipogenesis (DNL), a process where excess acetyl-CoA is converted to fatty acids via fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC). Unlike glucose, fructose is metabolized independently of insulin, bypassing glycolytic regulation and overwhelming hepatic triglyceride synthesis capacity.

Biochemical Pathway Overview:
1. Fructose Metabolism:

  • Fructose is rapidly phosphorylated by ketohexokinase in the liver, generating fructose-1-phosphate, which enters glycolysis as glyceraldehyde and dihydroxyacetone phosphate (DHAP).
  • DHAP is converted to glycerol-3-phosphate, a backbone for triglyceride assembly.
  • Excess acetyl-CoA from fructose metabolism drives malonyl-CoA production, inhibiting carnitine palmitoyltransferase-1 (CPT-1) and reducing fatty acid oxidation, further promoting lipogenesis.

    • 2. VLDL Overproduction:

  • Triglycerides synthesized via DNL are packaged into very low-density lipoproteins (VLDL) for secretion.
  • Chronic VLDL overproduction saturates lipoprotein lipase (LPL) activity, delaying triglyceride clearance and increasing circulating TRL levels.
  • LDL cholesterol remains relatively stable because dietary cholesterol absorption and hepatic LDL receptor activity are less sensitive to carbohydrate-induced lipogenesis.

    • Comparative Impact on Lipid Profiles:

  • High-carbohydrate diets (e.g., >55% of total calories) elevate triglycerides by 20–50% within weeks, while LDL cholesterol changes by <10%.
  • Low-fat, high-carbohydrate diets (e.g., Mediterranean-style with olive oil) reduce triglycerides by 30–40% without significantly lowering LDL, demonstrating the selective metabolic response.

    • Insulin Resistance and Hepatic Lipid Dysregulation

    Insulin resistance is the central mediator of elevated triglycerides in the absence of LDL abnormalities. Hyperinsulinemia, a compensatory response to peripheral insulin resistance, exerts dual effects on lipid metabolism:
    1. Stimulation of Hepatic Lipogenesis:
  • Insulin activates sterol regulatory element-binding protein-1c (SREBP-1c), a transcription factor that upregulates FAS, ACC, and glycerol-3-phosphate acyltransferase (GPAT), accelerating triglyceride synthesis.
  • Insulin suppresses adenosine monophosphate-activated protein kinase (AMPK), reducing fatty acid oxidation and amplifying DNL.

    • 2. Suppression of Lipoprotein Lipase (LPL) Activity:

  • Insulin inhibits LPL in adipose tissue, reducing triglyceride hydrolysis from chylomicrons and VLDL, thereby prolonging their circulation.
  • Postprandial hypertriglyceridemia becomes pronounced due to delayed clearance, even in the absence of dietary fat excess.

    • 3. Selective Sparing of LDL Cholesterol:

  • LDL levels are regulated by hepatic LDL receptor activity, which is primarily influenced by cholesterol homeostasis (via HMG-CoA reductase and PCSK9 pathways) rather than insulin.
  • Insulin resistance may modestly reduce LDL receptor expression due to leptin resistance (discussed later), but the effect is less pronounced than the rise in VLDL-TG.

    • Insulin Signaling Pathway in Triglyceride Metabolism:

    Key Nodes:
  • Insulin → PI3K/AKT → mTORC1 → SREBP-1c (↑ DNL)
  • Insulin → PKB → Inhibition of LPL (↓ Triglyceride clearance)
  • Insulin → Suppression of AMPK (↓ Fatty acid oxidation)
    • Clinical Correlates:
  • Fasting insulin >15 µU/mL correlates with triglycerides >200 mg/dL in insulin-resistant individuals, even with normal LDL (<130 mg/dL).
  • Metabolic syndrome (defined by waist circumference, blood pressure, glucose, and triglycerides) exhibits triglycerides ≥150 mg/dL in ~70% of cases, with LDL often in the optimal range (<100 mg/dL).

    • Metabolic Disorders Associated with Isolated Hypertriglyceridemia

    The following table summarizes metabolic conditions where triglycerides are disproportionately elevated relative to LDL cholesterol, highlighting hormonal imbalances, diagnostic criteria, and lipid profiles.
    Condition Key Hormonal Imbalances Diagnostic Criteria Typical Triglyceride Range (mg/dL) LDL Cholesterol Profile (mg/dL)
    Metabolic Syndrome
    • Hyperinsulinemia (fasting insulin >10 µU/mL)
    • Leptin resistance (↑ leptin, ↓ leptin receptor sensitivity)
    • Cortisol excess (↑ 11-deoxycortisol in some cases)
    • Waist circumference ≥40" (men) or ≥35" (women)
    • Triglycerides ≥150 mg/dL
    • HDL-C <40 (men) or <50 (women)
    • Blood pressure ≥130/85 mmHg
    • Fasting glucose ≥100 mg/dL
    		 150–500 70–130 (often normal or borderline)
    Type 2 Diabetes Mellitus
    • Chronic hyperinsulinemia → ↓ insulin receptor sensitivity
    • ↑ Glucagon (↓ hepatic fatty acid oxidation)
    • ↑ Free fatty acids (↑ VLDL secretion)
    • Fasting glucose ≥126 mg/dL or HbA1c ≥6.5%
    • Triglycerides ≥150 mg/dL in ~50–60% of cases
    • Often accompanied by hypertension or albuminuria
    		 150–600 60–120 (LDL may be low due to ↑ LPL activity)
    Polycystic Ovary Syndrome (PCOS)
    • Hyperandrogenism (↑ testosterone, ↓ SHBG)
    • Insulin resistance (↑ cortisol, ↓ adiponectin)
    • Leptin resistance (↑ visceral adiposity)
    • Oligomenorrhea or anovulation
    • Clinical/hormonal hyperandrogenism
    • Triglycerides ≥150 mg/dL in ~40% of cases
    • Often coexists with metabolic syndrome
    		 150–400 70–120 (LDL typically unaffected)
    Hyp

    what causes high triglycerides but normal cholesterol - Ilustrasi 2

    Dietary and Lifestyle Triggers of Elevated Triglycerides with Normal LDL Cholesterol

    High triglycerides (TGs) with stable LDL cholesterol levels often stem from specific dietary patterns and lifestyle factors that disproportionately stimulate hepatic very-low-density lipoprotein (VLDL) secretion without significantly altering LDL synthesis or clearance. Unlike LDL, which reflects long-term cholesterol metabolism, triglycerides respond acutely to macronutrient composition, insulin resistance, and metabolic stress. Research demonstrates that excessive dietary fructose, refined carbohydrates, and certain fatty acids—particularly when consumed in isolation or in imbalanced ratios—can elevate TGs by 20–50% within hours to days, while leaving LDL and HDL relatively unchanged. This phenomenon is particularly evident in high-carbohydrate/low-fat (HCLF) diets, where insulin-mediated lipogenesis dominates, and in omega-6/omega-3 imbalances, where pro-inflammatory eicosanoids impair lipoprotein lipase (LPL) activity. Below, the mechanisms, hidden dietary triggers, and fat-specific responses are examined with clinical evidence.

    Macronutrient Ratios and Triglyceride Disproportion

    The acute and chronic effects of macronutrient ratios on triglycerides are mediated by distinct metabolic pathways. Unlike LDL, which is primarily influenced by dietary cholesterol and saturated fats, triglycerides are highly sensitive to carbohydrate load, de novo lipogenesis (DNL), and fatty acid oxidation efficiency. Key ratios and their mechanisms include:

    - High-Carbohydrate/Low-Fat (HCLF) Diets (60–70% carbs, <20% fat)
    Studies show that low-fat, high-carbohydrate diets—particularly those rich in refined starches and sugars—increase TG levels by 30–60% within 24–48 hours due to:

  • Insulin-mediated suppression of hormone-sensitive lipase (HSL), reducing free fatty acid (FFA) release from adipose tissue.
  • Enhanced hepatic DNL, where excess glucose is converted to fatty acids via acetyl-CoA, packaged into VLDL, and secreted into circulation.
  • Reduced LPL activity, as insulin resistance impairs TG hydrolysis in peripheral tissues.
    • Clinical Evidence: A 2016 meta-analysis (Journal of the American Heart Association) found that low-fat diets high in refined carbs raised TGs by 1.2 mmol/L (105 mg/dL) compared to moderate-fat diets, with no significant change in LDL.

    - Omega-6 to Omega-3 Imbalance (>10:1 ratio)
    The omega-6/omega-3 ratio critically influences TG metabolism through:

  • Prostaglandin and leukotriene synthesis: Excess omega-6 (linoleic acid, LA) promotes pro-inflammatory eicosanoids, which impair LPL function and increase hepatic VLDL secretion.
  • Competitive inhibition of omega-3 metabolism: High LA intake reduces EPA/DHA incorporation into cell membranes, blunting their TG-lowering effects (via reduced hepatic DNL and increased β-oxidation).
    • Clinical Evidence: A 2019 study in The American Journal of Clinical Nutrition demonstrated that replacing 5% of energy from LA with EPA/DHA lowered TGs by 22% in metabolic syndrome patients, while maintaining LDL levels.

    - Very Low-Carbohydrate/Ketogenic Diets (VLCKD, <50g carbs/day)
    While VLCKDs are effective for short-term TG reduction, their long-term impact depends on fat quality and protein intake:

  • Initial TG drop (1–3 weeks): Ketosis reduces DNL and increases FFA oxidation, lowering TGs by 30–40%.
  • Plateau or rebound (3+ months): If dietary fat is high in omega-6 or trans fats, TG levels may stabilize at elevated levels due to increased VLDL secretion and reduced LPL sensitivity.
    • Clinical Evidence: A 2020 randomized trial (Nutrients) found that VLCKDs with high monounsaturated fats (MUFAs) reduced TGs by 35% after 6 months, whereas those with high polyunsaturated fats (PUFAs) showed only a 15% reduction.

    Hidden Dietary Culprits and Sugar/Fructose Sources

    Excessive fructose and refined sugars—often concealed in processed foods—are primary drivers of TG elevation due to their direct hepatic lipogenic pathway and minimal satiety effect. Unlike glucose, fructose is metabolized exclusively in the liver, bypassing insulin regulation and accelerating DNL.

    Common Sources of Hidden Sugars/Fructose:
    Fructose is not just in obvious sweets but also in savory processed foods, "healthy" snacks, and alcohol. Below are the most potent TG-raising sources, ranked by fructose content per serving and metabolic impact:

    • High-Fructose Corn Syrup (HFCS) and Sucrose
    • Present in sodas, energy drinks, and fruit-flavored yogurts.
    • 12–15g fructose per 100mL in sugary beverages; a single can of soda (~355mL) delivers 40–50g fructose, equivalent to 2–3 times the liver’s capacity for metabolism per hour.
    • Mechanism: HFCS-55 (55% fructose) increases urric acid and VLDL-TG secretion more than sucrose (50% fructose, 50% glucose) due to faster hepatic uptake.
    • "Healthy" Snacks and Low-Fat Processed Foods
    • Granola bars, protein bars, and "diet" cereals often contain 15–25g added sugars per serving, primarily as isomaltulose (palatinose) or agave syrup—both metabolized like fructose.
    • Example: A single "low-fat" muffin may contain 12g fructose, triggering a 30% spike in postprandial TGs within 3 hours (Journal of Nutrition, 2017).
    • Condiments and Sauces
    • Ketchup, BBQ sauce, and salad dressings contain 5–10g sugar per 2 tbsp, with ~40% as fructose.
    • Case Study: A 2018 study in Diabetologia found that consuming 50g fructose from condiments (e.g., 5 tbsp ketchup) raised postprandial TGs by 25% compared to glucose.
    • Dried Fruits and Fruit Juices
    • Raisins, apricots, and apple juice are concentrated fructose sources—1 cup of apple juice = 35g fructose, similar to a soda.
    • Metabolic Impact: Juices bypass fiber, leading to rapid fructose absorption and hepatic TG synthesis without compensatory glucose-induced insulin suppression.
    • Alcohol and Alcohol-Free Cocktails
    • Beer and sweet wines contain 5–10g fructose per serving from fermentation residues.
    • Alcohol-free cocktails (e.g., mocktails with grenadine, fruit syrups) can deliver 20–30g added sugars per drink, with ~50% as fructose.
    • Dual Mechanism:
    • Direct hepatic TG synthesis: Alcohol metabolism (via ADH and MEOS pathways) generates NADH, which shunts acetyl-CoA toward TG synthesis rather than oxidation.
    • HDL-raising effect: Moderate alcohol (1 drink/day) may increase HDL by 5–10% via increased apoA-I synthesis, but this is offset by TG elevation in heavy drinkers (>2 drinks/day).
    Step-by-Step Guide to Identify Hidden Sugar/Fructose Sources:
    1. Scan Nutrition Labels for "Added Sugars"
  • Look for terms: high-fructose corn syrup, sucrose, dextrose, maltose, agave, honey, maple syrup, fruit juice concentrates.
  • Fructose is often listed under "other carbohydrates" if not explicitly named.

    • 2. Avoid "Low-Fat" or "Diet" Foods

  • Manufacturers compensate for fat removal with added sugars (e.g., fat-free yogurt may contain 20g sugar/serving).

    • 3. Check Condiments and Sauces

  • Ketchup, BBQ sauce, and teriyaki sauce can add 10–20g sugar per meal. Opt for sugar-free versions or homemade alternatives.

    • 4. Limit Fruit

    what causes high triglycerides but normal cholesterol - Ilustrasi 3

    Hormonal and Endocrine Disruptions in Elevated Triglycerides with Normal LDL Cholesterol

    Endocrine and hormonal imbalances represent a critical yet often underappreciated mechanism underlying isolated hypertriglyceridemia, where triglyceride (TG) levels rise independently of low-density lipoprotein cholesterol (LDL-C). These disruptions alter lipid metabolism through direct effects on hepatic lipogenesis, lipoprotein clearance, and peripheral fat mobilization, often without significantly impacting LDL-C due to compensatory regulatory pathways. Thyroid dysfunction, sex hormone fluctuations, and chronic stress-mediated cortisol excess exemplify how endocrine axes intersect with lipid metabolism, necessitating a mechanistic understanding for accurate diagnosis and targeted intervention.

    The following sections delineate the pathophysiological pathways by which thyroid disorders, hormonal contraceptives, menopause, and stress-related cortisol excess contribute to elevated triglycerides while sparing LDL-C. Emphasis is placed on actionable diagnostic criteria, comparative hormonal effects, and clinical decision-support frameworks to guide endocrine-driven lipid management.

    Thyroid Dysfunction and Lipid Metabolism: Mechanistic Pathways to Isolated Hypertriglyceridemia

    Thyroid hormones exert profound control over lipid metabolism via thyroid hormone receptors (THRs) in the liver, adipose tissue, and skeletal muscle. Dysregulation—whether hypothyroidism or hyperthyroidism—disrupts the balance between triglyceride synthesis, clearance, and oxidation, often resulting in selective TG elevation without parallel changes in LDL-C. The underlying mechanisms involve altered lipoprotein lipase (LPL) activity, hepatic very-low-density lipoprotein (VLDL) overproduction, and subclinical thyroid dysfunction, which may evade conventional diagnostic thresholds.

    Key Mechanistic Overview:

  • Hypothyroidism: Reduced thyroid hormone (T3/T4) activity decreases LPL activity in adipose tissue and skeletal muscle, impairing TG hydrolysis from chylomicrons and VLDL. Concurrently, hepatic lipase (HL) activity declines, prolonging VLDL circulation and promoting TG enrichment. Hepatic steatosis and increased fatty acid uptake further drive VLDL secretion, exacerbating hypertriglyceridemia. LDL-C may remain normal due to compensatory reductions in LDL receptor activity or altered apolipoprotein B (apoB) metabolism.
  • Hyperthyroidism: Elevated thyroid hormones enhance LPL activity, accelerating chylomicron clearance but simultaneously increasing hepatic VLDL secretion via upregulated sterol regulatory element-binding protein (SREBP)-1c. The net effect is often a biphasic TG response: moderate hypertriglyceridemia in early stages (due to VLDL overproduction) with eventual normalization as LPL-mediated clearance dominates. LDL-C may decrease due to enhanced LDL receptor activity or reduced apoB synthesis.

    • Diagnostic Thresholds for Subclinical Thyroid Disorders:
    Subclinical hypothyroidism (elevated TSH with normal free T4) and subclinical hyperthyroidism (suppressed TSH with normal free T4) are frequently associated with mild-to-moderate TG elevation. Key diagnostic cutoffs include:

  • Subclinical hypothyroidism: TSH ≥ 4.5–10 mIU/L (varies by guideline; ATA suggests ≥ 4.5 mIU/L as a threshold for intervention in high-risk patients).
  • Subclinical hyperthyroidism: TSH < 0.1–0.4 mIU/L, with free T4 in the upper normal range.
  • Reverse T3 (rT3) elevation: In non-thyroidal illness or severe hypothyroidism, rT3 competes with T3 for THR binding, exacerbating lipid dysregulation. Monitoring rT3 may identify occult thyroid resistance in hypertriglyceridemic patients.

    • Comparative Lipid Profiles:

    ConditionTriglyceridesLDL-CHDL-CVLDL
    Hypothyroidism↑↑ (300–1000 mg/dL)Normal or ↓ (if apoB ↓)↓ (reduced LCAT activity)↑↑ (prolonged clearance)
    Hyperthyroidism↑ (150–300 mg/dL)↓ (if LDL receptor ↑)↑ (increased CETP)↑ (early phase), then ↓

    Hormonal Contraceptives and Menopause: Estrogen-Progesterone Dynamics in Triglyceride Regulation

    Sex hormones modulate lipid metabolism through estrogen receptor (ER)-mediated hepatic lipogenesis, progesterone-induced insulin resistance, and apolipoprotein regulation. The ratio of estrogen to progesterone, route of administration (oral vs. transdermal), and menopausal status dictate the magnitude and selectivity of TG responses, often dissociating TG elevation from LDL-C changes.

    Estrogen/Progesterone Ratios and Triglyceride Synthesis:

  • Estrogen dominance (e.g., high-dose estrogen therapy or oral contraceptives with low-progesterone content) suppresses hepatic lipogenesis via ERα activation, reducing VLDL secretion. However, progesterone excess (e.g., progestin-only contraceptives or combined oral contraceptives with high androgenic activity) promotes:
  • Insulin resistance (via progesterone receptor modulation of GLUT4 translocation).
  • Increased hepatic diacylglycerol acyltransferase (DGAT2) activity, enhancing TG synthesis.
  • Reduced LPL activity, impairing TG clearance.
  • Postmenopausal hormone therapy (MHT): Selective estrogen receptor modulators (SERMs) like conjugated equine estrogen (CEE) + bazedoxifene may lower TGs via ERβ agonism, whereas unopposed estrogen (e.g., CEE alone) can elevate TGs by 10–20% due to unchecked hepatic lipogenesis.

    • Oral vs. Transdermal Contraceptives: Route-Specific Effects

  • Oral contraceptives: First-pass metabolism in the liver induces shunt hyperlipidemia via:
  • Ethinyl estradiol (EE)-mediated induction of SREBP-1c, increasing fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC) activity.
  • Progestin-induced insulin resistance, amplifying VLDL secretion.
  • Net effect: TG increases by 20–40% in susceptible individuals, with minimal LDL-C changes due to compensatory LDL receptor upregulation.
  • Transdermal contraceptives: Bypass hepatic first-pass metabolism, reducing SREBP-1c induction. TG elevations are mild (~10–20%) and less consistent, with LDL-C often unaffected.

    • Postmenopausal Hormone Therapy: Selective Impact on Triglycerides vs. LDL-C

  • Estrogen-only MHT: Elevates TGs by 15–30% via ERα-mediated hepatic lipogenesis, but may lower LDL-C by 10–20% through LDL receptor upregulation.
  • Combined MHT (estrogen + progestin): TG responses vary by progestin type:
  • Micronized progesterone: Minimal TG impact; LDL-C may rise slightly.
  • Synthetic progestins (e.g., medroxyprogesterone acetate): TG increases by 20–50%, with LDL-C often unchanged or mildly elevated.

    • Decision Tree for Clinicians: Assessing Endocrine-Related Causes
    The following framework integrates symptoms, lab tests, and red flags to prioritize endocrine evaluations in hypertriglyceridemic patients with normal LDL-C.

    Step 1: Symptom Inquisition (Red Flags for Endocrine Dysfunction)
  • Thyroid dysfunction:
  • Fatigue, cold intolerance, dry skin (hypothyroidism).
  • Heat intolerance, palpitations, weight loss (hyperthyroidism).
  • Subclinical clues: Unexplained bradycardia/tachycardia, delayed deep tendon reflexes (hypothyroidism), or atrial fibrillation (hyperthyroidism).
  • Hormonal contraceptives/menopause:
  • Recent initiation or change in contraceptive type.
  • Postmenopausal symptoms (vasomotor instability, vaginal dryness) with concurrent TG elevation.
  • Menstrual irregularities: Oligomenorrhea (progesterone deficiency) or amenorrhea (estrogen dominance).
  • Cortisol excess:
  • Central obesity, moon facies, proximal muscle weakness (Cushing’s syndrome).
  • Sleep disturbances, chronic fatigue, or adrenal fatigue symptoms (e.g., orthostatic hypotension).
    • Step 2: Laboratory Evaluation Beyond Lipids
  • Thyroid panel:
  • TSH, free T4, free T3, reverse T3 (in non-thyroidal illness), and thyroid peroxidase antibodies (TPO-Ab) for autoimmune thyroiditis.
  • Diagnostic algorithm: If TSH is normal but TG > 150 mg/dL, consider TSH < 2.5 mIU/L as a cutoff for subclinical hypothyroidism in high-risk patients.
  • Sex hormones:
  • Estradiol, progesterone (luteal phase), sex hormone-binding globulin (SH

    The dissociation between high triglycerides and normal cholesterol underscores a nuanced metabolic landscape where dietary triggers, insulin resistance, and endocrine dysfunction converge. While fructose and refined carbohydrates directly fuel hepatic lipogenesis, hormonal imbalances—such as those in thyroid disorders or polycystic ovary syndrome—exacerbate triglyceride accumulation through altered lipoprotein lipase activity and VLDL secretion. Clinicians must adopt a systematic approach, integrating genetic screening, fasting lipid panels, and endocrine assessments to identify underlying drivers. Ultimately, addressing this condition requires a multifaceted strategy: optimizing macronutrient intake, mitigating insulin resistance, and targeting specific hormonal or genetic pathways to normalize triglycerides without compromising cholesterol profiles.

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