FOR IMMEDIATE RELEASE
Orthomolecular Medicine News Service, January 10, 2025

Understanding the Root Causes of Dyslipidemia in Atherosclerotic Cardiovascular Disease

Richard Z. Cheng, M.D., Ph.D., Thomas E. Levy, M.D., J.D.

Highlights

A paradigm shift from the cholesterol-centric focus on symptom management to addressing the root causes of ASCVD has demonstrated potential for prevention and reversal, as shown by our recently reported 10 ASCVD reversal cases(1).

Abstract

Dyslipidemia has long been the primary target for atherosclerotic cardiovascular disease (ASCVD) treatment. However, we have recently presented compelling evidence demonstrating that dyslipidemia is an intermediary mechanistic step, not a root cause of ASCVD, and that the American Heart Association’s decades-long cholesterol-centric dogma is both unreasonable and potentially unethical, bordering on criminal negligence (2).

In our international consultation services, we have shifted from this outdated paradigm to an orthomolecular medicine-based integrative approach, focusing on restoring biochemical balance (between nutrients and toxins) and physiological harmony (among various hormones). Using this approach, we recently reported a series of 10 successful ASCVD reversal cases (1).

This paper explores the multifactorial root causes contributing to dyslipidemia, including dietary factors, nutritional deficiencies, infections, physical inactivity, and hormonal imbalances. Special attention is given to the roles of high-carbohydrate diets, ultra-processed foods, seed oils (containing high amounts of omega-6 PUFA), and high-fructose consumption. The effects of micronutrient deficiencies, such as those of vitamins B, C, D, E, and magnesium, are examined in the context of lipid metabolism. Additionally, the paper highlights the impact of chronic infections, sedentary lifestyles, and hormonal dysregulation on lipid abnormalities.

Understanding these key root causes provides a foundation for more effective prevention and treatment strategies (3). In future papers, we plan to explore these topics in greater detail, advocating for a paradigm shift from cholesterol-centric management to addressing the underlying causes of dyslipidemia and ASCVD.

Introduction

Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of morbidity and mortality worldwide. For decades, cholesterol and dyslipidemia have been central to ASCVD management strategies. However, our prior critiques of the cholesterol-centric paradigm have underscored that dyslipidemia is not the root cause but rather an intermediary mechanism of ASCV (2). Here we explore the multifactorial root causes underlying dyslipidemia, and advocate for prevention and treatment strategies that address these root causes. We focus here on categorizing the primary root causes contributing to ASCVD through dyslipidemia. More comprehensive discussions on these root causes will be presented where appropriate in subsequent papers in this series.

1. Dietary factors and dyslipidemia

• High-carbohydrate diets have been strongly associated with dyslipidemia, particularly characterized by increased triglycerides and decreased HDL cholesterol levels (4–6). This effect is especially pronounced with high glycemic index carbohydrates (5). The mechanism may involve reduced clearance of LDL particles and increased production of their precursors (7). Carbohydrate-induced hypertriglyceridemia occurs when dietary carbohydrate exceeds 55% of energy intake, despite reduced dietary fat (8). This paradoxical effect may be due to enhanced intestinal de novo lipogenesis and mobilization of stored lipids (9). However, the impact of carbohydrates on lipid metabolism is complex, with some studies suggesting that low-carbohydrate diets may have beneficial effects on atherogenic dyslipidemia (10).
• Low-carbohydrate ketogenic diets (KDs) have shown promising effects in improving metabolic disorders, particularly dyslipidemia. KDs can lead to significant reductions in triglycerides, total cholesterol, and LDL cholesterol, while increasing HDL cholesterol (11,12). These diets have been found to improve insulin sensitivity, reverse atherogenic dyslipidemia, and reduce inflammatory biomarkers associated with cardiovascular disease (13,14). KDs have also demonstrated benefits in managing obesity, metabolic syndrome, and type 2 diabetes (15,16). Studies have shown that KDs can decrease fasting serum insulin concentrations, improve LDL particle size, and reduce postprandial lipemia (11,12). While the optimal carbohydrate proportion and diet duration require further investigation, KDs appear to be a safe and effective approach for treating metabolic disorders (17,18).
• Ultra-processed foods and dyslipidemia. High consumption of ultra-processed foods (UPF) has been shown to be associated with an increased risk of dyslipidemia and other cardiometabolic disorders. Multiple prospective cohort studies have found that individuals with higher UPF intake have significantly greater odds of developing hypertriglyceridemia, low HDL cholesterol, and hypercholesterolemia (19,20). This association has been observed in both adults and adolescents (21,22). Systematic reviews and meta-analyses confirm these findings, reporting consistent positive associations between UPF consumption and increased risk of dyslipidemia, as well as diabetes, hypertension, and obesity (23,24). Longitudinal studies in children have also shown that higher UPF intake is associated with elevated total cholesterol and triglyceride levels (25). Proposed mechanisms include altered food matrix, toxicity from additives, and processing-induced contaminants affecting lipid metabolism, gut microbiota, and inflammatory pathways (26).
• Seed oils (rich in omega-6 PUFA) and dyslipidemia. Research suggests that high intake of omega-6 polyunsaturated fatty acids (PUFAs) from seed oils may contribute to inflammation, oxidative stress, and atherosclerosis (27). Despite recommendations for omega-6 PUFA consumption, some studies indicate potential long-term side effects, including hyperinsulinemia and increased cancer risk (28). Flaxseed and its oil, rich in omega-3 fatty acids, have demonstrated positive impacts on cardiovascular risk factors and dyslipidemia (29,30). Adjusting the omega-6 to omega-3 PUFA ratio may be crucial in managing chronic diseases (30). During cooking, both omega-3 and omega-6 high PUFA seed oils are readily oxidized, become rancid, and may produce harmful trans-fats (72).
• High fructose (found in HFCS and fruits). Research suggests that high fructose consumption, particularly from high-fructose corn syrup (HFCS), may contribute to dyslipidemia and other metabolic disorders. Studies have shown that fructose intake can increase postprandial triglycerides, LDL cholesterol, and apolipoprotein B levels (32,33). Fructose consumption has also been linked to visceral adiposity, insulin resistance, and hepatic de novo lipogenesis (fatty liver disease) (34,35). The metabolic effects of fructose differ from glucose due to its rapid hepatic conversion and extraction (36). While some studies found no significant metabolic differences between HFCS and sucrose (37), others suggest that HFCS consumption at 25% of energy requirements can increase cardiovascular disease risk factors comparably to fructose (32). Recent research emphasizes the synergistic effects of glucose and fructose on lipid metabolism, supporting public health efforts to reduce sugar intake (38,39).

2. Nutritional deficiency and dyslipidemia

Many vitamins and micronutrients play critical roles in lipid and energy metabolism, and deficiencies—whether isolated or combined—can lead to metabolic disturbances. Below are some key examples:

• B vitamins. Niacin and vitamin B6 have shown significant potential in managing dyslipidemia and associated cardiovascular risks. Niacin supplementation can lower triglycerides, LDL, and VLDL levels while increasing HDL (40). B vitamin supplementation improves lipid metabolism and reduces inflammation in patients with stable coronary artery disease (41). Animal studies have demonstrated antihyperlipidemic and hepatoprotective effects of vitamin B6 (42). Deficiencies in vitamins B6 and B12 are frequently reported in hyperlipidemic patient (43). Higher dietary niacin intake is associated with a reduced risk of dyslipidemia (44).
• Vitamin C and dyslipidemia. Research demonstrates that vitamin C supplementation can improve lipid profiles by lowering total cholesterol, LDL cholesterol, and triglycerides, particularly in individuals with hypercholesterolemia or diabetes (45–47). Some studies also report increases in HDL cholesterol (48,49). Beneficial effects of vitamin C have been observed across diverse groups, including diabetics, hemodialysis patients, and oil workers exposed to petroleum fumes (50,51). A meta-analysis of 13 randomized controlled trials confirmed that vitamin C supplementation significantly reduces LDL cholesterol and triglycerides in hypercholesterolemic individuals (46). The effects of vitamin C vary depending on dosage, duration, and individual health status (47). Dr. Linus Pauling's pioneering work on vitamin C and cardiovascular disease laid the foundation for understanding its role in vascular health, indirectly linking it to lipid metabolism. We plan to dedicate a paper to further explore Pauling’s insights and their relevance to dyslipidemia and ASCVD. One of us (TEL) discusses vitamin C’s role in improving lipid profiles, combating oxidative stress, and supporting vascular health in the books Primal Panacea (52) and Stop America's Number One Killer (53).
• Vitamin D and dyslipidemia. Vitamin D deficiency is significantly associated with dyslipidemia. Studies reveal that individuals with lower serum 25-hydroxyvitamin D levels are more likely to exhibit abnormal lipid profiles, including elevated total cholesterol, LDL, and triglycerides, and decreased HDL (54–57). This relationship persists even after adjusting for confounding factors. Vitamin D deficiency is linked to alterations in metabolomic profiles, particularly sphingolipid pathway (58). Interactions with other micronutrients, such as vitamin A, zinc, and magnesium, may influence vitamin D’s impact on lipid metabolism (59). Our recent comprehensive review of vitamin D demonstrates that maintaining optimal serum levels above 40 ng/mL reduces the risk of cardiovascular disease incidence and mortality (60) (accepted for publication by Nutrients).
• Vitamin E and dyslipidemia. Vitamin E has shown anti-atherosclerotic properties (61). Research on vitamin E and dyslipidemia shows mixed results. Some studies suggest that vitamin E supplementation can improve lipid profiles in dyslipidemic patients, reducing total cholesterol, LDL-C, and triglycerides (62,63). Higher serum vitamin E levels have been associated with a more favorable lipid profile (64). Vitamin E supplementation has been shown to suppress elevated plasma lipid peroxides and increase serum antioxidant activity (65). The impact of antioxidative vitamins on lipid profiles varies based on dosage, duration, and individual health status (47).
• Magnesium and dyslipidemia. Hypomagnesemia has been linked to metabolic abnormalities and dyslipidemia (66–70). Studies report negative correlations between serum magnesium and triglycerides, LDL, and total cholesterol, while positive correlations are observed with HDL cholesterol (70,71).

3. Infections and dyslipidemia

• Infections promote dyslipidemia. Dyslipidemia is a common complication in HIV-infected patients and those with COVID-19, associated with increased severity and mortality (72). It is characterized by elevated total cholesterol, LDL, and triglycerides, with decreased HDL (73,74). The pathogenesis involves inflammation, oxidative stress, and lipid peroxidation (75). These lipid abnormalities may increase cardiovascular risk in HIV patients (76,77). Research suggests a significant association between oral infections, particularly periodontitis, and systemic metabolic disturbances. Periodontitis has been linked to increased risk of cardiovascular diseases and dyslipidemia (78,79). Studies have found higher levels of total cholesterol, LDL cholesterol, and triglycerides, along with lower HDL cholesterol, in individuals with periodontitis (80,81). Chronic oral infection with Porphyromonas gingivalis, a key periodontal pathogen, has been shown to accelerate atheroma formation by altering lipid profiles in animal models (82). The relationship between periodontitis and hyperlipidemia appears bidirectional, with elevated triglycerides potentially modulating inflammatory responses to periodontal pathogens (83). The underlying mechanisms involve systemic inflammation, metabolic endotoxemia, and genetic factors that influence both oral infections and cardiometabolic diseases (84). These findings highlight the complex interplay between oral health and systemic metabolism.
• Infection control improves dyslipidemia. Periodontal treatment has been shown to improve lipid control (85). Eradication of Helicobacter pylori infection may decrease the risk of dyslipidemia (86).

4. Physical inactivity and dyslipidemia/high cholesterol.

Research consistently shows an inverse relationship between physical activity (PA) and dyslipidemia. Higher PA levels are associated with increased HDL-C and decreased triglycerides in both men and women (87,88). Sedentary behavior increases the risk of dyslipidemia, while moderate-to-vigorous PA (MVPA) may reduce this risk (89,90). The prevalence of dyslipidemia is high in some populations, with limited awareness and treatment (91). Individuals meeting PA guidelines have lower odds of dyslipidemia, even with poor diet quality (91). However, adults with hypercholesterolemia are less likely to meet PA recommendations compared to those without (92). PA patterns, including timing and intensity, may influence lipid profiles differently (90). Overall, habitual PA is associated with more favorable lipid profiles and reduced cardiovascular disease risk (93,94).

5. Hormonal imbalance and dyslipidemia/high cholesterol.

• Thyroid dysfunction, particularly hypothyroidism, is strongly associated with dyslipidemia and increased cardiovascular risk (95,96). Both overt and subclinical hypothyroidism can lead to elevated total cholesterol, LDL cholesterol, and apolipoprotein B levels, while potentially affecting HDL cholesterol and triglycerides (97,98). These lipid abnormalities are primarily due to reduced LDL receptor activity and altered regulation of cholesterol biosynthesis (99). Thyroid hormone replacement therapy has been shown to improve lipid profiles in overt hypothyroidism, but its benefits in subclinical hypothyroidism remain debated (99,100). Recent studies have also highlighted the role of thyroid hormones in regulating HDL function and cholesterol efflux (98). Given the prevalence of thyroid dysfunction and its impact on lipid metabolism, screening for thyroid disorders is recommended in patients with dyslipidemia (101).
• Cortisol imbalance significantly contributes to dyslipidemia, high cholesterol, and increased cardiovascular risk. Excess cortisol, such as in Cushing's syndrome, is associated with elevated triglycerides, total cholesterol, and LDL cholesterol levels (102). Similarly, stress-induced cortisol elevation disrupts lipid metabolism, promoting atherogenesis and increasing the risk of atherosclerosis (103). Conversely, patients with metabolic syndrome and low cortisol levels exhibit less pronounced lipid disturbances (104). Elevated basal cortisol levels and reduced circadian variability have been linked to unfavorable lipid profiles, particularly in individuals with depressive and anxiety disorders (105). Additionally, the cortisol-to-DHEA ratio has been positively correlated with atherogenic lipid profiles in HIV patients with lipodystrophy (106). Glucocorticoid therapy, a common cause of cortisol excess, can lead to dyslipidemia and hypertension, further heightening cardiovascular disease risk (107). Excess cortisol is also strongly associated with obesity, hypertension, and metabolic syndrome (108,109). Furthermore, studies have found that elevated long-term cortisol levels, as measured in scalp hair, are linked to a history of cardiovascular disease (110). In obesity, higher cortisol concentrations are directly correlated with an increased risk of cardiovascular comorbidities (111). These findings highlight the multifaceted role of cortisol in dyslipidemia and emphasize the need to manage cortisol levels to mitigate cardiovascular risks effectively.
• Estrogen imbalance significantly impacts lipid metabolism and cholesterol levels. During menopause, estrogen deficiency leads to increased total cholesterol, LDL cholesterol, and triglycerides, while decreasing HDL cholesterol (112). High maternal estradiol levels can induce dyslipidemia in newborns by upregulating HMGCR expression in fetal hepatocytes (113). Estrogen administration in premenopausal women increases VLDL and HDL constituents, enhancing VLDL apoB and HDL apoA-I production (114). In postmenopausal women, estrogen therapy lowers LDL cholesterol levels (115). Estrogen treatment in cholesterol-fed rabbits attenuates atherosclerosis development by modulating lipoprotein metabolism (116,117). Endogenous sex hormones play a role in regulating lipid metabolism in postmenopausal women, with SHBG associated with a more favorable lipid profile (118). Estrogen administration in postmenopausal women decreases LDL cholesterol and hepatic triglyceride lipase activity while increasing HDL cholesterol (119).
• Progesterone imbalance can significantly impact lipid metabolism and cholesterol levels. Progesterone administration in rats led to increased hepatic triglycerides and cholesterol esters, while decreasing plasma cholesterol levels (120). In cultured cells, progesterone inhibited cholesterol biosynthesis (121). Dyslipidemia affected ovarian steroidogenesis in mice through oxidative stress, inflammation, and insulin resistance (122). In premenopausal women, ovarian lipid metabolism influenced circulating lipids (123). Estrogen plus progesterone replacement therapy in postmenopausal women lowered lipoprotein[a] levels and improved overall lipid profiles (124). High-dose medroxyprogesterone decreased total, LDL, and HDL cholesterol in postmenopausal women (125). In children, progesterone/estradiol ratios were associated with LDL-cholesterol levels (126). Female runners with menstrual irregularities showed altered steroid hormone and lipid profiles compared to eumenorrheic counterparts (127).
• Testosterone imbalance can significantly impact lipid metabolism and cholesterol levels. Research suggests a complex relationship between testosterone and lipid profiles. Low testosterone levels are associated with adverse lipid profiles, including higher total cholesterol and triglycerides, and lower high-density lipoprotein (HDL) cholesterol (128,129). Conversely, higher testosterone levels correlate with increased HDL cholesterol in men, particularly those with cardiovascular disease (130,131). Testosterone deficiency may contribute to hypercholesterolemia through altered expression of hepatic PCSK9 and LDL receptors (132). The effect of testosterone on lipids varies with age, gender, race/ethnicity, and menopausal status (133). Exogenous testosterone administration in hypogonadal men may improve lipid profiles by decreasing LDL and total cholesterol, although it may also decrease HDL cholesterol (134). While testosterone's influence on lipids is evident, its overall impact on cardiovascular disease risk remains unclear and requires further investigation (134,135).

Conclusion

Dyslipidemia, long regarded as a primary target in ASCVD management, is increasingly understood as an outcome of complex, multifactorial root causes. These root causes include dietary factors, such as high-carbohydrate diets, ultra-processed foods, seed oils, and high-fructose consumption, which significantly influence lipid metabolism. Nutritional deficiencies, including vitamins B, C, D, and E, and magnesium, further exacerbate dyslipidemia, while chronic infections and physical inactivity compound cardiovascular risk. Hormonal imbalances, including dysfunctions in thyroid hormones, estrogen, progesterone, testosterone, and cortisol, also play a pivotal role in lipid abnormalities.

Addressing these underlying factors presents an opportunity to move beyond the traditional cholesterol-centric paradigm. Strategies such as dietary modifications, increased physical activity, infection control, and optimization of nutritional and hormonal balance can significantly improve lipid profiles, reduce cardiovascular risk, and even reverse ASCVD in some cases, as we have demonstrated in our recent report (1).

By focusing on the root causes of dyslipidemia, healthcare providers can offer more personalized and effective interventions, shifting the emphasis from symptom management to true disease prevention and reversal. This approach has the potential to improve not only ASCVD outcomes but also overall cardiovascular health and longevity. Future studies should prioritize the integration of these multifaceted strategies into clinical practice, emphasizing the importance of addressing the root causes of dyslipidemia for sustainable cardiovascular health.

References:

1. Cheng RZ, Levy TE (2025) The Mismanagement of ASCVD: A Call for Root Cause Solutions Beyond Cholesterol. Orthomol Med News Serv. 21(2). https://orthomolecular.org/resources/omns/v21n02.shtml

2. Cheng RZ, Duan L, Levy TE (2024) A Holistic Approach to ASCVD: Summary of a Novel Framework and Report of 10 Case Studies. Orthomol Med News Serv. 20(20). https://orthomolecular.org/resources/omns/v20n20.shtml

3. Cheng RZ (2024) Integrative Orthomolecular Medicine Protocol for ASCVD. https://www.drwlc.com/blog/2024/08/01/integrative-orthomolecular-medicine-protocol-for-ascvd

4. Polacow VO, Lancha Junior AH (2007) [High-carbohydrate diets: effects on lipid metabolism, body adiposity and its association with physical activity and cardiovascular disease risk.] Arq Bras Endocrinol Metabol. 51:389-400. https://pubmed.ncbi.nlm.nih.gov/17546237

5. Shin W-K, Shin S, Lee J-k, et al. (2024) Carbohydrate Intake and Hyperlipidemia among Population with High-Carbohydrate Diets: The Health Examinees Gem Study. Mol Nutr Food Res. https://onlinelibrary.wiley.com/doi/10.1002/mnfr.202000379

6. Jackson RL, Yates MT, McNerney CA, Kashyap ML (1987) Diet and HDL Metabolism: High Carbohydrate vs. High Fat Diets. In: Malmendier CL, Alaupovic P, editors. Lipoproteins and Atherosclerosis. Boston, MA: Springer US; Adv Exp Med Biol. 210:165-172. https://doi.org/10.1007/978-1-4684-1268-0_24 ，Https://pubmed.ncbi.nlm.nih.gov/3591547

7. Houttu V, Grefhorst A, Cohn DM, et al. (2023) Severe Dyslipidemia Mimicking Familial Hypercholesterolemia Induced by High-Fat, Low-Carbohydrate Diets: A Critical Review. Nutrients, 15:962. https://pubmed.ncbi.nlm.nih.gov/36839320

8. Parks EJ (2001) Effect of dietary carbohydrate on triglyceride metabolism in humans. J Nutr. 131:2772S-2774S. https://pubmed.ncbi.nlm.nih.gov/11584104

9. Stahel P, Xiao C, Lewis GF (2018) Control of intestinal lipoprotein secretion by dietary carbohydrates. Curr Opin Lipidol. 29:24-29. https://pubmed.ncbi.nlm.nih.gov/29135691

10. Musunuru K (2010) Atherogenic dyslipidemia: cardiovascular risk and dietary intervention. Lipids, 45:907-914. https://pubmed.ncbi.nlm.nih.gov/20524075

11. Sharman MJ, Kraemer WJ, Love DM, et al. (2002) A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr. 132:1879-1885. https://pubmed.ncbi.nlm.nih.gov/12097663

12. Hickey JT, Hickey L, Yancy WS, et al. (2003) Clinical use of a carbohydrate-restricted diet to treat the dyslipidemia of the metabolic syndrome. Metab Syndr Relat Disord. 1:227-232. https://pubmed.ncbi.nlm.nih.gov/18370666

13. O'Neill BJ (2020) Effect of low-carbohydrate diets on cardiometabolic risk, insulin resistance, and metabolic syndrome. Curr Opin Endocrinol Diabetes Obes. 27:301-307. https://pubmed.ncbi.nlm.nih.gov/32773574

14. Zhang W, Guo X, Chen L, et al. (2021) Ketogenic Diets and Cardio-Metabolic Diseases. Front Endocrinol. 12:753039. https://pubmed.ncbi.nlm.nih.gov/34795641

15. Moreno-Sepúlveda J, Capponi M (2020) [The impact on metabolic and reproductive diseases of low-carbohydrate and ketogenic diets]. Rev Med Chil. 148:1630-1639. https://pubmed.ncbi.nlm.nih.gov/33844769

16. Sakr HF, Sirasanagandla SR, Das S, et al. (2023) Low-Carbohydrate Ketogenic Diet for Improvement of Glycemic Control: Mechanism of Action of Ketosis and Beneficial Effects. Curr Diabetes Rev. 19:82-93. https://doi.org/10.2174/1573399818666220511121629 ， https://pubmed.ncbi.nlm.nih.gov/35546779

17. Charlot A, Zoll J (2022) Beneficial Effects of the Ketogenic Diet in Metabolic Syndrome: A Systematic Review. Diabetology. 3:292-309. https://www.mdpi.com/2673-4540/3/2/20

18. Kayode TO, Rotimi ED, Afolayan AO, Kayode AAA (2020) Ketogenic diet: A nutritional remedy for some metabolic disorders. J Educ Health Sport. 10:180-188. https://eprints.federalpolyilaro.edu.ng/1359

19. Donat-Vargas C, Sandoval-Insausti H, Rey-García J, et al. (2021) High Consumption of Ultra-Processed Food is Associated with Incident Dyslipidemia: A Prospective Study of Older Adults. J Nutr. 151:2390-2398. https://pubmed.ncbi.nlm.nih.gov/34038538

20. Scaranni P de O da S, de Oliveira Cardoso L, Griep RH, et al. (2023) Consumption of ultra-processed foods and incidence of dyslipidemias: the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Br J Nutr. 129:336-344. https://pubmed.ncbi.nlm.nih.gov/35450540 ， https://www.cambridge.org/core/services/aop-cambridge-core/content/view/FD39D494B4DF7FD1A3173BCEA3A5D91E/S0007114522001131a.pdf

21. Lima LR, Nascimento LM, Gomes KRO, et al. (2020) [Association between ultra-processed food consumption and lipid parameters among adolescents]. Cienc Saude Coletiva. 25:4055-4064. https://pubmed.ncbi.nlm.nih.gov/33027399

22. Beserra JB, Soares NI da S, Marreiros CS, et al. (2020) [Do children and adolescents who consume ultra-processed foods have a worse lipid profile? A systematic review]. Cienc Saude Coletiva. 25:4979-4989. https://pubmed.ncbi.nlm.nih.gov/33295516

23. Vitale M, Costabile G, Testa R, et al. (2024) Ultra-Processed Foods and Human Health: A Systematic Review and Meta-Analysis of Prospective Cohort Studies. Adv Nutr. 15:100121. https://pubmed.ncbi.nlm.nih.gov/38245358

24. Mambrini SP, Menichetti F, Ravella S, et al. (2023) Ultra-Processed Food Consumption and Incidence of Obesity and Cardiometabolic Risk Factors in Adults: A Systematic Review of Prospective Studies. Nutrients, 15:2583. https://pubmed.ncbi.nlm.nih.gov/37299546

25. Leffa PS, Hoffman DJ, Rauber F, et al. (2020)S Longitudinal associations between ultra-processed foods and blood lipids in childhood. Br J Nutr. 124:341-348. https://pubmed.ncbi.nlm.nih.gov/32248849

26. Juul F, Vaidean G, Lin Y, et al. (2021) Ultra-Processed Foods and Incident Cardiovascular Disease in the Framingham Offspring Study. J Am Coll Cardiol. 77:1520-1531. https://pubmed.ncbi.nlm.nih.gov/33766258

27. DiNicolantonio JJ, O'Keefe J (2021) The Importance of Maintaining a Low Omega-6/Omega-3 Ratio for Reducing the Risk of Autoimmune Diseases, Asthma, and Allergies. Mo Med. 118:453-459. https://pubmed.ncbi.nlm.nih.gov/34658440

28. Yam D, Eliraz A, Berry EM (1996) Diet and disease--the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet. Isr J Med Sci. 32:1134-1143. https://pubmed.ncbi.nlm.nih.gov/8960090

29. Vashishtha V, Barhwal K, Kumar A, et al. (2017) Effect of seabuckthorn seed oil in reducing cardiovascular risk factors: A longitudinal controlled trial on hypertensive subjects. Clin Nutr Edinb Scotl. 36:1231-1238. https://pubmed.ncbi.nlm.nih.gov/27522605

30. Fawzy M, Nagi HM, Mourad R. (2020) Beneficial effect of flaxseed oil by adjusting omega6:omega3 ratio on lipid metabolism in high cholesterol diet fed rats. J Spec Educ Res. 2020(58):117-142. https://journals.ekb.eg/article_130822_0.html

31. Obi J, Sakamoto T, Furihata K, et al. (2025) Vegetables containing sulfur compounds promote trans-isomerization of unsaturated fatty acids in triacylglycerols during the cooking process. Food Res Int. 200:115425. https://www.sciencedirect.com/science/article/abs/pii/S0963996924014959

32. Stanhope KL, Bremer AA, Medici V, et al. (2011) Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. J Clin Endocrinol Metab. 96:E1596-E1605. https://pubmed.ncbi.nlm.nih.gov/21849529

33. Stanhope KL, Medici V, Bremer AA, et al. (2015) A dose-response study of consuming high-fructose corn syrup-sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. Am J Clin Nutr. 101:1144-1154. https://pubmed.ncbi.nlm.nih.gov/25904601

34. Stanhope KL, Havel PJ (2008) Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. Curr Opin Lipidol. 19:16-24. https://pubmed.ncbi.nlm.nih.gov/18196982

35. Tappy L, Lê KA (2010) Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 90:23-46. https://pubmed.ncbi.nlm.nih.gov/20086073

36. Schaefer EJ, Gleason JA, Dansinger ML (2009) Dietary fructose and glucose differentially affect lipid and glucose homeostasis. J Nutr. 139:1257S-1262S. https://pubmed.ncbi.nlm.nih.gov/19403705

37. Angelopoulos TJ, Lowndes J, Zukley L, et al. (2009) The effect of high-fructose corn syrup consumption on triglycerides and uric acid. J Nutr. 139:1242S-1245S. https://pubmed.ncbi.nlm.nih.gov/19403709

38. Gugliucci A (2023) Sugar and Dyslipidemia: A Double-Hit, Perfect Storm. J Clin Med. 12:5660. https://pubmed.ncbi.nlm.nih.gov/37685728

39. Stanhope KL (2012) Role of fructose-containing sugars in the epidemics of obesity and metabolic syndrome. Annu Rev Med. 63:329-343. https://pubmed.ncbi.nlm.nih.gov/22034869

40. Dayi T, Hoca M (2022) [Is Niacin A Potential Agent in Reduction of Dyslipidemia Risk?] Istanbul Devel Univ J Health Sci.17:626-635. https://dergipark.org.tr/tr/pub/igusabder/issue/72351/1112685

41. Liu M, Wang Z, Liu S, et al. (2020) Effect of B vitamins supplementation on cardio-metabolic factors in patients with stable coronary artery disease: A randomized double-blind trial. Asia Pac J Clin Nutr. 29:245-252. https://pubmed.ncbi.nlm.nih.gov/32674231

42. Zhang Q, Zhang DL, Zhou XL, et al. (2021) Antihyperlipidemic and Hepatoprotective Properties of Vitamin B6 Supplementation in Rats with High-Fat Diet-Induced Hyperlipidemia. Endocr Metab Immune Disord Drug Targets, 21:2260-2272. https://pubmed.ncbi.nlm.nih.gov/34370653

43. Al-Qusous MN, Al Madanat WKJ, Mohamed Hussein R (2023) Association of Vitamins D, B6, and B12 Deficiencies with Hyperlipidemia Among Jordanian Adults. Rep Biochem Mol Biol. 12:415-424. https://pubmed.ncbi.nlm.nih.gov/38618263

44. Altschul R, Hoffer A, Stephen JD (1955) Influence of nicotinic acid on serum cholesterol in man. Arch Biochem Biophys. 54:558-559. Https://pubmed.ncbi.nlm.nih.gov/14350806， https://www.cabidigitallibrary.org/doi/full/10.5555/19551404120

45. Chaudhari HV, Dakhale GN, Chaudhari S, et al. (2012) The beneficial effec of vitamin C suppllemtation on serum lipids in type 2 diabetic patients: a randomized double blind study. Int J Diabetes Metab. 20:53-58. https://karger.com/ijd/article-abstract/20/2/53/175532

46. McRae MP (2008) Vitamin C supplementation lowers serum low-density lipoprotein cholesterol and triglycerides: a meta-analysis of 13 randomized controlled trials. J Chiropr Med. 7:48-58. https://pubmed.ncbi.nlm.nih.gov/19674720

47. Mohseni S, Tabatabaei-Malazy O, Shadman Z, et al. (2021) Targeting dyslipidemia with antioxidative vitamins C, D, and E; a systematic review of meta-analysis studies. J Diabetes Metab Disord. 20:2037-2047. https://pubmed.ncbi.nlm.nih.gov/34900839

48. Ness AR, Khaw KT, Bingham S, Day NE (1996) Vitamin C status and serum lipids. Eur J Clin Nutr. 50:724-729. https://pubmed.ncbi.nlm.nih.gov/8933118

49. Cerná O, Ramacsay L, Ginter E (1992) Plasma lipids, lipoproteins and atherogenic index in men and women administered vitamin C. Cor Vasa. 34:246-254. https://pubmed.ncbi.nlm.nih.gov/1306421

50. El Mashad GM, ElSayed HM, Nosair NA (2016) Effect of vitamin C supplementation on lipid profile, serum uric acid, and ascorbic acid in children on hemodialysis. Saudi J Kidney Dis Transplant, 27:1148-1154. https://pubmed.ncbi.nlm.nih.gov/27900959 , https://journals.lww.com/sjkd/fulltext/2016/27060/effect_of_vitamin_c_supplementation_on_lipid.6.aspx

51. George-Opuda IM, Etuk EJ, Elechi-Amadi KN, et al. (2024) Vitamin C Supplementation Lowered Atherogenic Lipid Parameters among Oil and Gas Workers Occupationally Exposed to Petroleum Fumes in Port Harcourt, Rivers State, Nigeria. J Adv Med Pharm Sci. 26:45-52. http://journal.article2publish.com/id/eprint/3636

52. Levy TE, Gordon G (2012) Primal Panacea. Second Printing edition. Henderson, NV: Medfox Pub. ISBN-13: 978-0983772704 https://www.amazon.com/Primal-Panacea-Thomas-Levy/dp/0983772800

53. Levy TE (2015) Stop America's #1 Killer. ‎ 2nd ed. Edition. Henderson, NV: Medfox Pub. ISBN-13: 978-0977952007. https://www.amazon.com/Stop-Americas-Killer-MD-Levy/dp/0977952002

54. Sharba ZF, Shareef RH, Abd BA, Hameed EN (2021) Association between Dyslipidemia and Vitamin D Deficiency: a Cross-Sectional Study. Folia Med (Plovdiv). 63:965-969. https://pubmed.ncbi.nlm.nih.gov/35851223

55. Chaudhuri JR, Mridula KR, Anamika A, et al. (2013) Deficiency of 25-Hydroxyvitamin D and Dyslipidemia in Indian Subjects. J Lipids, 2013:623240. https://pubmed.ncbi.nlm.nih.gov/24455278

56. Jiang X, Peng M, Chen S, et al. (2019) Vitamin D deficiency is associated with dyslipidemia: a cross-sectional study in 3788 subjects. Curr Med Res Opin. 35:1059-1063. https://pubmed.ncbi.nlm.nih.gov/24455278

57. Doddamani DS, Shetty DP (2019) The Association between Vitamin D Deficiency and Dyslipidemia. Int J Res Rev. 6:5-8. https://www.ijrrjournal.com/IJRR_Vol.6_Issue.9_Sep2019/IJRR002.pdf

58. Mousa H, Elrayess MA, Diboun I, et al. (2022) Metabolomics Profiling of Vitamin D Status in Relation to Dyslipidemia. Metabolites, 12:771. https://pubmed.ncbi.nlm.nih.gov/36005643

59. Khosravi-Boroujeni H, Ahmed F, Sarrafzadegan N (2015) Is the Association between Vitamin D and Metabolic Syndrome Independent of Other Micronutrients? Int J Vitam Nutr Res. 85:245-260. https://pubmed.ncbi.nlm.nih.gov/27439768

60. Grant, W.B.; Wimalawansa, S.J.; Pludowski, P.; Cheng, R.Z. Vitamin D: Evidence-Based Health Benefits and Recommendations for Population Guidelines. Nutrients 2025, 17, 277. https://www.mdpi.com/2072-6643/17/2/277

61. Saggini A, Anogeianaki A, Angelucci D, et al. (2011) Cholesterol and vitamins: revisited study. J Biol Regul Homeost Agents. 25:505-515. https://pubmed.ncbi.nlm.nih.gov/22217984

62. Vasanthi B, Kalaimathi B. (2012) Therapeutic Effect of Vitamin E in Patients with Dyslipidaemia. [cited 2025 Jan 5]. Available from: https://www.semanticscholar.org/paper/Therapeutic-Effect-of-Vitamin-E-in-Patients-with-Vasanthi-Kalaimathi/2856f54306f952ff20d346526b46f31e4b462e23

63. Manimegalai R, Geetha A, Rajalakshmi K (1993) Effect of vitamin-E on high fat diet induced hyperlipidemia in rats. Indian J Exp Biol. 31:704-707. https://pubmed.ncbi.nlm.nih.gov/8270285

64. Barzegar-Amini M, Ghazizadeh H, Seyedi SMR, et al. (2019) Serum vitamin E as a significant prognostic factor in patients with dyslipidemia disorders. Diabetes Metab Syndr. 2019;13:666-671. https://pubmed.ncbi.nlm.nih.gov/30641786

65. Szczeklik A, Gryglewski RJ, Domagala B, et al. (1985)Dietary supplementation with vitamin E in hyperlipoproteinemias: effects on plasma lipid peroxides, antioxidant activity, prostacyclin generation and platelet aggregability. Thromb Haemost. 54:425-430. https://pubmed.ncbi.nlm.nih.gov/3909500

66. Guerrero-Romero F, Rodríguez-Morán M (2019) Magnesium and dyslipidemia 1st Edition. CRC Press; 2019 [cited 2025 Jan 5]. Available from: https://www.taylorfrancis.com/chapters/edit/10.1201/9780429029141-5/magnesium-dyslipidemia-fernando-guerrero-romero-martha-rodr%C3%ADguez-mor%C3%A1n

67. Levy T (2019) Magnesium: Reversing Disease. Medfox Pub. https://www.amazon.com/Magnesium-Reversing-MD-Jd-Levy/dp/0998312401 ISBN-13: 978-0998312408

68. Dean C (2017) The Magnesium Miracle, Second Ed.:‎ Ballantine Books ISBN-13: 978-0399594441. Available from: https://www.amazon.com/Magnesium-Miracle-Second-Carolyn-Dean/dp/0399594442

69. Mishra S, Padmanaban P, Deepti G, et al. (2012) Serum Magnesium and Dyslipidemia in Type-2 Diabetes Mellitus. Biomed Res - Tokyo. [cited 2025 Jan 5]; Available from: https://www.semanticscholar.org/paper/Serum-Magnesium-and-Dyslipidemia-in-Type-2-Diabetes-Mishra-Padmanaban/8d23a2bd9017cb57bb6ddda98789ba81c176b53c， https://www.academia.edu/96013524/Serum_Magnesium_and_Dyslipidemia_in_Type_2_Diabetes_Mellitus?sm=b

70. Sajjan N, Shamsuddin M (2016) A study of serum magnesium and dyslipidemia in type 2 diabetes mellitus patients. Int J Clin Biochem Res. 3:36-41. https://www.researchgate.net/profile/Viyatprajna-Acharya/publication/304336811_Oxidative_stress_in_post_menopausal_women_with_cardiovascular_risk_factors/links/58fc5eb1aca2723d79d89335/Oxidative-stress-in-post-menopausal-women-with-cardiovascular-risk-factors.pdf#page=42

71. Deepti R, Nalini G, Anbazhagan (2014) Relationship between hypomagnesemia and dyslipidemia in type 2 diabetes. Asian J Pharm Res Health Care. [cited 2025 Jan 5]; https://www.semanticscholar.org/paper/RELATIONSHIP-BETWEEN-HYPOMAGNESEMIA-AND-IN-TYPE-2-Deepti-Nalini/5fd9c00eacce8aa45f93c3e5ea0961969ec3223b

72. Hariyanto TI, Kurniawan A (2020) Dyslipidemia is associated with severe coronavirus disease 2019 (COVID-19) infection. Diabetes Metab Syndr. 14:1463-1465. https://pubmed.ncbi.nlm.nih.gov/32771919

73. Lo J (2011) Dyslipidemia and lipid management in HIV-infected patients. Curr Opin Endocrinol Diabetes Obes. 18:144-147. Available from: https://journals.lww.com/co-endocrinology/abstract/2011/04000/dyslipidemia_and_lipid_management_in_hiv_infected.9.aspx

74. Green ML (2002) Evaluation and management of dyslipidemia in patients with HIV infection. J Gen Intern Med. 17:797-810. https://pubmed.ncbi.nlm.nih.gov/12390557

75. Feingold KR, Grunfeld C (2000) The Effect of Inflammation and Infection on Lipids and Lipoproteins. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext. South Dartmouth (MA): MDText.com, Inc.; 2000 [cited 2024 Dec 29]. https://www.ncbi.nlm.nih.gov/books/NBK326741

76. Kulasekaram R, Peters BS, Wierzbicki AS (2005) Dyslipidaemia and cardiovascular risk in HIV infection. Curr Med Res Opin. 21:1717-1725. https://pubmed.ncbi.nlm.nih.gov/16307691

77. Kotler DP (2008) HIV and Antiretroviral Therapy: Lipid Abnormalities and Associated Cardiovascular Risk in HIV-Infected Patients. JAIDS J Acquir Immune Defic Syndr. 49:S79-S85. https://pubmed.ncbi.nlm.nih.gov/18725816

78. Mattila KJ, Pussinen PJ, Paju S (2005) Dental infections and cardiovascular diseases: a review. J Periodontol. 76:2085-2088. https://pubmed.ncbi.nlm.nih.gov/16277580

79. Ma W, Zou Z, Yang L, et al. (2024) Exploring the bi-directional relationship between periodontitis and dyslipidemia: a comprehensive systematic review and meta-analysis. BMC Oral Health. 24:508. https://pubmed.ncbi.nlm.nih.gov/38684998

80. Moeintaghavi A, Haerian-Ardakani A, Talebi-Ardakani M, Tabatabaie I (2005) Hyperlipidemia in patients with periodontitis. J Contemp Dent Pract. 6:78-85. https://pubmed.ncbi.nlm.nih.gov/16127475

81. Nibali L, D'Aiuto F, Griffiths G, et al. (2007) Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case-control study. J Clin Periodontol. 34:931-937. https://pubmed.ncbi.nlm.nih.gov/17877746

82. Maekawa T, Takahashi N, Tabeta K, et al. (2011) Chronic Oral Infection with Porphyromonas gingivalis Accelerates Atheroma Formation by Shifting the Lipid Profile. Cardona PJ, editor. PLoS ONE. 6(5):e20240. https://pubmed.ncbi.nlm.nih.gov/21625524

83. Cutler CW, Shinedling EA, Nunn M, et al. (1999) Association between periodontitis and hyperlipidemia: cause or effect? J Periodontol. 70:1429-1434. https://pubmed.ncbi.nlm.nih.gov/10632517

84. Janket SJ, Javaheri H, Ackerson LK, et al. (2015) Oral Infections, Metabolic Inflammation, Genetics, and Cardiometabolic Diseases. J Dent Res. 94(9 Suppl):119S-127S. https://pubmed.ncbi.nlm.nih.gov/25840582

85. Fentoğlu O, Sözen T, Oz SG, et al. (2010) Short-term effects of periodontal therapy as an adjunct to anti-lipemic treatment. Oral Dis. 16:648-654. https://pubmed.ncbi.nlm.nih.gov/20412449

86. Park Y, Kim TJ, Lee H, et al. (2021) Eradication of Helicobacter pylori infection decreases risk for dyslipidemia: A cohort study. Helicobacter. 26(2):e12783. https://pubmed.ncbi.nlm.nih.gov/33508177

87. Dancy C, Lohsoonthorn V, Williams MA (2008) Risk of dyslipidemia in relation to level of physical activity among Thai professional and office workers. Southeast Asian J Trop Med Public Health. 39:932-941. https://pubmed.ncbi.nlm.nih.gov/19058592

88. Meireles De Pontes L (2008) Standard of physical activity and influence of sedentarism in the occurrence of dyslipidemias in adults. Fit Perform J. 7:245-250. https://openurl.ebsco.com/EPDB%3Agcd%3A2%3A7102866/detailv2?sid=ebsco%3Aplink%3Ascholar&id=ebsco%3Agcd%3A35447259

89. Zhou J, Zhou Q, Wang DP, et al. (2017) [Associations of sedentary behavior and physical activity with dyslipidemia]. Beijing Da Xue Xue Bao. 49:418-423. https://pubmed.ncbi.nlm.nih.gov/28628141

90. Wang X, Wang Y, Xu Z, et al. (2023) Trajectories of 24-Hour Physical Activity Distribution and Relationship with Dyslipidemia. Nutrients. 15:328. https://pubmed.ncbi.nlm.nih.gov/36678199

91. Mutalifu M, Zhao Q, Wang Y, et al. (2024) Joint association of physical activity and diet quality with dyslipidemia: a cross-sectional study in Western China. Lipids Health Dis. 23:46. https://pubmed.ncbi.nlm.nih.gov/38341553

92. Churilla JR, Johnson TM, Zippel EA (2013) Association of physical activity volume and hypercholesterolemia in US adults. QJM Mon J Assoc Physicians, 106:333-340. https://pubmed.ncbi.nlm.nih.gov/23256179

93. Gordon DJ, Witztum JL, Hunninghake D, et al. (1983) Habitual physical activity and high-density lipoprotein cholesterol in men with primary hypercholesterolemia. The Lipid Research Clinics Coronary Primary Prevention Trial. Circulation, 67:512-520. https://pubmed.ncbi.nlm.nih.gov/6821893

94. Delavar M, Lye M, Hassan S, et al. (2011) Physical activity, nutrition, and dyslipidemia in middle-aged women. Iran J Public Health, 40:89-98. https://pubmed.ncbi.nlm.nih.gov/23113107

95. Brenta G, Fretes O (2014) Dyslipidemias and hypothyroidism. Pediatr Endocrinol Rev. 11:390-399. https://pubmed.ncbi.nlm.nih.gov/24988692

96. Neves C, Alves M, Medina JL, Delgado JL (2008) Thyroid diseases, dyslipidemia and cardiovascular pathology. Rev Port Cardiol. 27:1211-1236. https://pubmed.ncbi.nlm.nih.gov/19178025

97. Peppa M, Betsi G, Dimitriadis G (2011) Lipid abnormalities and cardiometabolic risk in patients with overt and subclinical thyroid disease. J Lipids. 2011:575840. https://pubmed.ncbi.nlm.nih.gov/21789282

98. Jung KY, Ahn HY, Han SK, et al. (2017) Association between thyroid function and lipid profiles, apolipoproteins, and high-density lipoprotein function. J Clin Lipidol. 11:1347-1353. https://pubmed.ncbi.nlm.nih.gov/28958565

99. Duntas LH, Brenta G (2018) A Renewed Focus on the Association Between Thyroid Hormones and Lipid Metabolism. Front Endocrinol. 9:511. https://pubmed.ncbi.nlm.nih.gov/30233497

100. Liberopoulos EN, Elisaf MS (2002) Dyslipidemia in patients with thyroid disorders. Hormones (Athens) 2002;1:218-223. https://pubmed.ncbi.nlm.nih.gov/17018450

101. Asranna A, Taneja RS, Kulshreshta B (2012) Dyslipidemia in subclinical hypothyroidism and the effect of thyroxine on lipid profile. Indian J Endocrinol Metab. 16:S347-S349. https://pubmed.ncbi.nlm.nih.gov/23565423

102. Arnaldi G, Scandali VM, Trementino L, et al. (2010) Pathophysiology of dyslipidemia in Cushing’s syndrome. Neuroendocrinology. 92:86-90. https://pubmed.ncbi.nlm.nih.gov/20829625

103. Marcondes FK, Das Neves VJ, Costa R, et al. (2012) Dyslipidemia Induced by Stress. In: Kelishadi R, editor, Dyslipidemia - From Prevention to Treatment, InTechOpen. ISBN-13: 978-9533079042. https://www.intechopen.com/chapters/27506

104. Nadolnik L, Polubok V, Gonchar K (2020) Blood Cortisol Level in Patients with Metabolic Syndrome and Its Correlation with Parameters of Lipid and Carbohydrate Metabolisms. Int J Biochem Res Rev. 29:149-158. https://journalijbcrr.com/index.php/IJBCRR/article/view/676

105. Veen G, Giltay EJ, DeRijk RH, et al. (2009) Salivary cortisol, serum lipids, and adiposity in patients with depressive and anxiety disorders. Metabolism. 58:821-827. https://pubmed.ncbi.nlm.nih.gov/19375126

106. Christeff N, Melchior JC, de Truchis P, et al. (1999) Lipodystrophy defined by a clinical score in HIV-infected men on highly active antiretroviral therapy: correlation between dyslipidaemia and steroid hormone alterations. AIDS, 13:2251-2260. https://pubmed.ncbi.nlm.nih.gov/10563710

107. Sholter DE, Armstrong PW (2000) Adverse effects of corticosteroids on the cardiovascular system. Can J Cardiol. 16:505-511. https://pubmed.ncbi.nlm.nih.gov/10787466

108. Anagnostis P, Athyros VG, Tziomalos K, et al. (2009) Clinical review: The pathogenetic role of cortisol in the metabolic syndrome: a hypothesis. J Clin Endocrinol Metab. 94:2692-2701. https://pubmed.ncbi.nlm.nih.gov/19470627

109. van der Valk ES, Savas M, van Rossum EFC (2018) Stress and Obesity: Are There More Susceptible Individuals? Curr Obes Rep. 7:193-203. https://pubmed.ncbi.nlm.nih.gov/29663153

110. Manenschijn L, Schaap L, van Schoor NM, et al. (2013) High long-term cortisol levels, measured in scalp hair, are associated with a history of cardiovascular disease. J Clin Endocrinol Metab. 98:2078-2083. https://pubmed.ncbi.nlm.nih.gov/23596141

111. Vicennati V, Pasqui F, Cavazza C, et al. (2009) Stress-related development of obesity and cortisol in women. Obesity (Silver Spring) 17:1678-1683. https://pubmed.ncbi.nlm.nih.gov/19300426

112. Torosyan N, Visrodia P, Torbati T, et al. (2022) Dyslipidemia in midlife women: Approach and considerations during the menopausal transition. Maturitas. 166:14-20. https://pubmed.ncbi.nlm.nih.gov/36027726

113. Meng Y, Lv PP, Ding GL, et al. (2015) High Maternal Serum Estradiol Levels Induce Dyslipidemia in Human Newborns via a Hepatic HMGCR Estrogen Response Element. Sci Rep. 5:10086. https://pubmed.ncbi.nlm.nih.gov/25961186

114. Schaefer EJ, Foster DM, Zech LA, et al. (1983) The effects of estrogen administration on plasma lipoprotein metabolism in premenopausal females. J Clin Endocrinol Metab. 57:262-267. https://pubmed.ncbi.nlm.nih.gov/6408108

115. Wahl P, Walden C, Knopp R, et al. (1983) Effect of estrogen/progestin potency on lipid/lipoprotein cholesterol. N Engl J Med. 308:862-867. https://pubmed.ncbi.nlm.nih.gov/6572785

116. Henriksson P, Stamberger M, Eriksson M, et al. (1989) Oestrogen-induced changes in lipoprotein metabolism: role in prevention of atherosclerosis in the cholesterol-fed rabbit. Eur J Clin Invest. 19:395-403. https://pubmed.ncbi.nlm.nih.gov/2550241

117. Kushwaha RS, Hazzard WR (1981) Exogenous estrogens attenuate dietary hypercholesterolemia and atherosclerosis in the rabbit. Metabolism. 30:359-366. https://pubmed.ncbi.nlm.nih.gov/7207207

118. Mudali S, Dobs AS, Ding J, et al. (2005) Endogenous postmenopausal hormones and serum lipids: the atherosclerosis risk in communities study. J Clin Endocrinol Metab. 90:1202-1209. https://pubmed.ncbi.nlm.nih.gov/15546905

119. Applebaum-Bowden D, McLean P, Steinmetz A, et al. (1989) Lipoprotein, apolipoprotein, and lipolytic enzyme changes following estrogen administration in postmenopausal women. J Lipid Res. 30:1895-1906. https://pubmed.ncbi.nlm.nih.gov/2621417

120. Gandarias JM, Abad C, Lacort M, Ochoa B (1979) [Effect of progesterone on rat plasma and liver lipid levels (author's transl)]. Rev Esp Fisiol. 35:470-473. https://pubmed.ncbi.nlm.nih.gov/542709 ， https://revistas.unav.edu/index.php/ref/article/view/49652/38926

121. Metherall JE, Waugh K, Li H (1996) Progesterone inhibits cholesterol biosynthesis in cultured cells. Accumulation of cholesterol precursors. J Biol Chem. 271:2627-2633. https://pubmed.ncbi.nlm.nih.gov/8576232

122. Abreu JM, Santos GB, Carvalho MDGDS, et al. (2021) Dyslipidemia's influence on the secretion ovarian's steroids in female mice. Res Soc Dev. 10:e298101321369. https://rsdjournal.org/index.php/rsd/article/view/21369

123. Jensen JT, Addis IB, Hennebold JD, Bogan RL (2017) Ovarian Lipid Metabolism Modulates Circulating Lipids in Premenopausal Women. J Clin Endocrinol Metab. 102:3138-3145. https://pubmed.ncbi.nlm.nih.gov/28323981

124. Soma MR, Osnago-Gadda I, Paoletti R, et al. (1993) The lowering of lipoprotein[a] induced by estrogen plus progesterone replacement therapy in postmenopausal women. Arch Intern Med. 153:1462-1468. https://pubmed.ncbi.nlm.nih.gov/8390232

125. Grönroos M, Lehtonen A (1983) Effect of high dose progestin on serum lipids. Atherosclerosis. 47:101-105. https://pubmed.ncbi.nlm.nih.gov/6870984

126. Srinivasan SR, Sundaram GS, Williamson GD, et al. (1985) Serum lipoproteins and endogenous sex hormones in early life: observations in children with different lipoprotein profiles. Metabolism. 34:861-867. https://pubmed.ncbi.nlm.nih.gov/3162076

127. Thompson DL, Snead DB, Seip RL, et al. (1997) Serum lipid levels and steroidal hormones in women runners with irregular menses. Can J Appl Physiol. 22:66-77. https://pubmed.ncbi.nlm.nih.gov/9018409

128. Haring R, Baumeister SE, Völzke H, et al. (2011) Prospective association of low total testosterone concentrations with an adverse lipid profile and increased incident dyslipidemia. Eur J Cardiovasc Prev Rehabil. 18:86-96. https://pubmed.ncbi.nlm.nih.gov/20562628

129. Zhang N, Zhang H, Zhang X, et al. (2014) The relationship between endogenous testosterone and lipid profile in middle-aged and elderly Chinese men. Eur J Endocrinol. 170:487-494. https://pubmed.ncbi.nlm.nih.gov/24394726

130. Page ST, Mohr BA, Link CL, et al. (2008) Higher testosterone levels are associated with increased high-density lipoprotein cholesterol in men with cardiovascular disease: results from the Massachusetts Male Aging Study. Asian J Androl. 10:193-200. https://pubmed.ncbi.nlm.nih.gov/18097527

131. Nordøy A, Aakvaag A, Thelle D (1979) Sex hormones and high density lipoproteins in healthy males. Atherosclerosis. 34:431-436. https://pubmed.ncbi.nlm.nih.gov/229880

132. Cai Z, Xi H, Pan Y, et al. (2015) Effect of testosterone deficiency on cholesterol metabolism in pigs fed a high-fat and high-cholesterol diet. Lipids Health Dis. 14:18. https://pubmed.ncbi.nlm.nih.gov/25889601

133. Self A, Zhang J, Corti M, Esani M (2019) Correlation between Sex Hormones and Dyslipidemia. Am Soc Clin Lab Sci. 32:106. https://clsjournal.ascls.org/content/32/3/106

134. Monroe AK, Dobs AS (2013) The effect of androgens on lipids. Curr Opin Endocrinol Diabetes Obes. 20:132-139. https://pubmed.ncbi.nlm.nih.gov/23422242

135. Gutai J, LaPorte R, Kuller L, et al. (1981) Plasma testosterone, high density lipoprotein cholesterol and other lipoprotein fractions. Am J Cardiol. 48:897-902. https://pubmed.ncbi.nlm.nih.gov/7304438

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