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In our international consultation services, we have shifted from this outdated paradigm to an orthomolecular medicine-based integrative approach, focusing on restoring biochemical balance (between nutrients and toxins) and physiological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, Duan L, Levy TE. A Holistic Approach to ASCVD: Summary of a Novel Framework and Report of 10 Case Studies. Orthomol Med News Serv [Internet]. 2024 Nov 27;20(20). Available from: https://orthomolecular.org/resources/omns/v20n20.shtml

2. Cheng RZ, Levy TE. The Mismanagement of ASCVD: A Call for Root Cause Solutions Beyond Cholesterol. Orthomol Med News Serv [Internet]. 2025 Jan 2 [cited 2025 Jan 5]; Available from: https://orthomolecular.activehosted.com/index.php?action=social&chash=0bb4aec1710521c12ee76289d9440817.345

3. Cheng RZ. Integrative Orthomolecular Medicine Protocol for ASCVD [Internet]. 2024. Available from: https://www.drwlc.com/blog/2024/08/01/integrative-orthomolecular-medicine-protocol-for-ascvd/

4. Polacow VO, Lancha Junior AH. [High-carbohydrate diets: effects on lipid metabolism, body adiposity and its association with physical activity and cardiovascular disease risk]. Arq Bras Endocrinol Metabol. 2007 Apr;51(3):389–400.

5. Shin WK, Shin S, Lee Jo koo. Carbohydrate Intake and Hyperlipidemia among Population with High‐Carbohydrate Diets: The Health Examinees Gem Study - Shin - 2021 - Molecular Nutrition & Food Research - Wiley Online Library. Mol Nutr Food Res [Internet]. [cited 2024 Dec 29]; Available from: https://onlinelibrary.wiley.com/doi/10.1002/mnfr.202000379

6. Jackson RL, Yates MT, McNerney CA, Kashyap ML. Diet and HDL Metabolism: High Carbohydrate vs. High Fat Diets. In: Malmendier CL, Alaupovic P, editors. Lipoproteins and Atherosclerosis [Internet]. Boston, MA: Springer US; 1987 [cited 2024 Nov 5]. p. 165–72. Available from: https://doi.org/10.1007/978-1-4684-1268-0_24

7. Houttu V, Grefhorst A, Cohn DM, Levels JHM, Roeters van Lennep J, Stroes ESG, et al. Severe Dyslipidemia Mimicking Familial Hypercholesterolemia Induced by High-Fat, Low-Carbohydrate Diets: A Critical Review. Nutrients. 2023 Feb 15;15(4):962.

8. Parks EJ. Effect of dietary carbohydrate on triglyceride metabolism in humans. J Nutr. 2001 Oct;131(10):2772S-2774S.

9. Stahel P, Xiao C, Lewis GF. Control of intestinal lipoprotein secretion by dietary carbohydrates. Curr Opin Lipidol. 2018 Feb;29(1):24–9.

10. Musunuru K. Atherogenic dyslipidemia: cardiovascular risk and dietary intervention. Lipids. 2010 Oct;45(10):907–14.

11. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gómez AL, Scheett TP, et al. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr. 2002 Jul;132(7):1879–85.

12. Hickey JT, Hickey L, Yancy WS, Hepburn J, Westman EC. Clinical use of a carbohydrate-restricted diet to treat the dyslipidemia of the metabolic syndrome. Metab Syndr Relat Disord. 2003 Sep;1(3):227–32.

13. O’Neill BJ. Effect of low-carbohydrate diets on cardiometabolic risk, insulin resistance, and metabolic syndrome. Curr Opin Endocrinol Diabetes Obes. 2020 Oct;27(5):301–7.

14. Zhang W, Guo X, Chen L, Chen T, Yu J, Wu C, et al. Ketogenic Diets and Cardio-Metabolic Diseases. Front Endocrinol. 2021;12:753039.

15. Moreno-Sepúlveda J, Capponi M. [The impact on metabolic and reproductive diseases of low-carbohydrate and ketogenic diets]. Rev Med Chil. 2020 Nov;148(11):1630–9.

16. Sakr HF, Sirasanagandla SR, Das S, Bima AI, Elsamanoudy AZ. Low-Carbohydrate Ketogenic Diet for Improvement of Glycemic Control: Mechanism of Action of Ketosis and Beneficial Effects. Curr Diabetes Rev. 2023;19(2):e110522204580.

17. Charlot A, Zoll J. Beneficial Effects of the Ketogenic Diet in Metabolic Syndrome: A Systematic Review. Diabetology. 2022 Apr 24;3(2):292–309.

18. Kayode TO, Rotimi ED, Afolayan AO, Kayode AAA. Ketogenic diet: A nutritional remedy for some metabolic disorders. J Educ Health Sport. 2020 Aug 10;10(8):180–8.

19. Donat-Vargas C, Sandoval-Insausti H, Rey-García J, Moreno-Franco B, Åkesson A, Banegas JR, et al. High Consumption of Ultra-Processed Food is Associated with Incident Dyslipidemia: A Prospective Study of Older Adults. J Nutr. 2021 Aug 7;151(8):2390–8.

20. Scaranni P de O da S, de Oliveira Cardoso L, Griep RH, Lotufo PA, Barreto SM, da Fonseca M de JM. Consumption of ultra-processed foods and incidence of dyslipidemias: the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Br J Nutr. 2022 Apr 22;1–22.

21. Lima LR, Nascimento LM, Gomes KRO, Martins M do C de CE, Rodrigues MTP, Frota K de MG. [Association between ultra-processed food consumption and lipid parameters among adolescents]. Cienc Saude Coletiva. 2020 Oct;25(10):4055–64.

22. Beserra JB, Soares NI da S, Marreiros CS, Carvalho CMRG de, Martins M do C de CE, Freitas B de JES de A, et al. [Do children and adolescents who consume ultra-processed foods have a worse lipid profile? A systematic review]. Cienc Saude Coletiva. 2020 Dec;25(12):4979–89.

23. Vitale M, Costabile G, Testa R, D’Abbronzo G, Nettore IC, Macchia PE, et al. Ultra-Processed Foods and Human Health: A Systematic Review and Meta-Analysis of Prospective Cohort Studies. Adv Nutr Bethesda Md. 2024 Jan;15(1):100121.

24. Mambrini SP, Menichetti F, Ravella S, Pellizzari M, De Amicis R, Foppiani A, et al. Ultra-Processed Food Consumption and Incidence of Obesity and Cardiometabolic Risk Factors in Adults: A Systematic Review of Prospective Studies. Nutrients. 2023 May 31;15(11):2583.

25. Leffa PS, Hoffman DJ, Rauber F, Sangalli CN, Valmórbida JL, Vitolo MR. Longitudinal associations between ultra-processed foods and blood lipids in childhood. Br J Nutr. 2020 Aug 14;124(3):341–8.

26. Juul F, Vaidean G, Lin Y, Deierlein AL, Parekh N. Ultra-Processed Foods and Incident Cardiovascular Disease in the Framingham Offspring Study. J Am Coll Cardiol. 2021 Mar 30;77(12):1520–31.

27. DiNicolantonio JJ, O’Keefe J. The Importance of Maintaining a Low Omega-6/Omega-3 Ratio for Reducing the Risk of Autoimmune Diseases, Asthma, and Allergies. Mo Med. 2021;118(5):453–9.

28. Yam D, Eliraz A, Berry EM. Diet and disease--the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet. Isr J Med Sci. 1996 Nov;32(11):1134–43.

29. Vashishtha V, Barhwal K, Kumar A, Hota SK, Chaurasia OP, Kumar B. Effect of seabuckthorn seed oil in reducing cardiovascular risk factors: A longitudinal controlled trial on hypertensive subjects. Clin Nutr Edinb Scotl. 2017 Oct;36(5):1231–8.

30. Fawzy M, Nagi HM, Mourad R. BENEFICIAL EFFECT OF FLAXSEED AND FLAXSEED OIL BY ADJUSTING OMEGA6:OMEGA3 RATIO ON LIPID METABOLISM IN HIGH CHOLESTEROL DIET FED RATS. J Spec Educ Res. 2020 Apr 1;2020(58):117–42.

31. Obi J, Sakamoto T, Furihata K, Sato S, Honda M. Vegetables containing sulfur compounds promote trans-isomerization of unsaturated fatty acids in triacylglycerols during the cooking process. Food Res Int. 2025 Jan 1;200:115425.

32. Stanhope KL, Bremer AA, Medici V, Nakajima K, Ito Y, Nakano T, et al. 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. 2011 Oct;96(10):E1596-1605.

33. Stanhope KL, Medici V, Bremer AA, Lee V, Lam HD, Nunez MV, et al. 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. 2015 Jun;101(6):1144–54.

34. Stanhope KL, Havel PJ. Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. Curr Opin Lipidol. 2008 Feb;19(1):16–24.

35. Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010 Jan;90(1):23–46.

36. Schaefer EJ, Gleason JA, Dansinger ML. Dietary fructose and glucose differentially affect lipid and glucose homeostasis. J Nutr. 2009 Jun;139(6):1257S-1262S.

37. Angelopoulos TJ, Lowndes J, Zukley L, Melanson KJ, Nguyen V, Huffman A, et al. The effect of high-fructose corn syrup consumption on triglycerides and uric acid. J Nutr. 2009 Jun;139(6):1242S-1245S.

38. Gugliucci A. Sugar and Dyslipidemia: A Double-Hit, Perfect Storm. J Clin Med. 2023 Aug 31;12(17):5660.

39. Stanhope KL. Role of fructose-containing sugars in the epidemics of obesity and metabolic syndrome. Annu Rev Med. 2012;63:329–43.

40. Dayi T, Hoca M. Niasin Dislipidemi Riskini Azaltmada Potansiyel Bir Ajan Mıdır? İstanbul Gelişim Üniversitesi Sağlık Bilim Derg. 2022 Aug 29;(17):626–35.

41. Liu M, Wang Z, Liu S, Liu Y, Ma Y, Liu Y, et al. 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. 2020;29(2):245–52.

42. Zhang Q, Zhang DL, Zhou XL, Li Q, He N, Zhang J, et al. Antihyperlipidemic and Hepatoprotective Properties of Vitamin B6 Supplementation in Rats with High-Fat Diet-Induced Hyperlipidemia. Endocr Metab Immune Disord Drug Targets. 2021;21(12):2260–72.

43. Al-Qusous MN, Al Madanat WKJ, Mohamed Hussein R. Association of Vitamins D, B6, and B12 Deficiencies with Hyperlipidemia Among Jordanian Adults. Rep Biochem Mol Biol. 2023 Oct;12(3):415–24.

44. Altschul R, Hoffer A, Stephen JD. Influence of nicotinic acid on serum cholesterol in man. Arch Biochem Biophys. 1955 Feb;54(2):558–9.

45. Chaudhari HV, Dakhale GN, Chaudhari S, Kolhe S, Hiware S, Mahatme M. The beneficial effec of vitamin C suppllemtation on serum lipids in type 2 diabetic patients: a randomized double blind study. Int J Diabetes Metab. 2012;20(2):53–8.

46. McRae MP. Vitamin C supplementation lowers serum low-density lipoprotein cholesterol and triglycerides: a meta-analysis of 13 randomized controlled trials. J Chiropr Med. 2008 Jun;7(2):48–58.

47. Mohseni S, Tabatabaei-Malazy O, Shadman Z, Khashayar P, Mohajeri-Tehrani M, Larijani B. Targeting dyslipidemia with antioxidative vitamins C, D, and E; a systematic review of meta-analysis studies. J Diabetes Metab Disord. 2021 Oct 21;20(2):2037–47.

48. Ness AR, Khaw KT, Bingham S, Day NE. Vitamin C status and serum lipids. Eur J Clin Nutr. 1996 Nov;50(11):724–9.

49. Cerná O, Ramacsay L, Ginter E. Plasma lipids, lipoproteins and atherogenic index in men and women administered vitamin C. Cor Vasa. 1992;34(3):246–54.

50. El Mashad GM, ElSayed HM, Nosair NA. Effect of vitamin C supplementation on lipid profile, serum uric acid, and ascorbic acid in children on hemodialysis. Saudi J Kidney Dis Transplant Off Publ Saudi Cent Organ Transplant Saudi Arab. 2016;27(6):1148–54.

51. George-Opuda IM, Etuk EJ, Elechi-Amadi KN, Okolonkwo BN, Adegoke OA, Ohaka TP, et al. 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. 2024 Feb 19;26(3):45–52.

52. Levy TE, Gordon G. Primal Panacea. 2012 Second Printing edition. Henderson, NV: Medfox Publishing; 2011. 352 p.

53. Levy TE. Stop America’s #1 Killer: MD JD Levy, MD Julian Whitaker: 9780977952007: Amazon.com: Gateway [Internet]. [cited 2019 Jul 6]. Available from: https://www.amazon.com/Stop-Americas-Killer-MD-Levy/dp/0977952002/ref=sr_1_1?crid=2GE3D8VO3QMJL&keywords=stop+america+s+%231+killer&qid=1562416934&s=gateway&sprefix=stop+america%2Caps%2C428&sr=8-1

54. Sharba ZF, Shareef RH, Abd BA, Hameed EN. Association between Dyslipidemia and Vitamin D Deficiency: a Cross-Sectional Study. Folia Med (Plovdiv). 2021 Dec 31;63(6):965–9.

55. Chaudhuri JR, Mridula KR, Anamika A, Boddu DB, Misra PK, Lingaiah A, et al. Deficiency of 25-Hydroxyvitamin D and Dyslipidemia in Indian Subjects. J Lipids. 2013;2013:1–7.

56. Jiang X, Peng M, Chen S, Wu S, Zhang W. Vitamin D deficiency is associated with dyslipidemia: a cross-sectional study in 3788 subjects. Curr Med Res Opin. 2019 Jun 3;35(6):1059–63.

57. Doddamani DS, Shetty DP. The Association between Vitamin D Deficiency and Dyslipidemia. In 2020 [cited 2025 Jan 5]. Available from: https://www.semanticscholar.org/paper/The-Association-between-Vitamin-D-Deficiency-and-Doddamani-Shetty/50aa5e70d0f7a9edc9d72c5c7a8b0af5fca58866

58. Mousa H, Elrayess MA, Diboun I, Jackson SK, Zughaier SM. Metabolomics Profiling of Vitamin D Status in Relation to Dyslipidemia. Metabolites. 2022 Aug 22;12(8):771.

59. Khosravi-Boroujeni H, Ahmed F, Sarrafzadegan N. Is the Association between Vitamin D and Metabolic Syndrome Independent of Other Micronutrients? Int J Vitam Nutr Res Int Z Vitam- Ernahrungsforschung J Int Vitaminol Nutr. 2015 Dec;85(5–6):245–60.

60. Grant WB, Wimalawansa SJ, Pludowski P, Cheng RZ. Vitamin D: Evidence-Based Health Benefits and Recommendations for Population Guidelines. Nutrients [Internet]. Available from: www.mdpi.com/journal/nutrients

61. Saggini A, Anogeianaki A, Angelucci D, Cianchetti E, D’Alessandro M, Maccauro G, et al. Cholesterol and vitamins: revisited study. J Biol Regul Homeost Agents. 2011;25(4):505–15.

62. Vasanthi B, Kalaimathi B. Therapeutic Effect of Vitamin E in Patients with Dyslipidaemia. In 2012 [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. Effect of vitamin-E on high fat diet induced hyperlipidemia in rats. Indian J Exp Biol. 1993 Aug;31(8):704–7.

64. Barzegar-Amini M, Ghazizadeh H, Seyedi SMR, Sadeghnia HR, Mohammadi A, Hassanzade-Daloee M, et al. Serum vitamin E as a significant prognostic factor in patients with dyslipidemia disorders. Diabetes Metab Syndr. 2019;13(1):666–71.

65. Szczeklik A, Gryglewski RJ, Domagala B, Dworski R, Basista M. Dietary supplementation with vitamin E in hyperlipoproteinemias: effects on plasma lipid peroxides, antioxidant activity, prostacyclin generation and platelet aggregability. Thromb Haemost. 1985 Aug 30;54(2):425–30.

66. Guerrero-Romero F, Rodríguez-Morán M. Magnesium and dyslipidemia [Internet]. 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. Magnesium: Reversing Disease: Levy MD, Jd: 9780998312408: Amazon.com: Books [Internet]. 2019 [cited 2022 Feb 12]. Available from: https://www.amazon.com/Magnesium-Reversing-MD-Jd-Levy/dp/0998312401/ref=pd_lpo_2?pd_rd_i=0998312401&psc=1

68. Dean C. The Magnesium Miracle (Second Edition): Dean M.D. N.D., Carolyn: 9780399594441: Amazon.com: Books [Internet]. 2017 [cited 2022 Feb 12]. Available from: https://www.amazon.com/Magnesium-Miracle-Second-Carolyn-Dean/dp/0399594442

69. Mishra S, Padmanaban P, Deepti G, G.Sarkar, Sumathi S, Toora BD. Serum Magnesium and Dyslipidemia in Type-2 Diabetes Mellitus. Biomed Res-Tokyo [Internet]. 2012 [cited 2025 Jan 5]; Available from: https://www.semanticscholar.org/paper/Serum-Magnesium-and-Dyslipidemia-in-Type-2-Diabetes-Mishra-Padmanaban/8d23a2bd9017cb57bb6ddda98789ba81c176b53c

70. Sajjan N, Shamsuddin M. A study of serum magnesium and dyslipidemia in type 2 diabetes mellitus patients. Int J Clin Biochem Res. 2016;3(1):36.

71. Deepti R, Nalini G, Anbazhagan. RELATIONSHIP BETWEEN HYPOMAGNESEMIA AND DYSLIPIDEMIA IN TYPE 2 DIABETES MELLITUS. Asian J Pharm Res Health Care [Internet]. 2014 Jul 1 [cited 2025 Jan 5]; Available from: https://www.semanticscholar.org/paper/RELATIONSHIP-BETWEEN-HYPOMAGNESEMIA-AND-IN-TYPE-2-Deepti-Nalini/5fd9c00eacce8aa45f93c3e5ea0961969ec3223b

72. Hariyanto TI, Kurniawan A. Dyslipidemia is associated with severe coronavirus disease 2019 (COVID-19) infection. Diabetes Metab Syndr. 2020;14(5):1463–5.

73. Lo J. Dyslipidemia and lipid management in HIV-infected patients. Curr Opin Endocrinol Diabetes Obes [Internet]. 2011 Apr [cited 2024 Dec 29];18(2). Available from: https://journals.lww.com/co-endocrinology/abstract/2011/04000/dyslipidemia_and_lipid_management_in_hiv_infected.9.aspx

74. Green ML. Evaluation and management of dyslipidemia in patients with HIV infection. J Gen Intern Med. 2002 Oct 1;17(10):797–810.

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

76. Kulasekaram R, Peters BS, Wierzbicki AS. Dyslipidaemia and cardiovascular risk in HIV infection. Curr Med Res Opin. 2005 Nov;21(11):1717–25.

77. Kotler DP. HIV and Antiretroviral Therapy: Lipid Abnormalities and Associated Cardiovascular Risk in HIV-Infected Patients. JAIDS J Acquir Immune Defic Syndr. Sept. 1, 20008;49:S79–85.

78. Mattila KJ, Pussinen PJ, Paju S. Dental infections and cardiovascular diseases: a review. J Periodontol. 2005 Nov;76(11 Suppl):2085–8.

79. Ma W, Zou Z, Yang L, Lin D, Guo J, Shan Z, et al. Exploring the bi-directional relationship between periodontitis and dyslipidemia: a comprehensive systematic review and meta-analysis. BMC Oral Health. 2024 Apr 29;24(1):508.

80. Moeintaghavi A, Haerian-Ardakani A, Talebi-Ardakani M, Tabatabaie I. Hyperlipidemia in patients with periodontitis. J Contemp Dent Pract. 2005 Aug 15;6(3):78–85.

81. Nibali L, D’Aiuto F, Griffiths G, Patel K, Suvan J, Tonetti MS. Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case-control study. J Clin Periodontol. 2007 Nov;34(11):931–7.

82. Maekawa T, Takahashi N, Tabeta K, Aoki Y, Miyashita H, Miyauchi S, et al. Chronic Oral Infection with Porphyromonas gingivalis Accelerates Atheroma Formation by Shifting the Lipid Profile. Cardona PJ, editor. PLoS ONE. 2011 May 19;6(5):e20240.

83. Cutler CW, Shinedling EA, Nunn M, Jotwani R, Kim BO, Nares S, et al. Association between periodontitis and hyperlipidemia: cause or effect? J Periodontol. 1999 Dec;70(12):1429–34.

84. Janket SJ, Javaheri H, Ackerson LK, Ayilavarapu S, Meurman JH. Oral Infections, Metabolic Inflammation, Genetics, and Cardiometabolic Diseases. J Dent Res. 2015 Sep;94(9 Suppl):119S-27S.

85. Fentoğlu O, Sözen T, Oz SG, Kale B, Sönmez Y, Tonguç MO, et al. Short-term effects of periodontal therapy as an adjunct to anti-lipemic treatment. Oral Dis. 2010 Oct;16(7):648–54.

86. Park Y, Kim TJ, Lee H, Yoo H, Sohn I, Min YW, et al. Eradication of Helicobacter pylori infection decreases risk for dyslipidemia: A cohort study. Helicobacter. 2021 Apr;26(2):e12783.

87. Dancy C, Lohsoonthorn V, Williams MA. Risk of dyslipidemia in relation to level of physical activity among Thai professional and office workers. Southeast Asian J Trop Med Public Health. 2008 Sep;39(5):932–41.

88. Meireles De Pontes L. Standard of physical activity and influence of sedentarism in the occurrence of dyslipidemias in adults. Fit Perform J. 2008 Jul 1;7(4):245–50.

89. Zhou J, Zhou Q, Wang DP, Zhang T, Wang HJ, Song Y, et al. [Associations of sedentary behavior and physical activity with dyslipidemia]. Beijing Da Xue Xue Bao. 2017 Jun 18;49(3):418–23.

90. Wang X, Wang Y, Xu Z, Guo X, Mao H, Liu T, et al. Trajectories of 24-Hour Physical Activity Distribution and Relationship with Dyslipidemia. Nutrients. 2023 Jan 9;15(2):328.

91. Mutalifu M, Zhao Q, Wang Y, Hamulati X, Wang YS, Deng L, et al. Joint association of physical activity and diet quality with dyslipidemia: a cross-sectional study in Western China. Lipids Health Dis. 2024 Feb 10;23(1):46.

92. Churilla JR, Johnson TM, Zippel EA. Association of physical activity volume and hypercholesterolemia in US adults. QJM Mon J Assoc Physicians. 2013 Apr;106(4):333–40.

93. Gordon DJ, Witztum JL, Hunninghake D, Gates S, Glueck CJ. Habitual physical activity and high-density lipoprotein cholesterol in men with primary hypercholesterolemia. The Lipid Research Clinics Coronary Primary Prevention Trial. Circulation. 1983 Mar;67(3):512–20.

94. Delavar M, Lye M, Hassan S, Khor G, Hanachi P. Physical activity, nutrition, and dyslipidemia in middle-aged women. Iran J Public Health. 2011 Dec;40(4):89–98.

95. Brenta G, Fretes O. Dyslipidemias and hypothyroidism. Pediatr Endocrinol Rev PER. 2014 Jun;11(4):390–9.

96. Neves C, Alves M, Medina JL, Delgado JL. Thyroid diseases, dyslipidemia and cardiovascular pathology. Rev Port Cardiol Orgao Of Soc Port Cardiol Port J Cardiol Off J Port Soc Cardiol. 2008 Oct;27(10):1211–36.

97. Peppa M, Betsi G, Dimitriadis G. Lipid abnormalities and cardiometabolic risk in patients with overt and subclinical thyroid disease. J Lipids. 2011;2011:575840.

98. Jung KY, Ahn HY, Han SK, Park YJ, Cho BY, Moon MK. Association between thyroid function and lipid profiles, apolipoproteins, and high-density lipoprotein function. J Clin Lipidol. 2017;11(6):1347–53.

99. Duntas LH, Brenta G. A Renewed Focus on the Association Between Thyroid Hormones and Lipid Metabolism. Front Endocrinol. 2018;9:511.

100. Liberopoulos EN, Elisaf MS. Dyslipidemia in patients with thyroid disorders. Horm Athens Greece. 2002;1(4):218–23.

101.Asranna A, Taneja RS, Kulshreshta B. Dyslipidemia in subclinical hypothyroidism and the effect of thyroxine on lipid profile. Indian J Endocrinol Metab. 2012 Dec;16(Suppl 2):S347-349.

102. Arnaldi G, Scandali VM, Trementino L, Cardinaletti M, Appolloni G, Boscaro M. Pathophysiology of dyslipidemia in Cushing’s syndrome. Neuroendocrinology. 2010;92 Suppl 1:86–90.

103. Marcondes FK, Das Neves VJ, Costa R, Sanches A, Sousa T, Sampaio Moura MJC, et al. Dyslipidemia Induced by Stress. In: Kelishadi R, editor. InTech; 2012 [cited 2025 Jan 5]. Available from: http://www.intechopen.com/books/dyslipidemia-from-prevention-to-treatment/dyslipidemia-induced-by-stress

104. Nadolnik L, Polubok V, Gonchar K. Blood Cortisol Level in Patients with Metabolic Syndrome and Its Correlation with Parameters of Lipid and Carbohydrate Metabolisms. Int J Biochem Res Rev. 2020 Dec 31;149–58.

105. Veen G, Giltay EJ, DeRijk RH, van Vliet IM, van Pelt J, Zitman FG. Salivary cortisol, serum lipids, and adiposity in patients with depressive and anxiety disorders. Metabolism. 2009 Jun;58(6):821–7.

106. Christeff N, Melchior JC, de Truchis P, Perronne C, Nunez EA, Gougeon ML. Lipodystrophy defined by a clinical score in HIV-infected men on highly active antiretroviral therapy: correlation between dyslipidaemia and steroid hormone alterations. AIDS Lond Engl. 1999 Nov 12;13(16):2251–60.

107. Sholter DE, Armstrong PW. Adverse effects of corticosteroids on the cardiovascular system. Can J Cardiol. 2000 Apr;16(4):505–11.

108. Anagnostis P, Athyros VG, Tziomalos K, Karagiannis A, Mikhailidis DP. Clinical review: The pathogenetic role of cortisol in the metabolic syndrome: a hypothesis. J Clin Endocrinol Metab. 2009 Aug;94(8):2692–701.

109. van der Valk ES, Savas M, van Rossum EFC. Stress and Obesity: Are There More Susceptible Individuals? Curr Obes Rep. 2018 Jun;7(2):193–203.

110. Manenschijn L, Schaap L, van Schoor NM, van der Pas S, Peeters GMEE, Lips P, et al. High long-term cortisol levels, measured in scalp hair, are associated with a history of cardiovascular disease. J Clin Endocrinol Metab. 2013 May;98(5):2078–83.

111. Vicennati V, Pasqui F, Cavazza C, Pagotto U, Pasquali R. Stress-related development of obesity and cortisol in women. Obes Silver Spring Md. 2009 Sep;17(9):1678–83.

112. Torosyan N, Visrodia P, Torbati T, Minissian MB, Shufelt CL. Dyslipidemia in midlife women: Approach and considerations during the menopausal transition. Maturitas. 2022 Dec;166:14–20.

113. Meng Y, Lv PP, Ding GL, Yu TT, Liu Y, Shen Y, et al. High Maternal Serum Estradiol Levels Induce Dyslipidemia in Human Newborns via a Hepatic HMGCR Estrogen Response Element. Sci Rep. 2015 May 11;5:10086.

114. Schaefer EJ, Foster DM, Zech LA, Lindgren FT, Brewer HB, Levy RI. The effects of estrogen administration on plasma lipoprotein metabolism in premenopausal females. J Clin Endocrinol Metab. 1983 Aug;57(2):262–7.

115. Wahl P, Walden C, Knopp R, Hoover J, Wallace R, Heiss G, et al. Effect of estrogen/progestin potency on lipid/lipoprotein cholesterol. N Engl J Med. 1983 Apr 14;308(15):862–7.

116. Henriksson P, Stamberger M, Eriksson M, Rudling M, Diczfalusy U, Berglund L, et al. Oestrogen-induced changes in lipoprotein metabolism: role in prevention of atherosclerosis in the cholesterol-fed rabbit. Eur J Clin Invest. 1989 Aug;19(4):395–403.

117. Kushwaha RS, Hazzard WR. Exogenous estrogens attenuate dietary hypercholesterolemia and atherosclerosis in the rabbit. Metabolism. 1981 Apr;30(4):359–66.

118. Mudali S, Dobs AS, Ding J, Cauley JA, Szklo M, Golden SH, et al. Endogenous postmenopausal hormones and serum lipids: the atherosclerosis risk in communities study. J Clin Endocrinol Metab. 2005 Feb;90(2):1202–9.

119. Applebaum-Bowden D, McLean P, Steinmetz A, Fontana D, Matthys C, Warnick GR, et al. Lipoprotein, apolipoprotein, and lipolytic enzyme changes following estrogen administration in postmenopausal women. J Lipid Res. 1989 Dec;30(12):1895–906.

120. Gandarias JM, Abad C, Lacort M, Ochoa B. [Effect of progesterone on rat plasma and liver lipid levels (author’s transl)]. Rev Esp Fisiol. 1979 Dec;35(4):470–3.

121. Metherall JE, Waugh K, Li H. Progesterone inhibits cholesterol biosynthesis in cultured cells. Accumulation of cholesterol precursors. J Biol Chem. 1996 Feb 2;271(5):2627–33.

122. Abreu JM, Santos GB, Carvalho MDGDS, Mencarelli JM, Cândido BRM, Prado BBDP, et al. Dyslipidemia’s influence on the secretion ovarian’s steroids in female mice. Res Soc Dev. 2021 Oct 12;10(13):e298101321369.

123. Jensen JT, Addis IB, Hennebold JD, Bogan RL. Ovarian Lipid Metabolism Modulates Circulating Lipids in Premenopausal Women. J Clin Endocrinol Metab. 2017 Sep 1;102(9):3138–45.

124. Soma MR, Osnago-Gadda I, Paoletti R, Fumagalli R, Morrisett JD, Meschia M, et al. The lowering of lipoprotein[a] induced by estrogen plus progesterone replacement therapy in postmenopausal women. Arch Intern Med. 1993 Jun 28;153(12):1462–8.

125. Grönroos M, Lehtonen A. Effect of high dose progestin on serum lipids. Atherosclerosis. 1983 Apr;47(1):101–5.

126. Srinivasan SR, Sundaram GS, Williamson GD, Webber LS, Berenson GS. Serum lipoproteins and endogenous sex hormones in early life: observations in children with different lipoprotein profiles. Metabolism. 1985 Sep;34(9):861–7.

127. Thompson DL, Snead DB, Seip RL, Weltman JY, Rogol AD, Weltman A. Serum lipid levels and steroidal hormones in women runners with irregular menses. Can J Appl Physiol Rev Can Physiol Appl. 1997 Feb;22(1):66–77.

128. Haring R, Baumeister SE, Völzke H, Dörr M, Felix SB, Kroemer HK, et al. Prospective association of low total testosterone concentrations with an adverse lipid profile and increased incident dyslipidemia. Eur J Cardiovasc Prev Rehabil Off J Eur Soc Cardiol Work Groups Epidemiol Prev Card Rehabil Exerc Physiol. 2011 Feb;18(1):86–96.

129. Zhang N, Zhang H, Zhang X, Zhang B, Wang F, Wang C, et al. The relationship between endogenous testosterone and lipid profile in middle-aged and elderly Chinese men. Eur J Endocrinol. 2014 Apr;170(4):487–94.

130. Page ST, Mohr BA, Link CL, O’Donnell AB, Bremner WJ, McKinlay JB. 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. 2008 Mar;10(2):193–200.

131. Nordøy A, Aakvaag A, Thelle D. Sex hormones and high density lipoproteins in healthy males. Atherosclerosis. 1979 Dec;34(4):431–6.

132. Cai Z, Xi H, Pan Y, Jiang X, Chen L, Cai Y, et al. Effect of testosterone deficiency on cholesterol metabolism in pigs fed a high-fat and high-cholesterol diet. Lipids Health Dis. 2015 Mar 7;14:18.

133. Self A, Zhang J, Corti M, Esani M. Correlation between Sex Hormones and Dyslipidemia. Am Soc Clin Lab Sci. 2019 Oct 14;ascls.119.002071.

134. Monroe AK, Dobs AS. The effect of androgens on lipids. Curr Opin Endocrinol Diabetes Obes. 2013 Apr;20(2):132–9.

135. Gutai J, LaPorte R, Kuller L, Dai W, Falvo-Gerard L, Caggiula A. Plasma testosterone, high density lipoprotein cholesterol and other lipoprotein fractions. Am J Cardiol. 1981 Nov;48(5):897–902.

Orthomolecular Medicine

Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org

Find a Doctor

To locate an orthomolecular physician near you: http://orthomolecular.org/resources/omns/v06n09.shtml

The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.

Editorial Review Board:

Albert G. B. Amoa, MB.Ch.B, Ph.D. (Ghana)
Seth Ayettey, M.B., Ch.B., Ph.D. (Ghana)
Ilyès Baghli, M.D. (Algeria)
Barry Breger, M.D. (Canada)
Ian Brighthope, MBBS, FACNEM (Australia)
Gilbert Henri Crussol, D.M.D. (Spain)
Carolyn Dean, M.D., N.D. (USA)
Ian Dettman, Ph.D. (Australia)
Susan R. Downs, M.D., M.P.H. (USA)
Ron Ehrlich, B.D.S. (Australia)
Hugo Galindo, M.D. (Colombia)
Gary S. Goldman, Ph.D. (USA)
William B. Grant, Ph.D. (USA)
Claus Hancke, MD, FACAM (Denmark)
Patrick Holford, BSc (United Kingdom)
Ron Hunninghake, M.D. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Dwight Kalita, Ph.D. (USA)
Felix I. D. Konotey-Ahulu, M.D., FRCP (Ghana)
Peter H. Lauda, M.D. (Austria)
Fabrice Leu, N.D., (Switzerland)
Alan Lien, Ph.D. (Taiwan)
Homer Lim, M.D. (Philippines)
Stuart Lindsey, Pharm.D. (USA)
Pedro Gonzalez Lombana, M.D., Ph.D. (Colombia)
Victor A. Marcial-Vega, M.D. (Puerto Rico)
Juan Manuel Martinez, M.D. (Colombia)
Mignonne Mary, M.D. (USA)
Dr.Aarti Midha M.D., ABAARM (India)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Karin Munsterhjelm-Ahumada, M.D. (Finland)
Sarah Myhill, MB, BS (United Kingdom)
Tahar Naili, M.D. (Algeria)
Zhiyong Peng, M.D. (China)
Isabella Akyinbah Quakyi, Ph.D. (Ghana)
Selvam Rengasamy, MBBS, FRCOG (Malaysia)
Jeffrey A. Ruterbusch, D.O. (USA)
Gert E. Schuitemaker, Ph.D. (Netherlands)
Thomas N. Seyfried, Ph.D. (USA)
Han Ping Shi, M.D., Ph.D. (China)
T.E. Gabriel Stewart, M.B.B.CH. (Ireland)
Jagan Nathan Vamanan, M.D. (India)

Andrew W. Saul, Ph.D. (USA), Founding Editor
Richard Cheng, M.D., Ph.D. (USA), Editor-In-Chief
Associate Editor: Robert G. Smith, Ph.D. (USA)
Editor, Japanese Edition: Atsuo Yanagisawa, M.D., Ph.D. (Japan)
Editor, Chinese Edition: Richard Cheng, M.D., Ph.D. (USA)
Editor, Norwegian Edition: Dag Viljen Poleszynski, Ph.D. (Norway)
Editor, Arabic Edition: Moustafa Kamel, R.Ph, P.G.C.M (Egypt)
Editor, Korean Edition: Hyoungjoo Shin, M.D. (South Korea)
Editor, Spanish Edition: Sonia Rita Rial, PhD (Argentina)
Editor, German Edition: Bernhard Welker, M.D. (Germany)
Associate Editor, German Edition: Gerhard Dachtler, M.Eng. (Germany)
Assistant Editor: Michael Passwater (USA)
Contributing Editor: Thomas E. Levy, M.D., J.D. (USA)
Contributing Editor: Damien Downing, M.B.B.S., M.R.S.B. (United Kingdom)
Contributing Editor: W. Todd Penberthy, Ph.D. (USA)
Contributing Editor: Ken Walker, M.D. (Canada)
Contributing Editor: Michael J. Gonzalez, N.M.D., Ph.D. (Puerto Rico)
Technology Editor: Michael S. Stewart, B.Sc.C.S. (USA)
Associate Technology Editor: Robert C. Kennedy, M.S. (USA)
Legal Consultant: Jason M. Saul, JD (USA)

Comments and media contact: editor@orthomolecular.org OMNS welcomes but is unable to respond to individual reader emails. Reader comments become the property of OMNS and may or may not be used for publication.

To Subscribe at no charge: http://www.orthomolecular.org/subscribe.html

To Unsubscribe from this list: http://www.orthomolecular.org/unsubscribe.html