The Power of Sleep in Metabolic and Cardiovascular Health and the Profound Cost of its Deprivation

Jesse Oswald • December 9, 2024

Key Points

  • Sleep deprivation disrupts glucose metabolism and the typical secretion patterns of the appetite hormones, contributing to metabolic dysfunctions. 
  • Sleep hygiene is a valuable tool for cardiovascular disease prevention.
  • Poor sleep quality shifts the autonomic nervous system balance towards sympathetic dominance, increasing the risk for cardiovascular disorders.
  • The circadian rhythms of cortisol, adrenaline, and melatonin influence cardiovascular parameters, with disruptions due to sleep deprivation compromising cardiovascular health.


Our previous article about sleep discussed basic sleep concepts, such as sleep quality and duration, and their impact on recovery and exercise performance. In closing the chapter about sleep and its broad influences on overall health and well-being, the impact of sleep on metabolic and cardiovascular health will be analyzed in the second part. Metabolic health aspects, such as glucose regulation, appetite hormones, and energy balance, as well as cardiovascular health aspects, such as autonomic nervous system regulation and hormones, will be considered. 


Sleep and metabolic health


Glucose regulation


In healthy individuals, glucose regulation appears to be under circadian control. Particularly, insulin sensitivity and glucose tolerance, which are major regulating factors of glucose metabolism, tend to be elevated during mornings and decrease as the day progresses. Circadian misalignment induced by sleep deprivation, poor sleep quality, or irregular sleeping patterns can disrupt these abilities, resulting in elevated blood glucose levels and extended time to restore normal levels. Thus, the chronically elevated blood sugar levels associated with systematic sleep deprivation can result in insulin resistance, leading to a high risk of developing a plethora of metabolic disorders, such as type II diabetes, obesity, and metabolic syndrome. Indicatively, robust data from experimental sleep restriction indicated that individuals with short sleep durations (≤6–7 h/night) are at 30% greater risk for developing type II diabetes.


Appetite hormones and energy balance


Another aspect of metabolism associated with circadian misalignment due to sleep disturbances is the 24-hour variation of the appetite hormones leptin and ghrelin. Leptin and ghrelin are primary coordinators of energy intake and energy expenditure throughout the day. Leptin is the satiety hormone that maintains energy balance by reducing caloric intake through decreased appetite, deterring fat production, and increasing energy expenditure. On the other hand, ghrelin is considered an orexigenic hormone, secreted mainly by the stomach. Ghrelin also plays a fundamental role in energy balance regulation with an opposite to leptin function. 


Their functions are synchronized with leptin levels, which typically rise during the early stages of sleep and reach their lowest early in the morning, while ghrelin follows an inverse pattern. Ghrelin declines during bedtime and reaches its peak early in the morning, remaining high before meals and typically returning to baseline postprandially. 


Although further research is required to elucidate the exact mechanisms, existing studies suggest that poor sleep quality and sleep deprivation interfere with appetite hormones’ secretion by altering the timing of their secretion, thus leading to dysregulation. Particularly, sleep restriction and irregular sleeping patterns are associated with diminished secretion of leptin and increased secretion of ghrelin, promoting elevated caloric intake and subsequent weight gain. From the evidence obtained so far, there might be a link between short sleep duration, adiposity, and the development of metabolic disorders.

The primary mechanism proposed for the dysregulation of appetite hormones due to sleep abnormalities is that sleep deprivation acts as a chronic stressor, affecting the hypothalamic-pituitary-adrenal axis function. The hypothalamic–pituitary–adrenal axis is responsible for cortisol production and secretion, an aforementioned stress hormone with catabolic properties. Sleep deprivation-induced stress can lead to elevated cortisol secretion by the brain, interfering with the normal signaling of the appetite hormones. As a consequence, leptin’s sensitivity is diminished, and even when the body has adequate energy reserves, the individual does not experience satiety. Additionally, cortisol can stimulate ghrelin secretion, further boosting feelings of hunger and potentially leading to weight gain.


Overall, sleep deprivation can have adverse effects on various aspects of metabolic health by disrupting glucose regulation, inducing stress, and potentially altering appetite control, resulting in a heightened risk of metabolic disorders like diabetes, type II diabetes, obesity, and metabolic syndrome. 


Sleep and cardiovascular health 


Autonomic Nervous System’s adaptations during healthy sleep 


Adequate and quality sleep is considered fundamental in preserving cardiovascular health, as underlined in the recent guidelines released by the American College of Cardiology/American Heart Association. These guidelines state that counseling on sleep and its hygiene is a valuable approach to cardiovascular disease (CVD) prevention.

This importance can be attributed to the vital rest period sleep offers the cardiovascular system. Particularly, during sleep, cardiovascular regulation is modified, and many biological functions slow down, allowing the heart to rest from the stress of waking hours and facilitating efficient restoration of the cardiovascular tissues. In this context, the autonomic nervous system (ANS), which controls physiological body processes that occur despite our control, plays a central role. Specifically, a suppression of the sympathetic nervous system and increased parasympathetic system activity occurs. In other words, our body transitions from an alert state, often called the «fight or flight» response, to a state of relaxation and rejuvenation. This shift is predominantly evident during stages N1, N2, and N3 of NREM sleep.


During NREM sleep, heart rate and arterial blood pressure tend to decrease. This is because a shift towards a more parasympathetic tone occurs, promoting vasodilation (widening of blood vessels), enhancing blood flow to peripheral tissues, and thus fostering relaxation and tissue repair. On the contrary, during REM sleep, which involves the transition from sleep to wakefulness, our nervous system is predominantly under sympathetic control, leading to elevated heart rate and arterial blood pressure values.


The interplay between the sympathetic and parasympathetic activities can be efficiently reflected by HRV, a marker that serves as an indicator of the fluctuations in the time intervals between consecutive heartbeats. HRV normal values differ between populations and depend on factors like age, gender, and fitness level. During sleep, higher HRV values, meaning broader time variation between heartbeats, are associated with balanced autonomic nervous system activity and resilience to stress. Conversely, lower HRV indicates autonomic dysregulation, diminished adaptivity between states of alertness and relaxation, and potential susceptibility to cardiovascular issues.


Autonomic Nervous System’s adaptations during sleep deprivation 


It’s becoming clear that the interplay between the two major branches of the autonomic nervous system (the sympathetic and parasympathetic nervous systems) is of great importance in achieving restful sleep. Disruptions of sleep duration and quality appear to disrupt this interplay, resulting in considerable predominance of the sympathetic nervous system’s activity. This suggests that sleep deprivation impairs the nervous system’s ability to adapt to shifting toward relaxation mode, subjecting individuals to a prolonged state of alertness and stress. As a result, a cascade of events occurs, including lower HRV values, increased proinflammatory cytokine secretion, and vasoconstriction, increasing the risk of hypertension, coronary artery disease, endothelial dysfunction, and other cardiovascular disorders.


Circadian Hormonal Dynamics and Cardiovascular Health


The circadian rhythm has implications for the cardiovascular system, as well. Hormones like cortisol, melatonin, and adrenaline, which follow circadian patterns, play a critical role in cardiovascular regulation.


As mentioned before, cortisol is a stress hormone, and its levels typically rise in the morning and reach their lowest during the night, enabling the anabolic hormones to facilitate recovery. However, chronic sleep deprivation can alter this hormonal synchronization, leading to dysregulated cortisol levels, potentially contributing to increased blood pressure and consequent risk of cardiovascular diseases.


Likewise, adrenaline, another hormone typically released as a response to stress stimuli, peaks throughout the day when the individual is active and the sympathetic nervous system governs. Sleep deprivation and irregular sleeping patterns can result in circadian misalignment associated with dysregulation of adrenaline secretion. This dysregulation leads to sympathetic nervous system dominance and, thus, elevated heart rate and blood pressure, meaning an increased risk for cardiovascular disorders.


Finally, melatonin, a hormone released by the brain, typically rises during the night as sleeping time approaches. Melatonin is known to exert cardioprotective effects through its antioxidant, anti-inflammatory, antiatherogenic, and lipid-lowering properties. Moreover, melatonin regulates blood pressure and vascular tone by contributing to blood pressure reduction during sleep. Hence, disruptions in melatonin secretion, often originating from chronic insufficient or poor sleep, pose a non-negligent risk for cardiovascular diseases. 


To sum up, adequate sleep quality is a good indicator of metabolic and cardiovascular health. Therefore, prioritizing sufficient and quality sleep for the optimal functioning of the cardiovascular and metabolic health system and thus for longevity is crucial and should not be ignored since sleep is, along with nutrition and exercise, amongst the main pillars of a healthy, long life.



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Lin J, Jiang Y, Wang G, Meng M, Zhu Q, Mei H, Liu S, Jiang F. Associations of short sleep duration with appetite-regulating hormones and adipokines: A systematic review and meta-analysis. Obes Rev. 2020 Nov;21(11):e13051. DOI: https://doi.org/10.1111/obr.13051


Liu S, Wang X, Zheng Q, Gao L, Sun Q. Sleep Deprivation and Central Appetite Regulation. Nutrients. 2022 Dec 7;14(24):5196. DOI: https://doi.org/10.3390/nu14245196


Morselli L, Leproult R, Balbo M, Spiegel K. Role of sleep duration in the regulation of glucose metabolism and appetite. Best Pract Res Clin Endocrinol Metab. 2010 Oct;24(5):687-702. DOI: https://doi.org/10.1016/j.beem.2010.07.005 


Rogers EM, Banks NF, Jenkins NDM. The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review. Diabetes Metab Res Rev. 2024 Feb;40(2):e3667. DOI: https://doi.org/10.1002/dmrr.3667


Tobaldini E, Costantino G, Solbiati M, Cogliati C, Kara T, Nobili L, Montano N. Sleep, sleep deprivation, autonomic nervous system and cardiovascular diseases. Neurosci Biobehav Rev. 2017 Mar;74(Pt B):321-329. DOI: https://doi.org/10.1016/j.neubiorev.2016.07.004 


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An Ounce of Prevention - Hyperion Health Blog

A woman is helping an older woman do exercises on an exercise ball in a gym.

What is a Kinesiologist?

By Jesse Oswald • January 29, 2025
What is a Kinesiologist?
A woman is wearing an oxygen mask while running on a treadmill.

Predicting Medical Costs with VO2max

By Jesse Oswald • January 20, 2025
Highlights Healthcare expenses are skyrocketing, with consumers and employers facing the significant brunt. Identifying those likely to get sick is critical as our resource-strapped healthcare system should focus on those likely to become the most significant burden to the system. VO2 max is a crucial longevity indicator that can also accurately predict healthcare expenses. The rampant chronic disease epidemic and the resulting surge in medical expenses is one of the most dire problems of modern societies, probably only second to climate change. Healthcare inflation is on a meteoric rise, and for those with limited or no healthcare coverage, a medical emergency is the equivalent of personal bankruptcy. A dire problem for employers In the US, employers and consumers who face rising health insurance premiums and astronomical out-of-pocket medical expenses feel the brunt of rising healthcare costs. Such is the problem that even large, well-capitalized corporations choose to send employees overseas for specific medical procedures since the cost of traveling and treatment in a foreign country is lower than the cost of care in the US. Another startling example is the infamous "northern caravan," a term that describes people with diabetes in the northern states who travel to Canada to secure their insulin supply. According to McKinsey , a survey conducted among over 300 employers highlighted that the average increase in the cost of health benefits over the past three years has been within the range of 6 to 7 percent. This survey also indicated that any rate increases exceeding 4 to 5 percent were deemed unsustainable. Interestingly, 95 percent of the surveyed employers expressed willingness to contemplate reducing benefits if costs surged by 4 percent or more. The primary cost-control measures that these employers indicated they might explore included elevating the portion of premium costs covered by employees and a potential transition to high-deductible health plans. Why is Breath Analysis relevant? Vis-a-vis this problem, the early and accurate estimation of who will get sick and how much they will cost is as critical as the treatment itself. The reason is that no other method of accurately identifying at-risk populations exists; it helps focus our scarce prevention resources and attention on those most in need. Breath analysis, AKA VO2max or metabolic testing, is an assessment that reveals two key biomarkers that provide significant predictive value for one's likelihood of developing costly chronic conditions. These two biomarkers are VO2max and the Respiratory Exchange Ratio. In this article, we will dive into VO2max to understand why it's a critical reflection of our overall health and, consequently, a window into our future healthcare spend. What is VO2max? Let's start with the basics. What is VO2max? VO2 max is the maximum amount of oxygen the human body can absorb. It is measured in terms of milliliters of oxygen consumed per kilogram of body weight. The below formula below indicates how VO2max is calculated: The numerator indicates the volume of oxygen your heart, lungs, and cells can absorb, expressed in milliliters per minute. The denominator indicates the weight of the individual represented in kilograms. 
There are many different types of fats in this picture.

Dietary Fat: An Essential Dietary Component Rather than the root of all Nutritional Health Issues

By Jesse Oswald • January 13, 2025
Key points A total fat intake between 20-35% ensures sufficient intake of essential fatty acids and fat-soluble vitamins Omega-6 PUFAs are primarily found in vegetable oils, while omega-3 PUFAs are primarily found in fatty fish and fish oils Both omega-3 PUFAs and MUFAs have established benefits for cardiovascular disease TFAs are the only dietary lipids that have a strong positive relationship with cardiovascular disease Omega-3 PUFA supplementation increases the beneficial bacteria of the human microbiome Over the last three decades, there has been a great revolution against fat due to its suspected association with several nutritional health issues, especially cardiovascular disease. There was a tremendous amount of evidence that indicated dietary cholesterol and saturated fat as the main culprits of cardiovascular disease, thus morbidity and mortality. It was when all the low-fat and no-fat dairy products started to launch, promising even complete substitution of the cholesterol-lowering heart medication if these products were exclusively consumed. Let’s start from the beginning. Dietary fat intake can vary significantly and still meet energy and nutrient needs. International guidelines suggest a total fat intake between 20% and 35% of the daily caloric consumption. This range ensures sufficient intake of essential fatty acids and fat-soluble vitamins. Not only does the quantity of the ingested fat matter, but most importantly, its quality. Some dietary fats have beneficial effects, with a significant role in maintaining good health, while others may threaten it. Which are, after all, the dietary fats? Dietary fats is a rather heterogeneous group of organic compounds, including four main types of fat, which are elaborately described in the following sections of this article. Polyunsaturated fatty acids (PUFAs) Polyunsaturated fatty acids (PUFAs) have two or more carbon-carbon double bonds. Omega-6 PUFAs and omega-3 PUFAs are the main types of PUFAs and are classified according to the location of the first unsaturated bond (sixth and third carbon atom, respectively). Alpha-Linolenic acid (ALA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and eicosapentaenoic acid (EPA) are the most important omega-3 PUFAs. ALA is an essential fatty acid that can only be obtained from diet and can be converted into EPA and then to DHA, but the rate of this conversion is finite, approximately 7.0%–21% for EPA and 0.01%–1% for DHA. In the same way, the most important omega-6 PUFAs are linoleic acid (LA) and arachidonic acid (ARA). LA is an essential fatty acid that, in order to give rise to ARA, needs to be ingested through the diet as the human body cannot synthesize it. The recommended intake for total PUFA ranges between 5% and 10% of the total energy intake, while a total omega-3 PUFA intake of 0.5%–2% and a total omega-6 PUFA intake of 2.5%-5% is suggested. A dietary ratio of omega−6/omega−3 PUFA is recommended to be 1:1–2:1 to balance their competing roles and achieve health benefits. Omega-6 and omega-3 PUFAs Omega-6 PUFAs, in the form of LA, are plentiful in most crop seeds and vegetable oils, such as canola, soybean, corn, and sunflower oils. In contrast to omega-6 PUFAs, omega-3 PUFAs are obtained from a limited range of dietary sources. Flax, chia, and perilla seeds are rich in ALA, with significant amounts also detected in green leafy vegetables. The consumption of fatty fish, such as salmon, sardines, tuna, trout, and herring, provides high amounts of EPA and DHA. Besides fish and their oils, small amounts of omega-3 PUFAs are also detected in red meat like beef, lamb, and mutton. All the above dietary sources provide EPA, DPA, DHA, LA, and ARA in different amounts, and their intake is necessary for normal physiological function. PUFAs play a critical role in many chronic diseases, affecting human cells by regulating inflammation, immune response, and angiogenesis. Omega-3 PUFAs’ role against hypertriglyceridemia has been clarified, and research indicates that systematically consuming oily fish can contribute to general heart protection. Supplementation with omega-3 PUFAs could potentially lower the risk of several cardiovascular outcomes, but the evidence is stronger for individuals with established coronary heart disease. Moreover, adequate EPA and DHA levels are necessary for brain anatomy, metabolism, and function. Although the mechanisms underlying omega-3 PUFAs' cardioprotective effects are still poorly understood, several studies have been conducted in this direction. Unfortunately, that does not hold true for their omega-6 counterparts, for which controversial emerging data tend to show anti-inflammatory behavior that needs to be further studied. Monounsaturated fatty acids (MUFAs) In contrast to PUFAs, monounsaturated fatty acids (MUFAs) are easily produced by the liver in response to the ingestion of carbohydrates. The main MUFA is oleic acid, found in plant sources, such as olive oil, olives, avocado, nuts, and seeds, while minimal amounts are also present in meat, eggs, and dairy products. Specific guidelines around MUFAs’ dietary consumption do not exist. Therefore, MUFAs are recommended to cover the remaining fat intake requirements to reach the total daily fat intake goal. A growing body of research shows that dietary MUFAs reduce or prevent the risk of metabolic syndrome, cardiovascular disease (CVD), and hypertension by positively affecting insulin sensitivity, blood lipid levels, and blood pressure, respectively. Moreover, olive oil contains several bioactive substances, possessing anti-tumor, anti-inflammatory, and antioxidant qualities. According to a meta-analysis, consuming olive oil was linked to a lower risk of developing any sort of cancer, especially breast cancer and cancer of the digestive system. Another study found that an isocaloric replacement of 5% of the energy from saturated fatty acids (SFAs) with plant MUFAs led to an 11% drop in cancer mortality over a 16-year follow-up period. Therefore, including MUFAs in the everyday diet offers multifaceted benefits in chronic disease prevention and management, including cancer and general health promotion.  Saturated fatty acids (SFAs) Saturated fatty acids (SFAs) form a heterogeneous group of fatty acids that contain only carbon-to-carbon single bonds. Whole-fat dairy, (unprocessed) red meat, milk chocolate, coconut, and palm kernel oil are all SFA-rich foods. These fatty acids have distinct physical and chemical profiles and varying effects on serum lipids and lipoproteins. Stearic, palmitic, myristic, and lauric acids are the principal SFAs found in most natural human diets. Dietary practice and guidelines recommend limiting SFA intake to <10% of the total energy (E%), while the American Heart Association suggests an even lower intake of <7 E% because total saturated fat consumption and LDL-C levels are positively correlated. However, the role of SFAs in CVDs is quite complex, and the evidence is heterogeneous. In a recent study with a 10.6-year follow-up period, which included 195,658 participants, there was no proof that consuming SFAs was linked to developing CVD while replacing saturated fat with polyunsaturated fat was linked to an increased risk of CVD. Moreover, according to 6 systematic reviews and meta-analyses, cardiovascular outcomes and total mortality were not significantly impacted by substituting saturated fat with polyunsaturated fat. Even if these analyses were to be challenged, due to heterogenous evidence, the possible reduction in CVD risk associated with replacing SFAs with PUFAs in several studies may not necessarily be an outcome of SFAs’ negative effect but rather a potential positive benefit of PUFAs. Regarding SFAs' effect on different types of cancers, associations of their intake with an increased risk of prostate and breast cancer have been indicated. Conversely, a meta-analysis showed no link between SFA intake and a higher risk of colon cancer; similarly, consuming MUFAs, PUFAs, or total fat did not affect colon cancer risk. Hence, the role of SFA consumption in preventing, promoting, or having a neutral role in serious chronic diseases has not been fully elucidated yet. Trans fatty acids (TFAs) Trans fatty acids (TFAs) are created industrially by partially hydrogenating liquid plant oils or can be naturally derived from ruminant-based meat and dairy products. TFAs are highly found in commercial baked goods, biscuits, cakes, fried foods, etc. Guidelines regarding TFAs are stringent and limit TFA intake to <1% of energy or as low as possible. In 2015, the US Food and Drug Administration declared that industrial TFAs are no longer generally recognized as safe and should be eliminated from the food supply as their consumption is strongly linked to various CVD risk factors. Specifically, TFA intake raises triglycerides and increases inflammation, endothelial dysfunction, and hepatic fat synthesis, leading to a significantly increased risk of coronary heart disease (CHD). A meta-analysis suggested that increased TFA intake led to an increase in total and LDL-cholesterol and a decrease in HDL-cholesterol concentrations. Data also indicates that TFAs may influence carcinogenesis through inflammatory pathways, but the reported data are debatable. A recent study investigated the effects of all types of dietary fat intake on CVD risk. While PUFA, MUFA, and SFA intake were not linked to higher CVD risk, dietary TFA intake showed a strong association with CVD risk. Analysis indicated PUFA intake and CVD risk were inversely correlated, and the relative risk of CVD was reduced by 5% in studies with a 10-year follow-up. Dietary lipids and the human microbiome Dietary lipids also affect human microbiota composition. Studies have identified a close association between the human microbiome and metabolic diseases, including obesity and type 2 diabetes. Diets with a high omega-6 PUFA, SFA, and TFA intake increase the amount of many detrimental bacteria in the microbiome and reduce the amount of the beneficial ones, altering the microbiota composition and inducing inflammation via the secretion of pro-inflammatory cytokines. These bacteria may disrupt the gut barrier function, allowing lipopolysaccharides (LPS) translocation, which are bacterial toxins. This condition is linked to metabolic perturbations such as dyslipidemia, insulin resistance, non-alcoholic fatty liver disease (NAFLD), and CVD. On the contrary, omega-3 PUFA (EPA and DHA) supplementation increases beneficial bacteria and limits harmful ones, enhancing intestinal barrier functioning and preventing LPS translocation and its implications. Omega-3 PUFA supplementation has also been studied as a means of mental health disorders management, but the evidence is still controversial. A possible protective impact of fish consumption on depression has been suggested by various studies, as well as a possible protective effect of dietary PUFAs on moderate cognitive impairment. A recent review of meta-analyses indicated that omega-3 PUFA supplementation might have potential value in mental health disorders, but data credibility is still weak. Dietary lipids and obesity Last but not least, obesity and its management is another field that dietary lipids intake seems to impact with their mechanisms. A diet high in PUFA has been shown to lower the total mass of subcutaneous white adipose tissue (the predominant fat type in human bodies), reduce blood lipid levels, and improve insulin sensitivity. In a study comparing PUFA and MUFA isocaloric intake, PUFA was more advantageous and lowered visceral adiposity in patients with central obesity. By stimulating brown adipose tissue, which aids energy expenditure through its elevated thermogenic activity, omega-3 PUFAs seem to elicit these positive effects in fat tissue, thus being useful in preventing and/or managing obesity. Another related study compared PUFA to SFA overfeeding in dietary surplus conditions that aimed to increase weight by 3%. While SFA overfeeding led to weight gain, primarily through the expansion of the visceral adipose tissue, PUFA overfeeding also led to weight gain, but because of a greater expansion of lean tissue mass. To sum up, dietary fats are an essential part of the human diet with many important physiologic functions, including cell function, hormone production, energy, and nutrient absorption. Moreover, dietary fat consumption is associated with positive outcomes in regard to cardiovascular disease, metabolic syndrome, cancer, and depression. Therefore, there is no reason to demonize this valuable dietary component, incriminating it for irrelevant adverse health outcomes, primarily weight loss failure and obesity. References 1. Astrup A, Magkos F, Bier DM, Brenna JT, de Oliveira Otto MC, Hill JO, King JC, Mente A, Ordovas JM, Volek JS, Yusuf S, Krauss RM. Saturated fats and health: A reassessment and proposal for food-based recommendations: JACC State-of-the-Art review. J Am Coll Cardiol. 2020;76(7):844-857. DOI: 10.1016/j.jacc.2020.05.077 2. Bojková B, Winklewski PJ, Wszedybyl-Winlewska M. Dietary fat and cancer-Which is good, which is bad, and the body of evidence. Int J Mol Sci. 2020;21(11):4114. DOI: 10.3390/ijms21114114 3. Custers, Emma EM, Kiliaan, Amanda J. Dietary lipids from body to brain. Prog Lipid Res. 2022;85:101144. DOI: 10.1016/j.plipres.2021.101144 4. de Souza RJ, Mente A, Maroleanu A, Cozma AI, Ha V, Kishibe T, Uleryk E, Budylowski P, Schünemann H, Beyene J, Anand SS. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ. 2015;351:h3978. DOI: 10.1136/bmj.h3978 5. Gao X, Su X, Han X, Wen X, Cheng C, Zhang S, Li W, Cai J, Zheng L, Ma J, Liao M, Ni W, Liu T, Liu D, Ma W, Han S, Zhu S, Ye Y, Zeng F-F. Unsaturated fatty acids in mental disorders: An umbrella review of meta-analyses. Adv Nutr. 2022;13(6):2217-2236. DOI: 10.1093/advances/nmac084 6. Liu AG, Ford NA, Hu FB, Zelman KM, Mozaffarian D, Kris-Etherton PM. A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion. Nutr J. 2017;16(1):53. DOI: 10.1186/s12937-017-0271-4 7. Poli A, Agostoni C, Visioli F. Dietary fatty acids and inflammation: Focus on the n-6 series. Int J Mol Sci. 2023;24(5):4567. DOI: 10.3390/ijms24054567 8. Saini RK, Keum Y-S. Omega-3 and omega-6 polyunsaturated fatty acids: Dietary sources, metabolism, and significance-A review. Life Sci. 2018;203:255-267. DOI: 10.1016/j.lfs.2018.04.049 9. Saini RK, Prasad P, Sreedhar RV, Naidu KA, Shang X, Keum Y-S. Omega-3 polyunsaturated fatty acids (PUFAS): Emerging plant and microbial sources, oxidative stability, bioavailability, and health benefits-A review. Antioxidants (Basel). 2021;10(10):1627. DOI: 10.3390/antiox10101627 10. Zhao M, Chiriboga D, Olendzki B, Xie B, Li Y, McGonigal LJ, Maldonado-Contreras A, Ma Y. Substantial increase in compliance with saturated fatty acid intake recommendations after one year following the American Heart Association diet. Nutrients. 2018;10(10):1486. DOI: 10.3390/nu10101486 11. Zhu Y, Bo Y, Liu Y. Dietary total fat, fatty acids intake, and risk of cardiovascular disease: a dose-response meta-analysis of cohort studies. Lipids Health Dis. 2019;18:91. DOI: 10.1186/s12944-019-1035-2
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