The Concept of Energy Balance and Its Implication in Health and Disease

Jesse Oswald • February 25, 2024

Key Points

  • Energy balance implies weight balance (weight maintenance), positive energy balance, weight gain, and negative energy balance weight loss.
  • Energy balance comprises two components: energy intake (the food we consume) and energy expenditure (the calories we burn at rest, through exercise, and food digestion)
  • Breath analysis, through measuring the volume of oxygen consumption (VO2) and carbon dioxide production (VCO2), is the gold standard method for determining energy balance.

 

Energy balance is based on the fundamental thermodynamic principle that energy cannot be destroyed and can only be gained, lost, or stored by an organism. It is defined as the state achieved when energy intake equals energy expenditure. When the body is in energy balance, body weight is stable; when the body is in positive energy balance, body weight increases; and when the body is in negative energy balance, body weight decreases. In other words, energy balance practically means weight balance, positive energy balance means weight gain and negative energy balance implies weight loss. This is also known as the calories in/calories out (CICO) rule, where weight loss occurs when the calories consumed are lower than the calories burnt, and weight gain occurs when the calories consumed are higher than the calories burnt. Weight maintenance occurs when the calories consumed are equal to the calories burnt.

 

To better understand energy balance, let’s delve into its two components: intake and expenditure. Energy intake refers to the calories humans ingest from protein, carbohydrates, fat, and alcohol through consuming foods and drinks. On the other hand, energy expenditure refers to the calories humans expend through the resting metabolic rate (RMR), the thermic effect of food (TEF), and physical activity. RMR is the energy required to fuel the body at rest to maintain vital body functions and homeostasis. RMR accounts for 60-75% of total daily energy expenditure and is proportional to muscle mass, meaning the greater the muscles somebody has, the higher their RMR. TEF refers to the energy required to absorb, digest, and metabolize the food consumed and typically accounts for 8-10% of total daily energy expenditure. Lastly, the energy expended through physical activity, the most variable component of total daily energy expenditure, involves the calories expended through voluntary and non-voluntary exercise, such as postural control and shivering. This is also known as non-exercise activity thermogenesis (NEAT).

 

Energy intake and energy expenditure are primarily controlled by the central nervous system (CNS). Upon food consumption, smell, taste, and texture inputs are sent to the cognitive and emotional brain, regulating eating behaviour. While food enters the gastrointestinal (GI) tract, physical distension of the stomach creates a satiation signal that is transmitted to the brain to stop eating. Moreover, digested food components such as fatty acids further promote satiation by stimulating short-term satiety hormones, such as cholecystokinin, from GI endocrine cells. Finally, after food consumption has terminated, hormones from the fat tissue (leptin) and the pancreas (insulin) are secreted, further suppressing appetite. The energy balance regulation is not only a short-term but, most importantly, a long-term process. The hypothalamus, a particular brain region, regulates long-term energy balance, thus body weight, by encoding information about total energy availability and reserve in the body.

 

A chronic positive energy balance caused by a combination of genetic (obesity genes) and environmental (food abundance, low cost of high fat and sugar palatable foods, lack of infrastructure, and motives for physical activity) factors leads to fat accumulation and eventually obesity. Conversely, energy expenditure must exceed energy intake (negative energy balance) to lose weight. However, the magnitude of this negative energy balance is highly debatable, and many theories have been developed over the years. One of the most popular ones is the ‘’3,500 kcal per pound’’ rule used to predict the weight-change time course of a dietary intervention. Specifically, this rule states that it takes a 3,500kcal calorie deficit for someone to lose 1 pound. This rule has been confirmed since it is generally acknowledged that compensatory changes occur with weight change in energy expenditure, rendering this balance more complex than a simple mathematical equation.

 

The shift of the energy balance towards a lower energy intake relative to the total energy expenditure has a host of distinct biological adaptations, including decreased RMR, reduced NEAT, and altered levels of circulating hormones that regulate appetite (increased levels of orexigenic or hunger hormones such as ghrelin and reduced levels of anorexigenic or satiating hormones such as leptin), known to influence weight loss but even more importantly long-term weight maintenance. The most powerful biological adaptations that occur during weight loss and operate against its continuum are the decrease in RMR and the increase in skeletal muscle activity efficiency, especially during low levels of exercise (previously referred to as NEAT). These adaptations are collectively referred to as adaptive thermogenesis (AT), where the cells in your body, and especially your skeletal muscle cells, burn fewer calories for their activities (mainly NEAT-type activities) per unit of weight compared to what they would normally do, given the hypocaloric environment did not exist. The abovementioned changes are the principal causes of weight loss plateau and complete or partial weight regain. Therefore, since the energy balance constitutes a susceptible mechanism that can easily be disrupted, especially through extreme and improper dietetic practices such as the very-low-calorie diets (VLCD), dieters should always refer to professional dietitians to guide them through this process.

 

Overweight and obesity arising from a chronic positive energy balance are major risk factors for serious chronic diseases, especially cancer, cardiovascular disease, and type II diabetes. Obesity is a causal factor for many types of cancer, including colorectum, endometrium, kidney, esophagus, pancreas, thyroid, breast, and prostate, among others. Adipose tissue is a metabolically active tissue producing hormones and inflammatory cytokines contributing to increased risk for certain cancers. Moreover, insulin resistance, a hallmark of obesity and a precursor of type II diabetes, causes hyperinsulinemia, which stimulates the production of insulin-like growth factor -1 (IGF-1), resulting in increased cancer risk. Obesity is also a strong risk factor for the development of cardiovascular disease, causing hypertension, hyperlipidemia, and endothelial dysfunction. Weight loss through adopting a healthy, balanced dietary pattern, such as the Mediterranean diet, diminishes the harmful effects of a long-term positive energy balance on the heart and the circulatory system in general.

A positive energy balance is not always unfortunate. Creating an adequate energy surplus is often a prerequisite, especially for lean athletes who attempt to gain muscle mass. The magnitude of this surplus so that the athlete can build 1 kg of skeletal muscle mass has not yet been defined due to inestimable variables such as genetics, age, sex, body composition, and training status. However, since muscle mass accretion through a positive energy balance is also associated with increased fat mass, the general recommendation is a surplus of 350-500kcal per day for an efficient anabolic context. A positive energy balance is insufficient, provided there is no adequate prescription for a resistance training program and adequate protein intake, the most critical macronutrient in skeletal muscle hypertrophy.

 

RMR, consequently, energy balance can be accurately measured through respiratory indirect calorimetry, which is the gold standard test for measuring energy expenditure. Breath analysis monitors gas exchange, namely the volume of oxygen consumption (VO2) and carbon dioxide production (VCO2) at rest and during exercise. The ratio of CO2 production to O2 consumption is known as the respiratory exchange ratio (RER) and represents fuel oxidation, specifically carbohydrate and fat relative contribution to energy expenditure. During pure carbohydrate oxidation, the amount of CO2 produced equals the amount of O2 consumed (RER=1.0), while during pure fat oxidation, RER equals 0.7. A greater ability to oxidize fat at rest is important for metabolic health, weight management, and body composition, while obese individuals with insulin resistance have impaired fat-burning efficiency. In addition, a high resting RER is predictive of fat mass regain after diet-induced reductions in body weight.

 

Overall, energy balance is a complex equilibrium with many components that may vary significantly among individuals. This equilibrium implicates complex biological mechanisms such as hormones and neural circuits, the disruption of which can have adverse long-term effects on metabolic health. While a chronic positive energy balance is related to obesity and other severe chronic health issues, it can also be desirable for athletes who strive to gain muscle mass. All people seeking a valid energy balance measurement should undertake breath analysis testing, the gold standard method for measuring energy expenditure, thus determining energy intake and, eventually, energy balance.

 

References

  •  

  • Cooney C, Daly E, McDonagh M, Ryan L. Evaluation of measured resting metabolic rate for dietary prescription in ageing adults with overweight and adiposity-based chronic disease. Nutrients. 2021;13(4):1229. DOI: 10.3390/nu13041229
  • Hall KD, Heymsfield SB, Kemnitz JW, Klein S, Schoeller DA, Speakman JR. Energy balance and its components: implications for body weight regulation. Am J Clin Nutr. 2012;95(4):989-994. DOI: 10.3945/ajcn.112.036350
  • Hill JO, Wyatt HR, Peters JC. The importance of energy balance. Eur Endocrinol. 2013;9(2):111-115. DOI: 10.17925/EE.2013.09.02.111
  • Hill JO, Wyatt HR, Peters JC. Energy balance and obesity. Circulation. 2012;126(1):126-132. DOI: https://doi.org/10.1161/CIRCULATIONAHA.111.087213
  • Pati S, Irfan W, Jameel A, Ahmed S, Shahid RK. Obesity and cancer: A current overview of epidemiology, pathogenesis, outcomes, and management. Cancers. 2023;15(2):485. DOI: https://doi.org/10.3390/cancers15020485
  • Powell-Wiley TM, Poirier P, Burke LE, Després J-P, Gordon-Larsen P, Lavie CJ, Lear SA, Ndumele CE, Neeland IJ, Sanders P, St-Onge M-P. Obesity and cardiovascular disease: A scientific statement from the American Heart Association. Circulation. 2021;143(21):e984-e1010. DOI: https://doi.org/10.1161/CIR.0000000000000973
  • Romieu I, Dossus L, Barquera S, Blottiére HM, Franks PW, Gunter M, Hwalla N, Hursting SD, Leitzmann M, Margetts B, Nishida C, Potischman N, Seidell J, Stepien M, Wang Y, Westerterp K, Winichagoon P, Wiseman M, Willett WC. Energy balance and obesity: what are the main drivers? Cancer Causes Control. 2017;28(3):247-258. DOI: 10.1007/s10552-017-0869-z
  • Rui L. Brain regulation of energy balance and body weights. Rev Endocr Metab Disord. 2013;14(4). DOI: 10.1007/s11154-013-9261-9
  • Slater GJ, Dieter BP, Marsh DJ, Helms ER, Shaw G, Iraki J. Is an energy surplus required to maximize skeletal muscle hypertrophy associated with resistance training? Front Nutr. 2019;6:131. DOI: 10.3389/fnut.2019.00131

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
SHOW MORE