Breath Analysis & Diabetes

Jesse Oswald • February 23, 2024

Key takeaways:

  • Diabetes begins with a condition called insulin resistance, which is caused by elevated free fatty acids and intramyocellular lipids.
  • The accumulation of free fatty acids and intramyocellular fat results from impaired fat-burn efficiency by our cells and/or weight gain.
  • Breath examination provides an excellent tool for tracking fat-burning efficiency and the likelihood of obesity. 


Unfortunately, diabetes is as common as it is misunderstood. Although pre-diabetes and diabetes are among the most common conditions, many of us, including doctors and health professionals, are unsure of their origin. As a result, we may claim that diabetes is a lifestyle disease, but we just cannot put our fingers on what exactly in our lifestyle causes it. This article explains the biological process of diabetes and how breath analysis provides an excellent tool for predicting its onset. 

What is diabetes?

Metabolism is the process by which our bodies transform the nutrients we eat into the energy we need to maintain essential functions (i.e., heartbeat, brain function, etc.), regulate temperature, and perform physical activities (e.g., move and exercise). Fat and carbohydrate are the two most commonly used nutrients in our metabolic process and thus supply more than 90% of our body's energy daily.

 

Although both macronutrients are used in significant amounts throughout the day, the process by which they are being treated varies vastly. This difference stems from the way they are stored. On the one hand, our body can store practically unlimited amounts of fat in adipose tissue (e.g., the fat accumulated around our abdomen, back, and other areas). Still, on the other hand, we can store only a minimal amount of carbohydrates. To put things into perspective, the average person may store up to 30,000 kcal worth of fat, which can increase tremendously by becoming overweight or obese, but can only store approximately 2,000 kcal of carbohydrates. The limited ability of our body to store carbohydrates ultimately means that whenever ingested, they need to be used immediately, stored in our small carbohydrate reserves (in case there is room), or converted into fat through a process called de-novo lipogenesis. Since the second pathway is unlikely and the third one energetically costly, our bodies will resort to the immediate burn of carbohydrates when ingesting them.

A diagram showing the process of ingestion of carbohydrates

Let’s now look into the process by which our body burns carbohydrates. Much like fats, carbohydrates must reach the inner part of our cells to be processed by the mitochondria, our body’s energy factory that converts fats or carbohydrates into the calories we use to survive and move. To achieve this, the following process takes place. Initially, carbohydrates need to be converted into glucose, which begins in our mouth but primarily in our small intestine. The intestine membranes absorb glucose, enter the bloodstream, and transfer it to the liver, where it is used, stored, or directed to other body parts. When it enters our muscle mass to be stored for future use, it is converted into glycogen.


As glucose levels rise in the blood, our body reacts through the secretion of insulin, a hormone required for managing glucose across our organs. Specifically, insulin is a substance that “latches” onto glucose molecules and enables them to enter cells, thus clearing them from the bloodstream. This is necessary because although glucose is a valuable nutrient that provides useful energy, it can be toxic for our organs if it remains in the bloodstream for too long. The toxic effects of lingering glucose in the blood slowly degrade all forms of tissue and can cause heart disease, neurodegenerative diseases such as Alzheimer's disease, and, in advanced cases, even require amputation of one’s leg. As a result, once glucose enters the bloodstream from the membranes of our small intestine, it needs to be stored in the liver or used by the working muscles immediately. Our body uses the hormone insulin, secreted from our pancreas, to enable glucose to enter our liver and muscle cells. This is where the route of diabetes lies. Specifically, diabetes occurs if our pancreas doesn’t produce enough insulin or our cells are not responsive enough to it, a condition also known as insulin resistance

A diagram of a cell with insulin glucose and pancreas function

What causes diabetes?

As described above, diabetes is a confluence of two conditions: cells becoming unresponsive to insulin and the pancreas not producing enough insulin. The combined effect of the two phenomena is that insulin production cannot clear glucose from the bloodstream. The lingering glucose thus causes widespread deterioration of all tissues across our body. Although both conditions need to coexist for diabetes to occur, their onset is not simultaneous but sequential.

 

The first of the two conditions is insulin resistance caused by excessive accumulation of intramyocellular lipids (IMCL) and plasma-freefatty acids (FFAs). Intramyocellular lipids are fat stores within muscles, whereas free fatty acids are fat molecules circulating in our bloodstream. The common denominator between the two is that they cause cells to become less responsive to insulin and thus cause insulin resistance. These two conditions occur when overall fat accumulation across the body increases, or in other words, when one starts to transition from average weight to an obese or overweight state.

 

To compensate for the fact that cells are now less responsive to insulin, the pancreas of an individual with early stages of insulin resistance starts to secret more insulin. This sets the person’s pancreas in a constant state of “overdrive,” meaning it constantly operates above its normal capacity. It is important to note, however, that this doesn’t always lead to pancreatic failure and insulin secretion shutdown. Nearly 80% of obese and overweight individuals live in a state where their pancreas is secreting excessive insulin to compensate for their varying degrees of insulin resistance. This state is also known as hyperinsulinemia.

 

However, in case hyperinsulinemia leads to partial or complete pancreatic failure. Insulin levels drop sharply, circulating blood glucose cannot penetrate cells, and ultimately, lingering blood glucose starts to cause its deleterious effects. This is when the onset of Type II Diabetes (T2D).

A diagram showing the causes of type 2 diabetes

Given the above mechanism, it is evident that fat accumulation is the underlying driver of T2D. This is corroborated by every piece of longitudinal data about the disease and its correlation with obesity levels. Specifically, T2D started to become a health concern and subsequently a dire epidemic at the same time that people began gaining weight. Given that obesity is founded on our unhealthy nutrition habits and lack of physical activity, it is an undeniable fact that T2D is largely a disease of our modern lifestyle.

A graph showing the number and percentage of u.s. population with diagnosed diabetes

The myth of carbs causing diabetes and fat treating it

The above mechanism elucidates the nature of T2D and how it is routed in weight gain and fat accumulation. However, it also sheds light on the fact that the macronutrient composition of one’s diet is irrelevant. In other words, following a low carb high, fat or low-fat high, carb diet can’t cause or cure diabetes. Besides, we describe in another one of our blogs, “Obesity Explained,” that through millennia, humans have followed all kinds of diets ranging from almost exclusively fat and animal protein-based to almost solely carb-based ones. Despite the wide range of diets followed by our ancestors, diabetes never became a health concern until obesity came along. As a result, weight loss and re-ignition of the cells’ insulin sensitivity through physical exercise to insulin are the only ways to mitigate the effects of T2D or, in some cases, even cure it.

How breath analysis provides an early warning for diabetes

Diabetes begins when insulin resistance occurs due to toxins secreted by free fatty acids (FFAs) and intramyocellular lipid (IMCL) accumulation. These toxins affect the cells’ ability to respond to insulin and thus prevent them from being able to absorb glucose that is circulating in the blood. In simple words, insulin becomes less effective when insulin resistance occurs as the “key” for glucose to enter cells. Therefore, we must first understand the root cause of fat accumulation to uncover the origins of insulin resistance. Specifically, the build-up of FFAs and IMCL can be traced back to two factors: 


  • Reduced ability to burn fat: Fat is a fuel source that requires oxygen and higher mitochondrial density compared to carbohydrates. Simply put, it requires “well-training” mitochondria as it’s a more complex fuel to process. Lack of exercise or constant consumption of high glycemic index carbs will gradually reduce mitochondrial density, making your cells less able to burn fat as a fuel source. Less fat oxidation means higher intramyocellular lipids and free fatty acids in the blood.
  • Obesity and visceral fat: Adipose tissue, in other words, accumulated body fat, impacts metabolism by releasing hormones and other substances, including leptin, cytokines, adiponectin, and proinflammatory substances. Another essential substance released in the process is FFAs. Individuals who are obese or overweight, therefore, have higher than average FFAs circulating in their blood. Out of the substances that adipose tissue releases that affect insulin sensitivity, the most are FFAs. The higher the level of circulating FFAs, the higher the insulin resistance and, thus, the likelihood of T2D.

 

Both phenomena can be traced or predicted through breath analysis. Specifically, the ability to utilize oxygen and burn fat at rest is assessed most accurately by analyzing the balance between oxygen and carbon dioxide in the breath, also known as the Respiratory Exchange Ratio. Studies have also proven this concept by showing that reduced fat oxidation at rest is a risk factor for diabetes even before the onset of elevated blood sugar levels during a fasted state (a condition also known as pre-diabetes). 

 

Moreover, the likelihood of obesity can be accurately assessed by determining the metabolic level of an individual, in other words, whether one’s metabolism is faster or slower than expected based on age, gender, and body size. The gold standard for analyzing a person’s metabolism is also breath analysis.

Conclusion

Diabetes is undeniably a lifestyle disease that stems from physical inactivity and poor nutrition habits. Combined, they lead to impaired cellular oxygen uptake ability and fat accumulation, leading to insulin resistance. As a result, addressing diabetes through nutrition and exercise should be a priority for everyone looking to avoid it or overcome it.

An Ounce of Prevention - Hyperion Health Blog

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