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Howevera€¦ many recent studies suggest that the true picture is more complicated than that. This article takes a detailed look at saturated fat and whether it is good or bad for your health. Each fat molecule is made of one glycerol molecule and three fatty acidsa€¦ which can be either saturated, monounsaturated or polyunsaturated. What this "saturation" stuff has to do with, is the number of double bonds in the molecule.
Saturated fatty acids have no double bonds, monounsaturated fatty acids have one double bond and polyunsaturated fatty acids have two or more double bonds. Foods that are high in saturated fat include fatty meats, lard, full-fat dairy products like butter and cream, coconuts, coconut oil, palm oil and dark chocolate. Even foods like beef also contain a significant amount of mono- and polyunsaturated fats (1). Fats that are mostly saturated (like butter) tend to be solid at room temperature, while fats that are mostly unsaturated (like olive oil) are liquid at room temperature.
Bottom Line: Saturated "fats" are fats that contain a high proportion of saturated fatty acids, which contain no double bonds. Back in the 20th century, there was a major epidemic of heart disease running rampant in America. It used to be a rare disease, but very quickly it skyrocketed and became the number one cause of deatha€¦ which it still is (2). Researchers learned that eating saturated fat seemed to increase levels of cholesterol in the bloodstream. This was an important finding at the time, because they also knew that having high cholesterol was linked to an increased risk of heart disease.
If saturated fat raises cholesterol (A causes B) and cholesterol causes heart disease (B causes C), then this must mean that saturated fat causes heart disease (A causes C). This hypothesis (called the "diet-heart hypothesis") was based on assumptions, observational data and animal studies (3). The diet-heart hypothesis then turned into public policy in 1977, before it was ever proven to be true (4).
Even though we now have plenty of experimental data in humans showing these initial assumptions to be wrong, people are still being told to avoid saturated fat in order to reduce heart disease risk. Bottom Line: Saturated fats have been assumed to cause heart disease by raising cholesterol in the blood.
HDL and LDL, the "good" and "bad" cholesterols, aren't actually cholesterola€¦ they are proteins that carry cholesterol around, known as lipoproteins. At first, scientists only measured "Total" cholesterol, which includes cholesterol within both LDL and HDL.
Because saturated fat raised LDL levels, it seemed logical to assume that this would increase the risk of heart disease.
Small, dense LDL: These are small lipoproteins that can penetrate the arterial wall easily, which drives heart disease. Large LDL: These lipoproteins are large and fluffy and don't easily penetrate the arteries.
The small, dense particles are also much more susceptible to becoming oxidized, which is a crucial step in the heart disease process (17, 18, 19). People with mostly small LDL particles have three times greater risk of heart disease, compared to those with mostly large LDL particles (20). Soa€¦ if we want to reduce our risk of heart disease, we want to have mostly large LDL particles and as little of the small ones as possible. Here's an interesting bit of information that is often ignored by "mainstream" nutritionistsa€¦ eating saturated fat changes the LDL particles from small, dense to Large (21, 22, 23). What this implies is that even though saturated fat can mildly raise LDL, they are changing the LDL to a benign subtype that is associated with a reduced risk of heart disease. Now scientists have realized that it's not just about the LDL concentration or the size of the particles, but the number of LDL particles (called LDL-p) floating in their bloodstreams. Low-carb diets, which tend to be high in saturated fat, can lower LDL-p, while low-fat diets can have an adverse effect and raise LDL-p (28, 29, 30, 31).
Bottom Line: Saturated fats raise HDL (the "good") cholesterol and change LDL from small, dense (bad) to Large LDL, which is mostly benign. The supposedly harmful effects of saturated fat are the cornerstone of modern dietary guidelines.
Howevera€¦ despite decades of research and billions of dollars spent, scientists still haven't been able to demonstrate a clear link. Several recent review studies that combined data from multiple other studies, found that there really is no link between saturated fat consumption and heart disease.
This includes a review of 21 studies with a total of 347,747 participants, published in 2010. Another review published in 2014 looked at data from 76 studies (both observational studies and controlled trials) with a total of 643,226 participants.
We also have a systematic review from the Cochrane collaboration, which combines data from numerous randomized controlled trials.
According to their review, published in 2011, reducing saturated fat has no effect on death or death from heart disease (34). However, they found that replacing saturated fats with unsaturated fats reduced the risk of cardiac events (but not death) by 14%.
This does not imply that saturated fats are "bad," just that certain types of unsaturated fats (mostly Omega-3s) are protective, while saturated fats are neutral.
Soa€¦ the biggest and best studies on saturated fat and heart disease show that there is no direct link. Unfortunately, the governments and "mainstream" health organizations seem reluctant to change their minds and continue to promote the old low-fat dogma.
Bottom Line: The link between saturated fat and heart disease has been studied intensely for decades, but the biggest and best studies show that there is no statistically significant association. This is the diet recommended by the USDA and mainstream health organizations all over the world.
This diet also recommends increased consumption of fruits, vegetables and whole grainsa€¦ along with reduced consumption of sugar. Other massive studies have confirmed thisa€¦ the low-fat diet provides no benefit for heart disease or the risk of death (39, 40).
Several studies that replaced saturated fat with polyunsaturated vegetable oils showed that more people in the vegetable oil groups ended up dying (41, 42). Of course, this graph alone doesn't prove anything (correlation does not equal causation), but it does make sense that replacing traditional foods like butter and meat with processed low-fat foods high in sugar had something to do with it.
It's also interesting when looking at the literature, that in almost every single study comparing the "expert approved" low-fat diet to other diets (including paleo, vegan, low-carb and Mediterranean), it loses (44, 45, 46, 47). Bottom Line: Studies on the low-fat diet do not show a reduced risk of heart disease or death and some studies show that replacing saturated fat with vegetable oils increases the risk. The studies clearly show that, on average, saturated fat does not raise the risk of heart disease.
Perhaps most individuals see no effecta€¦ while others experience decreased risk and yet others experience an increased risk. That being said, there are definitely some people who may want to minimize saturated fat in the diet. This includes individuals with a genetic disorder called Familial Hypercholesterolemia, as well as people who have a gene variant called ApoE4 (48).
With time, the science of genetics will most surely discover more ways in which diet affects our individual risk for disease. Bottom Line: Some people may want to minimize saturated fat intake, including people with Familial Hypercholesterolemia or a gene called ApoE4.
For this reason, coconut oil, lard and butter are all excellent choices for cooking, especially for high-heat cooking methods like frying. Foods that are naturally high in saturated fat also tend to be healthy and nutritious, as long as you're eating quality unprocessed foods.
Bottom Line: Saturated fats are excellent cooking fats and foods that are high in saturated fat tend to be both healthy and nutritious. The evidence points to saturated and monounsaturated fats being perfectly safe and maybe even downright healthy. We need to get these two types of fatty acids in a certain balance, but most people are eating way too many Omega-6 fatty acids these days (51). It is a good idea to eat plenty of Omega-3s (such as from fatty fish), but most people would do best by reducing their Omega-6 consumption (52). The best way to do that is to avoid seed- and vegetable oils like soybean and corn oils, as well as the processed foods that contain them. Trans fats are made by exposing polyunsaturated vegetable oils to a chemical process that involves high heat, hydrogen gas and a metal catalyst.
Studies show that trans fats lead to insulin resistance, inflammation, belly fat accumulation and drastically raise the risk of heart disease (53, 54, 55, 56).
So eat your saturated fats, monounsaturated fats and Omega-3sa€¦ but avoid trans fats and processed vegetable oils like the plague. Bottom Line: The truly harmful fats are artificial trans fats and processed vegetable oils high in Omega-6 fatty acids. The health authorities have spent an immense amount of resources studying the link between saturated fat and heart disease. Despite thousands of scientists, decades of work and billions of dollars spent, this hypothesis still hasn't been supported by any good evidence. The saturated fat myth wasn't proven in the past, isn't proven today and never will be provena€¦ because it's just flat out wrong. Humans and pre-humans have been eating saturated fat for hundreds of thousands (if not millions) of years, but the heart disease epidemic started a hundred years ago.
Governments here and abroad have been cautioning the public for decades on the dangers of high fat diets. One of the problems is that there is consistent inverse association in the percentage of energy coming from fats and sugars. That's no surprise as previous studies such as a two-year dietary study published in the journal Diabetologia showed that food with a lot of fat and few carbohydrates has a better effect on blood sugar levels and blood lipids. Research from the Hebrew University of Jerusalem shows that a carefully scheduled high-fat diet can lead to a reduction in body weight and a unique metabolism in which ingested fats are not stored, but rather used for energy at times when no food is available. Professor David Lawrence, an expert in nutrition and obesity data analysis, said recently in the journal BMC Medicine that the idea the idea of all calories being equal is flawed and based 'on an outdated understanding of the science'. Calories from different sources have different effects on the body, with calories from carbohydrates more likely to encourage weight gain. Calories from different sources have different effects on the body, with calories from carbohydrates more likely to encourage weight gain. Not only is the calorie theory under attack, but evidence is also emerging to show that lowering fat might not cut heart-disease risk after all.
A major study published in the authoritative New England Journal of Medicine compared the clinical benefits of a conventional low-fat diet with two types of Mediterranean diet, which are naturally considerably higher in fat.
The study had to be stopped early because the heart attack and stroke rate in the Mediterranean options was so much lower it was deemed irresponsible to keep patients on the conventional diet. A study led by Cara Ebbeling, PhD, associate director and David Ludwig, MD, director of the New Balance Foundation Obesity Prevention Center Boston Children's Hospital, found diets that reduce the surge in blood sugar after a meal--either low-glycemic index or very-low carbohydrate-may be preferable to a low-fat diet for those trying to achieve lasting weight loss.
Weight re-gain is often attributed to a decline in motivation or adherence to diet and exercise, but biology also plays an important role.
The study suggests that a low-glycemic load diet is more effective than conventional approaches at burning calories (and keeping energy expenditure) at a higher rate after weight loss. Faced with mounting evidence, Swedish dietary experts recently made a dramatic U-turn, recommending a low-carb, rather than low-fat, diet for weight loss.
The bombshell came from the Council on Health Technology Assessment, which advises the Swedish government. The most important of these hormones, and the one that's crucial for weight loss, is insulin. A low-carb and high-fat diet means less insulin, making it easier to lose weight because less fat is then stored.
Dramatic new evidence for this has come from a unique experiment conducted by a personal trainer. Now, according to the conventional wisdom, the weight gain would be the same on both regimens. Sam, who survived childhood cancer (Hodgkin's lymphoma), wondered if his usual low-carb diet was the key, and set about his experiment to find out. For the low-carb, high-fat part of the experiment, Sam got his 5,000 calories from foods such as eggs, mackerel (which is very fatty), steak, green veg and coconut oil, interspersed with three snacks of nuts - walnuts, pecans or almonds (which are naturally high in fat). While 72 percent of his total calorie intake came from fats, 22 percent came from protein and just 5.9 percent from carbs. With the high-carb diet, most of his calories (63 percent) came from carbohydrates, 13 percent from protein, and 22 percent from fat. He ate garlic bread, low-fat lasagna, crumpets, low-fat yogurts and rice pudding, chocolate muffins and wholewheat bread.
Admittedly the types of fat on his high-fat diet weren't your usual fatty foods, such as cream and butter. While Sam's experiment was by no means a scientific one, as well as the weight gain, what was even more striking was what an unhealthy effect the high carbohydrate regimen had on standard markers for heart health. For when Sam had his blood tested after his three weeks on high carbs, 'the diet effectively gave him metabolic syndrome which is a precursor to heart disease and diabetes. Particularly worrying was that his triglycerides (fats in his blood) had gone up four times, while his so-called 'good' (HDL) cholesterol had dropped. What's more, a level of inflammation in his liver had doubled, which is also linked with diabetes and heart disease. Did the fact that, as a personal trainer, Sam was obviously very fit at the start of his trial make a difference? Research has already shown that if you are eating a high-carb diet, and so have high levels of insulin, you are likely to have more fat in your blood than someone on a high-fat diet.
He argues that - as seen with Sam - a high-carb diet tends to lower the good HDL cholesterol that helps keep arteries clear. At the same time, as glucose from carbs is turned into fat for storage in the body, fatty acids are also produced. Recent research supports the idea that warning about saturated fat in the diet has probably been a mistake.
Demonizing fat and encouraging people to eat more carbs can be harmful to people with heart disease, says Dr Malhotra. Those eating low-carb these days are much more flexible about the amount of fat they get. Western governments have yet to acknowledge the Swedish style U-turn in healthy eating advice. We are spending billions trying to cope with metabolic diseases such as diabetes, cancer and obesity and the emphasis on low-fat diets is only promoting the metabolic pathways which encourage these diseases. The bottom line is to commit to educating yourself on the healthiest nutritional strategies for your health and not follow any recommendations by government, unless perhaps if you live in Sweden.
Natasha Longo has a master's degree in nutrition and is a certified fitness and nutritional counselor.
The information presented on this website is not intended as specific medical advice and is not a substitute for professional medical treatment or diagnosis. The morning I decide my family will finally start the low-sugar regimen I've been threatening them with, things are, to say the least, rocky. By clicking "Sign in", you confirm that you accept our terms of service and have read and understand privacy policy. By clicking "Create Account", you confirm that you accept our terms of service and have read and understand privacy policy. Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease.
Search the NHLBI, use the drop down list to select: the entire site, the Health Topics section only, or the News and Resources section. Atherosclerosis can lead to serious problems, including heart attack, stroke, or even death. Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms, legs, pelvis, and kidneys.


Coronary heart disease (CHD), also called coronary artery disease, occurs when plaque builds up in the coronary arteries. If blood flow to your heart muscle is reduced or blocked, you may have angina (chest pain or discomfort) or a heart attack. Carotid (ka-ROT-id) artery disease occurs if plaque builds up in the arteries on each side of your neck (the carotid arteries). If blood flow to these parts of your body is reduced or blocked, you may have numbness, pain, and, sometimes, dangerous infections.
You can control some risk factors, such as lack of physical activity, smoking, and an unhealthy diet. Improved treatments have reduced the number of deaths from atherosclerosis-related diseases. Describes how the build-up of plaque over time causes atherosclerosis which can lead to serious problems, including heart attack, stroke, or even death.
Scientists now report a new way to assess cholesterol that shows promise for evaluating the increased heart attack risk observed in patients with psoriasis, a common inflammatory skin disease.
Through the Healthy, Hunger-Free Kids Act championed by the First Lady and signed by President Obama, USDA made the first major changes in school meals in 15 years, which will help us raise a healthier generation of children.
The new standards align school meals with the latest nutrition science and the real world circumstances of America’s schools. Later they learned that while LDL was linked to increased risk, HDL was linked to reduced risk (5, 6, 7, 8, 9, 10). Although they increase LDL in the short-term, plenty of long-term observational studies find no link between saturated fat consumption and LDL levels (24, 25, 26).
For example, palmitic acid (16 carbons) may raise LDL, while stearic acid (18 carbons) does not (27). Their conclusion: there is absolutely no association between saturated fat and heart disease (32). It was a randomized controlled trial with 46,835 women, who were instructed to eat a low-fat diet.
Research published in the journal Critical Reviews in Food Science and Nutrition shows why people find it hard to follow government guidelines to cut their fat and sugar intake at the same time -- a phenomenon known as the sugar-fat seesaw. Despite the increased fat intake with a larger portion of saturated fatty acids, their lipoproteins did not get worse. Furthermore, the study found that the low-glycemic index diet had similar metabolic benefits to the very low-carb diet without negative effects of stress and inflammation as seen by participants consuming the very low-carb diet.
After weight loss, the rate at which people burn calories (known as energy expenditure) decreases, reflecting slower metabolism. Based on a review of 16,000 studies, it said the best sorts of food for losing weight were high fat foods which could include anything oils like olive and coconut. A high-carb diet increases the amount of glucose in the bloodstream, which in turn means you produce more insulin.
For three weeks he got these calories from a low-fat, high-carb diet; for another three, he ate more fat and cut right back on carbs.
I've personally been on many of these public policy and procurement programs investing hundreds of hours of my time trying to convince officials that food pyramids have to be thrown out the window along with many recommended foods they hold praise to. She has consulted on public health policy and procurement in Canada, Australia, Spain, Ireland, England and Germany. When I remind my husband, Pete, that for the next 2 weeks, he's off his usual breakfast of sugary cereal, he looks at me as if I've punched him in the gut.
It's not just the calories in the sugar that are making us fat; it's the fact that consuming megadoses of fructose interferes with our hormones, our digestive systems, our brains, and our bodies' natural ability to regulate appetite—so we just keep eating. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. IntroductionThe worldwide prevalence of obesity and its metabolic complications have increased substantially in recent decades. Arteries are blood vessels that carry oxygen-rich blood to your heart and other parts of your body. These treatments also have improved the quality of life for people who have these diseases. Making lifestyle changes and getting ongoing care can help you avoid the problems of atherosclerosis and live a long, healthy life. Shows how in atherosclerosis, plaque builds up inside the arteries which can cause a heart attack. These responsible reforms do what’s right for children’s health in a way that’s achievable in schools across the Nation. You'll still see this on most food pyramids regulated by government policy on diet and nutrition.
Lower energy expenditure adds to the difficulty of weight maintenance and helps explain why people tend to re-gain lost weight. I was really surprised that the damaging changes had happened so quickly," stated Dr. All content on this site may be copied, without permission, whether reproduced digitally or in print, provided copyright, reference and source information are intact and use is strictly for not-for-profit purposes.
I point out that it's not just the cereal itself—Rice Chex on a good day, but often, Frosted Flakes—but the fact that he adds 2 tablespoons of sugar on top, plus 3 more in his coffee. While glucose, a simple form of sugar found in plants, is a fuel source that almost every cell in our body needs, fructose is found naturally only in small quantities and usually in fruit that contains fiber, which helps limit how much fructose the body absorbs and how quickly. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. According to the World Health Organization, the global prevalence of obesity has nearly doubled between 1980 and 2008, and more than 10% of the adults aged 20 and over is obese in 2008 [1]. When the body is exposed to a high-carb low-fat meal, the pancreas works hard at overshooting the secretion of insulin which then causes the excess to be stored as fat.
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The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. The increased prevalence in obesity is also associated with increasing prevalence of nonalcoholic fatty liver disease (NAFLD).
In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Among the Americas, the prevalence of NAFLD is highest in the USA, Belize and Barbados and Mexico, which have a high prevalence of obesity [3]. The fact is, contrary to official advice by our diet dictocrats, high-fat diets lower blood sugar, improve blood lipids, and reduce obesity. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Obesity, especially abdominal obesity, is one of the predominant underlying risk factors for metabolic syndrome [4]. She starts to cry, then throws a pillow at me.I go to the kitchen and cut up some strawberries and bananas.
Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.
Obesity increases the risk of developing a variety of pathological conditions, including insulin resistance, type 2 diabetes, dyslipidemia, hypertension and NAFLD (Figure 1). I toast a piece of whole wheat bread, spread it with no-sugar peanut butter, and top it with more sliced strawberries.
Accumulating evidence suggests that chronic inflammation in adipose tissue may play a critical role in the development of obesity-related metabolic dysfunction [5–7].Adipose tissue has been recognized as an active endocrine organ and a main energy store of the body [8]. But I've never encountered a baguette, roll, plate of pasta, or glass of wine that didn't sing a siren song to me. Excess adiposity and adipocyte dysfunction result in dysregulation of a wide range of adipose tissue-derived secretory factors, referred to as adipokines, which may contribute to the development of various metabolic diseases via altered glucose and lipid homeostasis as well as inflammatory responses [9,10]. She looks at me as if I'd just killed a litter of kittens."These are all things you like," I say. As for my husband, when I was pregnant, Pete swore that he'd give up Coke, Oreos, and Frosted Flakes so our daughter wouldn't start out with a less-than-perfect dietary role model. In addition, excess fat accumulation promotes the release of free fatty acids into the circulation from adipocytes, which may be a critical factor in modulating insulin sensitivity [11,12].
However, plasma free fatty acid levels do not increase in proportion to the amount of body fat, since their basal adipose tissue lipolysis per kilogram of fat is lower in obese subjects than in lean subjects [13].
Erin, now 12, eats a reasonably balanced diet but, since she first trick-or-treated at 18 months, has devoted her life to the pursuit of sugar.
This finding has been supported by other studies of adipocytes from obese subjects [14,15] and it was associated with down-regulation of hormone sensitive lipase and adipose triglyceride lipase, key enzymes involved in intracellular degradation of triglycerides [14,16–18]. But this is what's for breakfast." I can feel the waves of hostility following me as I walk out of the room.So why have I decided to put my family through this torture? Lustig says are just as bad for you, since they contain so much concentrated fructose—and none of the fiber that can help counteract it.So I know we're not perfect. We will also review how the dysregulation of free fatty acids and inflammatory factors released by enlarged adipose tissue is associated with the pathogenesis of metabolic syndrome (insulin resistance, dyslipidemia and NAFLD).
In 1986, the last year the FDA formally studied the impact of "added" sugar (that's what manufacturers put in food, not what's naturally in, say, apples or carrots), Americans were eating 150 to 200 calories of added sugar a day. In particular, we will focus on the imbalance of pro-inflammatory and anti-inflammatory molecules secreted by adipose tissue which contribute to metabolic dysfunction.
That's 50 g, or a little more than what's in one can of Coke—and far less than what Pete's standard breakfast contains. Lustig tells me that the vicious hormonal cycles caused by excessive sugar consumption affect more than half of the US population—those who are obese, but also many who are normal weight.
Today Americans consume an average of 450 calories a day as added sugar, approximately one-fourth of a 2,000-calorie diet.The increase is partly because we're eating more plain old sugar (or sucrose, which is made up of half fructose, half glucose). And the more I think about how impossible it seems to reduce my family's sugar intake, the more important it seems to make it work. Function of Adipose TissueAdipose tissue is the major site for storage of excess energy in the form of triglycerides, and it contains multiple cell types, including mostly adipocytes, preadipocytes, endothelial cells and immune cells. But it's also due in large part to the invention of high fructose corn syrup, a form of grain-derived syrup that's been chemically manipulated to change some of its glucose molecules into sweeter-tasting fructose molecules, until the final product is about 55% fructose. During positive energy balance, adipose tissue stores excess energy as triglycerides in the lipid droplets of adipocytes through an increase in the number of adipocyte (hyperplasia) or an enlargement in the size of adipocytes (hypertrophy) [20]. HFCS really took off in the late 1970s, and it was added to all kinds of foods because it increases shelf life, makes low-fat processed foods and baked goods taste better, and is cheaper than regular sugar. The number of adipocytes is mainly determined in childhood and adolescence and remains constant during adulthood in both lean and obese subjects, even after marked weight loss [21]. It's become a staple of most of our oversweetened diets.But while our sugar consumption has been skyrocketing, so have rates of obesity, diabetes, lipid problems, high blood pressure, and heart disease, collectively termed metabolic syndrome, and research is starting to show that that's not a coincidence. Robert Lustig, MD, a pediatric endocrinologist and researcher at the University of California, San Francisco—and one of my neighbors—has been studying the biochemical effects of sugar on our bodies for more than 16 years. However, recent study has reported that normal-weight adults can expand lower-body subcutaneous fat, but not upper-body subcutaneous fat, via hyperplasia in response to overfeeding [22], suggesting hyperplasia of adipocytes can also occur in adulthood. His conclusion: Sugar is a toxin that's fueling a global obesity pandemic, and it's why we all, on average, weigh 25 pounds more today than people did 25 years ago.
These options won't hold my family for long, so I put a shout-out on Facebook, begging for low-sugar, low-refined-carb breakfast alternatives. Although overall obesity is associated with metabolic diseases, adipose tissue dysfunction caused by hypertrophy has been suggested to play an important role in the development of metabolic diseases such as insulin resistance [23–25]. In contrast to positive energy balance states, when energy is needed between meals or during physical exercise, triglycerides stored in adipocytes can be mobilized through lipolysis to release free fatty acids into circulation and the resulting free fatty acids are transported to other tissues to be used as an energy source. A high school pal suggests squash hash browns, noting that salty-crunchy things can help with sugar withdrawal, which, Dr. It is generally accepted that free fatty acids, a product of lipolysis, play a critical role in the development of obesity-related metabolic disturbances, especially insulin resistance. Lustig tells me, is a real thing, because fructose has an addictive effect on the body.Some are good ideas, and most of them work out well, but there's no way I'm going to get my peeps to eat squash hash browns. In obesity, free fatty acids can directly enter the liver via the portal circulation, and increased levels of hepatic free fatty acids induce increased lipid synthesis and gluconeogenesis as well as insulin resistance in the liver [26]. High levels of circulating free fatty acids can also cause peripheral insulin resistance in both animals and humans [26,27]. Moreover, free fatty acids serve as ligands for the toll-like receptor 4 (TLR4) complex [28] and stimulate cytokine production of macrophages [29], thereby modulating inflammation of adipose tissue which contributes to obesity-associated metabolic complications. However, circulating free fatty acid concentrations do not increase in proportion to fat mass and do not predict the development of metabolic syndrome [30–33], although many studies suggest a relationship between the release of free fatty acids from adipose tissue and obesity-related metabolic disorders.Adipose tissue also has a major endocrine function secreting multiple adipokines (including chemokines, cytokines and hormones) (Figure 2).
Many of the adipokines are involved in energy homeostasis and inflammation, including chemokines and cytokines. In the obese state, the adipocyte is integral to the development of obesity-induced inflammation by increasing secretion of various pro-inflammatory chemokines and cytokines [34,35]. No one even notices.The downside to eating less sugar is that it takes more time than most of us spend now getting a meal together. Many of them, including monocyte chemotactic protein (MCP)-1, tumor necrosis factor (TNF)-?, interlukin (IL)-1, IL-6 and IL-8, have been reported to promote insulin resistance [36–39].
One recent study found that 80% of the 600,000 food items sold in American supermarkets have added sugar, most of them convenience foods.
Moreover, the macrophage content of adipose tissue is positively correlated with both adipocyte size and body mass, and expression of pro-inflammatory cytokines, such as TNF-?, is mostly derived from macrophages rather than adipocytes [40].
Along with the increased number of macrophages in adipose tissue, obesity induces a phenotypic switch in these cells from an anti-inflammatory M2 polarization state to a pro-inflammatory M1 polarization state [41]. The accumulation of M1 macrophages in adipose tissue has been shown to result in secretion of a variety of pro-inflammatory cytokines and chemokines that potentially contribute to obesity-related insulin resistance [5,42].
In contrast, M2-polarized macrophages participate in remodeling of adipose tissue, including clearance of dead or dying adipocytes and recruitment and differentiation of adipocyte progenitors [43]. Decreased adipose macrophage infiltration or macrophage ablation reduces expression of inflammatory cytokines in adipose tissue and improves insulin sensitivity in diet-induced obese mice [44–47]. Furthermore, weight loss decreases macrophage infiltration and pro-inflammatory gene expression in adipose tissue in obese subjects [48,49].
In addition to M1 macrophages, levels of multiple pro-inflammatory immune cells, such as interferon (IFN)-?+ T helper type 1 cells and CD8+ T cells, are increased in adipose tissue in obesity [50]. I made a big batch of whole grain bran muffins, and he says they're a pretty good alternative to his usual sugary cereal.
In contrast, secretion of insulin-sensitizing adiponectin is reduced in obese subjects [51].
I've been pouring water or milk for my daughter to drink at meals, and she doesn't complain.[pagebreak]DAY 9I'm beginning to notice that I have more energy. Obesity and Insulin ResistanceInsulin resistance is an integral feature of metabolic syndrome and is a major predictor of the development of type 2 diabetes [52]. It has long been recognized that obesity is associated with type 2 diabetes, and the major basis for this link is the ability of obesity to induce insulin resistance.
Insulin resistance is defined as the decreased ability of tissues to respond to insulin action. Adipose tissue is one of the insulin-responsive tissues, and insulin stimulates storage of triglycerides in adipose tissue by multiple mechanisms, including promoting the differentiation of preadipocytes to adipocytes, increasing the uptake of glucose and fatty acids derived from circulating lipoproteins and lipogenesis in mature adipocytes, and inhibiting lipolysis [53]. I still like all those things, but it's not killing me to eat them less.DAY 10I desperately need to go grocery shopping but don't have time.
The metabolic effects of insulin are mediated by a complex insulin-signaling network (Figure 3). IRS-1, which is phosphorylated by the insulin receptor, activates PI3K by binding to its SH2 domain.
Ultimately, these signalling events result in the translocation of glucose transporter 4 to the plasma membrane, leading to an increase in adipocyte glucose uptake. The MAPK pathways are not implicated in mediating metabolic actions of insulin but rather in stimulating mitogenic and growth effects of insulin. She says it doesn't have much added sugar, and when I look up the recipe in The Cake Bible, I realize she's right: It's just chocolate, eggs, and butter.
In the adipose tissue, insulin also has an anti-lipolytic effect, whereby the activation of PI3K stimulates phosphodiesterase-3 so that more adenosine 3?,5?-cyclic monophosphate is hydrolyzed in adipocytes, which in turn limits the release of fatty acids from adipocytes. As discussed in the preceding text, free fatty acids and various adipokines released from adipose tissue have been involved in abnormal insulin signaling.


Lustig recommends indulging in this sort of thing once a week at most, and, I have to admit, it feels like such a treat.
It has been suggested that fatty acids and their metabolites, such as acyl-coenzyme A, ceramides and diacyglycerol, can impair insulin signaling by promoting protein kinases such as protein kinase C, MAPK, c-Jun N-terminal kinase (JNK), and the inhibitor of nuclear factor ?B kinase ? [54]. Saturated fatty acids, but not unsaturated fatty acids, induce the synthesis of ceramide, and inhibition of ceramide synthesis ameliorates saturated fatty acids-induced insulin resistance [55].
TNF-? also promotes ceramide accrual by activating sphingomyelinase, an enzyme that catalyzes the hydrolysis of sphingomyelin to ceramide [56], and ceramide mediates TNF-?-induced insulin resistance in adipocytes [57]. I get a press release from the American Heart Association about heart-healthy, low-sugar dishes, and I try to make the Greek salad recipe that calls for grated raw zucchini.
Obese subjects had greater whole body free fatty acids rates of appearance in plasma compared with lean subjects [60], and a sustained reduction in plasma free fatty acids levels after treatment of lipolysis inhibitor was associated with an improvement of insulin sensitivity in diabetic obese subjects [61]. The anti-lipolysis drug also decreased fasting plasma free fatty acids levels in lean control, obese nondiabetic, obese subjects with impaired glucose tolerance, and the lowering of plasma free fatty acids levels improved insulin resistance and glucose tolerance in obese subjects, regardless of the degree of their preexisting insulin resistance [62]. The real food—fruits, veggies, meat, milk, eggs, whole grains—exists on the fringes of the average supermarket.
Erin is perfectly happy with the whole wheat peanut butter toast and strawberries that begat a tantrum at the beginning.
Obesity-induced increases in lipolysis not only increases local extracellular lipid concentrations but also derives accumulation of macrophages in adipose tissue [64], which is associated with systemic hyperinsulinemia and insulin resistance in obese subjects [65]. I feel like we've done a real diet reset: Our table will feature more grains and proteins and fewer cookies, crackers, and cakes than before.So did we stick to our 200 calories a day? In fact, macrophage recruitment was increased with fat mass [54], and the phenotype of adipose macrophages and recruitment of macrophages and other immune cells to the adipose tissue play important roles in the development of obesity-related insulin resistance [66].Obesity-induced insulin resistance is also associated with increased secretion of cytokines and other bioactive substances from adipose tissue as well as the number of adipose macrophages. In the adipose tissue of obese humans and animals, there are a large number of macrophages infiltrations, and this recruitment is linked to the pathogenesis of obesity-induced inflammation and insulin resistance [5,40]. The production of most inflammatory factors by adipose tissue is also increased in the obese state and promotes obesity-linked metabolic diseases [67,68]. Adipocytes and immune cells (primarily macrophages) in the adipose tissue are the primary sources of many inflammatory proteins [67,68].
A number of pro-inflammatory proteins, including MCP-1, TNF-?, IL-6, IL-18, leptin, resistin, plasminogen activator inhibitor (PAI)-1, visfatin, retinol binding protein 4 (RBP4) and angiopoietin-like protein 2 (ANGPTL2), are described in more detail in the following text. It took a little more time, and the fresh fruit cost a little bit more than cookies, but we felt good. Additionally, we briefly discuss the metabolic properties of two anti-inflammatory adipokines, adiponectin and secreted frizzled-related protein 5 (SFRP5).
After about 10 days, we stopped thinking about sugar, and Pete even stopped making sugar jokes.
There are discrepancies between preclinical studies and clinical trials regarding some adipokines, including TNF-?, resistin and SFRP5.
Erin seemed calmer, less hyper.On day 15, I buy Pete a small box of Frosted Flakes as a thank-you. In addition, considering the wide spectrum of pro- and anti-inflammatory adipokines, which are altered in obesity, it is likely that crosstalk of many adipokines rather than a single adipokine in adipose tissue and other tissues may be involved in the metabolic dysregulation.
It initiates adipose inflammation by attracting inflammatory cells from the blood stream into adipose tissue [66,70]. Similarly, MCP-1 G-2518 gene variant was decreased the risk of type 2 diabetes in a Chinese and Turkey populations [76,77]. High levels of multiple chemokine ligands (CCL2, CCL3, CCL5, CCL7, CCL8, CCL11) and receptors (CCR1, CCR2, CCR3, CCR5) have been observed in adipose tissue of obese subjects and are associated with increased inflammation [69]. Thus, these studies suggest possibility that loss of one chemokine may be compensated by other chemokines. TNF-?TNF-? is a pro-inflammatory cytokine that may contribute to the pathogenesis of obesity and insulin resistance [36]. Expression of TNF-? is increased in obesity and insulin resistance in humans and is positively correlated with insulin resistance [36].
Treatment with TNF-? induces insulin resistance in adipose tissue [83], whereas deletion of TNF-? or its receptors improves insulin sensitivity in obese animals [84]. However, the correlation between plasma TNF-? levels and insulin resistance is relatively weak [36,85], and chronic neutralization of TNF-? does not improve insulin resistance in healthy overweight subjects with metabolic syndrome and insulin resistance, despite improvements in inflammatory status [86]. The absence of an effect on insulin sensitivity may be due to a compensatory role of other cytokines in the absence of TNF-?, since metabolic dysregulation has been attributed to numerous pro-inflammatory cytokines secreted by adipose tissue, including TNF-?, IL-1, and IL-6, all of which have been involved in disrupting insulin signaling [88]. TNF-? is a part of complex inflammation network and is capable of initiating cytokine cascades involving both synergistic and inhibitory reactions, which control the synthesis and expression of other cytokines, hormones, and their receptors [89]. Because IL-12 and TNF-? are co-stimulators for IFN-?, one of the essential cytokines for regulation of the inflammation and insulin resistance in obesity [91], the up-regulation of IL-12 in the absence of TNF-? could act in a compensatory manner to induce and maintain appropriate IFN-? levels.
In addition, TNF-? does not induce insulin resistance when IL-6 is down-regulated in adipose tissue [92]. IL-6 and IL-18IL-6 is another cytokine that plays an important role in the development of insulin resistance in obesity [93]. Adipose tissue contributes to 10%–35% of circulating IL-6 levels in humans [94], and hypertrophic enlargement of adipocytes is accompanied by increased production of IL-6 by adipose tissue [95]. Expression of adipose IL-6 positively correlates with insulin resistance both in vivo and in vitro [96]. Hyperglycemia results in increased IL-6 levels [97], and treatment with IL-6 induces hyperglycemia and insulin resistance in humans [98]. A lack of IL-6 has been shown to cause obesity and insulin resistance in mice [99], but Di Gregorio et al.
Treatment of IL-6 enhances insulin-stimulated glucose disposal in humans in vivo, and it increases glucose uptake and fatty acid oxidation in cultured L6 myotubes via activation of adenosine monophosphate-activated protein kinase (AMPK), as well as having an anti-inflammatory effect [101,102], whereas IL-6 induces insulin resistance in adipocytes [39]. Thus, the different tissue-specific functions of IL-6 may account for the controversial findings regarding the correlation between IL-6 and insulin resistance.IL-18 is also a pro-inflammatory cytokine and has been suggested to be produced by adipose tissue [103]. Circulating IL-18 levels have been shown to be increased in obese subjects and reduced with weight loss [104]. Moreover, overexpression of IL-18 aggravated insulin resistance in a rat model of metabolic syndrome [105]. However, a lack of IL-18 or its receptor in mice induces hyperphagia, obesity and insulin resistance [106]. Thus, further studies are needed to evaluate the role of IL-6 and IL-18 in the pathogenesis of obesity and insulin resistance.
LeptinLeptin is abundantly expressed in adipose tissue, specifically adipocytes and is involved in the regulation of energy homeostasis [107].
However, circulating leptin levels [108] and its mRNA expression in adipose tissue [109] are increased in obese subjects, probably due to the existence of leptin resistance [107]. Leptin also plays an important role in the regulation of glucose homeostasis, independent of actions on food intake, energy expenditure or body weight.
Leptin improves insulin sensitivity in the liver and skeletal muscle and regulates pancreatic ?-cell function [110], whereas it impairs insulin signaling in murine adipocytes [111,112].
In addition, leptin is suggested to have pro-inflammatory effects; Leptin has a cytokine-like structure, and its receptor is member of the class I cytokine receptor (gp130) superfamily [113].
It not only promotes the production of the pro-inflammatory cytokines, IL-2 and IFN-?, but also inhibits the production of the anti-inflammatory cytokine IL-4 by T cells or mononuclear cells [114].
Concomitantly, circulating leptin levels and its expression in adipose tissues are increased in response to pro-inflammatory cytokines (TNF, IL-1) and endotoxin (lipopolysaccharide, LPS) [115]. Accordingly, the interactions between leptin and inflammation are bidirectional: Pro-inflammatory cytokines increase the synthesis and release of leptin, which in turn contribute to maintain a chronic inflammatory state in obesity [113]. ResistinResistin is also an adipocyte-specific secreted adipokine, and it promotes both inflammation and insulin resistance in murine models.
Levels of circulating resistin are increased in obese mice and correlated with insulin resistance [116,117], whereas a lack of resistin protects mice from diet-induced hyperglycemia by increasing the activity of AMPK and decreasing the expression of gluconeogenic enzymes in the liver [118].
Moreover, resistin inhibits multiple steps involved in insulin signaling in 3T3-L1 adipocytes and induces the expression of suppressor of cytokine signaling-3 (SOCS-3), a known inhibitor of insulin signaling, in both 3T3-L1 adipocytes and murine adipose tissues [119]. However, there are conflicting reports of the potency of resistin in metabolic diseases in humans.
Several studies have consistently reported a close relationship between resistin levels and obesity, insulin resistance, or type 2 diabetes [120–124]. However, other studies have shown that circulating resistin levels and adipocyte expression are not associated with insulin resistance in humans [125,126]. Unlike mouse resistin, human resistin is exclusively expressed in mononuclear cells including macrophages [126], and macrophage-derived human resistin exacerbates adipose tissue inflammation and insulin resistance in mice [127].
PAI-1PAI-1, a primary inhibitor of fibrinolysis, is also synthesized by adipocytes as well as stromal vascular cells, such as preadipocytes, fibroblasts, vascular endothelial cells, and a variety of immune cells, in adipose tissue, and its levels in plasma are increased in obesity and insulin resistance [128,129]. A deficiency of PAI-1 decreases body weight gain, increases total energy expenditure, and improves insulin resistance in mice fed a high-fat diet [130]. Moreover, mice lacking PAI-1 have promoted adipocyte differentiation and enhanced basal glucose uptake as well as insulin-stimulated glucose uptake [131]. PAI-1 regulates expression of inflammatory factors, such as IL-8 and leukotriene B4, and monocyte migration, and its expression is regulated by various cytokine inducers such as cigarette smoke extraction and LPS [132]. VisfatinVisfatin, which was previously identified as a modulator of ?-cell differentiation that is expressed in a variety of tissues and cell types, including lymphocytes, bone marrow, muscle and liver [133], has been reported to be secreted by adipose tissue, especially visceral adipose tissue, and exhibit insulin-like activities in mice [134,135].
Visfatin was highly expressed in the visceral adipose tissue of mice as well as humans, and treatment with visfatin enhances glucose uptake in adipocytes and myocytes [134].
However, several studies have failed to confirm that visfatin is expressed predominantly in visceral white adipose tissue [136–139] and that expression of visfatin in adipose tissue is related to obesity [136,139,140].
Moreover, several studies have reported that circulating visfatin levels are high in subjects with obesity and type 2 diabetes and are positively associated with insulin resistance [139–141].
However, serum visfatin levels and expression of visfatin in adipose tissue are not correlated with glucose metabolism or insulin resistance [137,142]. A recent study has demonstrated that central visfatin improves hypothalamic insulin signaling and increases glucose-stimulated insulin secretion and ?-cell mass without changing serum visfatin levels in diabetic rats [143]. Therefore, further studies are needed to clarify the role of visfatin in the pathogenesis of obesity induced-insulin resistance. RBP4RBP4 is a hepatocyte-synthesized protein that is involved in the transport of vitamin A (retinol) in the body [145]. Recently, it has been suggested that RBP4 is also secreted by adipocytes and affects insulin sensitivity [146]. In states of obesity and insulin resistance, RBP4 is preferentially produced by visceral adipose tissue compared with subcutaneous adipose tissue, and thus it is linked to intra-abdominal adipose tissue expansion [147]. Expression of RBP4 is increased in adipose tissue in insulin-resistant mice, and adipose tissue RBP4 mRNA expression is correlated with changes in serum RBP4 levels [147]. Clinical studies have also reported that circulating RBP4 levels are associated with insulin resistance in subjects with obesity, impaired glucose tolerance, or type 2 diabetes as well as in nonobese subjects [149,150]. Along with markers of obesity and insulin resistance, RBP4 is correlated with inflammatory factors [151].
However, in several clinical studies, circulating RBP4 levels were not associated with obesity and insulin resistance [155,156]. Furthermore, some studies showed no correlation between serum RBP4 levels and expression of RBP4 in adipose tissue [155,157].
Thus, the relationship between adipose RBP4 expression, circulating levels of RBP4, obesity and insulin resistance in humans needs to be evaluated in future studies.
ANGPTL2ANGPTL2 was recently identified as an adipocyte-derived inflammatory mediator that promotes inflammation and insulin resistance [158]. Expression of ANGPTL2 in adipose tissue and circulating levels of ANGPTL2 are higher in diet-induced obese mice than in control mice, and circulating levels of ANGPTL2 are closely related to adiposity, insulin resistance, and inflammation in mice [158]. A deficiency of ANGPTL2 improves adipose tissue inflammation and insulin resistance in diet-induced obese mice, whereas its overexpression in adipose tissue promotes inflammation as well as insulin resistance in mice [158]. Further studies are needed to identify the association of human adipose ANGPTL2 expression with the development of type 2 diabetes.
AdiponectinAdiponectin is a well-known adipose-specific adipokine that produces insulin-sensitizing effects. Levels of adiponectin are low in obese subjects, and treatment with adiponectin increases insulin sensitivity in animal models [160,161]. Expression of adiponectin in adipose tissue is lower in subjects with obesity and insulin resistance than in lean subjects and is associated with higher degrees of insulin sensitivity and lower adipose TNF-? expression [162]. A deficiency of adiponectin in mice induces insulin resistance, whereas over-expression of adiponectin in mice improves insulin sensitivity and glucose tolerance [163]. It has been reported that the adiponectin receptors, adiponectin receptor (AdipoR)1 and AdipoR2 are reduced in obesity-related insulin resistance and mediate the anti-metabolic actions of adiponectin [164]. SFRP5SFRP5 is a new adipokine with insulin sensitizing and anti-inflammatory properties that exhibits beneficial effects on metabolic dysfunction [165].
The SFRP5 gene and protein are expressed at higher levels in adipose tissue than in other tissues and, in particular, gene expression is confined to adipocytes rather than stromal vascular cells [165]. A deficiency of SFRP5 in mice induced impaired insulin sensitivity, increased risk of developing NAFLD and aggravated adipose inflammation compared with control mice when fed a high-calorie diet, although SFRP5-deficient mice did not show detectable phenotype changes on a regular diet [165]. Conversely, administration of SFRP5 improves metabolic function and reduces adipose inflammation in obese and diabetic mice. The metabolic dysfunction observed in SFRP5-deficient mice is associated with increased accumulation of macrophages and enhanced production of pro-inflammatory cytokines in adipose tissue [165].
Furthermore, in SFRP5-deficient mice, JNK1 loss reverses the impaired insulin sensitivity and increased adipose inflammation [165], suggesting that a deficiency of SFRP5 promotes obesity-induced inflammation and metabolic dysfunction via activation of JNK1 in adipose tissue. Clinical study also demonstrated that plasma levels of SFRP5 were lower in adult subjects with impaired glucose intolerance and type 2 diabetes than normal glucose tolerance subjects, and its levels were negatively correlated with body mass index (BMI), waist-to-hip ratio and HOMA-IR [166,167].
In addition, circulating SFRP5 was associated with obesity and metabolic syndrome in obese children, and its levels were increased after weight loss [168]. Future clinical studies are required to determine the role of adipose SFRP5 in the control of obesity-related abnormalities in glucose homeostasis and insulin sensitivity.
Dyslipidemia is an abnormal amount of lipids, such as cholesterol and triglyceride, in the blood and is a widely accepted risk factor for cardiovascular disease. Obesity-related dyslipidemia is primarily characterized by increased levels of plasma free fatty acids and triglycerides, decreased levels of high-density lipoprotein (HDL), and abnormal low-density lipoprotein (LDL) composition (Figure 4).
The most significant contributing factor for obesity-related dyslipidemia is likely uncontrolled fatty acid release from adipose tissue, especially visceral adipose tissue, through lipolysis, which causes increased delivery of fatty acids to the liver and synthesis of very-low-density lipoprotein (VLDL). Increased levels of free fatty acids can decrease mRNA expression or activity of lipoprotein lipase (LPL) in adipose tissue and skeletal muscle, and increased synthesis of VLDL in the liver can inhibit lipolysis of chylomicrons, which promotes hypertriglyceridemia [170–172].
Hypertriglyceridemia further triggers a cholesterylester transfer protein-mediated exchange of triglycerides for cholesterol esters between triglyceride-rich lipoproteins (VLDL, immediate-density lipoprotein) and lipoproteins, which are relatively richer in cholesterol esters (LDL, HDL), which leads to a decreased HDL-cholesterol concentration and a reduction in triglyceride content in LDL [173].
The increased triglyceride content in LDL is hydrolyzed by hepatic lipase (HL) [173], leading to the formation of small, dense LDL particles that are associated with a higher risk of cardiovascular disease [174].
For decades, in clinical practice, LDL cholesterol has been the cornerstone measurement for assessing cardiovascular risk and is typically estimated using Friedewald formula [175].
As the formula is calculated based on measurements of total cholesterol, triglyceride, HDL cholesterol, the accuracy of Friedewald formula depends on the accuracy of these values. Therefore, recently, the limitation and errors of the Friedewald equation are not well appreciated by clinicians although well-documented.
Currently, there are several homogeneous assays for LDL cholesterol based on selective detergents or other elimination methods to separate chylomicrons, VLDL, and HDL from LDL [176]. A homogeneous assay for measurement of small, dense LDL cholesterol has also been developed [177].
The selective measurement of the small, dense LDL cholesterol concentration is crucial for evaluating the actual atherogenic risk of individuals, since a high concentration of small, dense LDL cholesterol is closely related to a high prevalence of cardiovascular disease [178]. Enlargement of adipocytes is associated with an increase in lipolysis [180], which leads to further increases in levels of circulating free fatty acids and their delivery to the liver to increase triglyceride synthesis. Along with triglyceride synthesis in the liver, the increased delivery of free fatty acids to the liver exacerbates insulin resistance, which promotes dyslipidemia.
Obese subjects have higher whole body fatty acid release compared with lean subjects because of their greater fat mass, although their basal adipose tissue lipolysis per kilogram of fat is lower [13]. A recent study reported the association between enlargement of visceral adipocytes, but not subcutaneous adipocytes, and dyslipidemia independent of body composition and fat distribution in obese subjects [181].
A relationship between visceral adipose tissue and dyslipidemia was also found in patients with type 2 diabetes [182]. The content of visceral adipose tissue is positively correlated with the number of VLDLs and LDLs, even when controlling for BMI and distribution of subcutaneous adipose tissue [182].



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