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 doi: https://doi.org/10.1136/bmj.h3978 (Published 12 August 2015) Cite this as: BMJ 2015;351:h3978
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Dear Editor:
It is provocative to peruse this systematic review and meta-analysis.1
Traditionally, saturated fatty acid (SFA) intake has been considered to be atherogenic, and it is suggested that reducing SFA intake prevents atherosclerotic diseases.2 Yet, some meta-analyses have indicated that greater dietary intake of SFA per se may not be associated with increased risk of coronary disease,3,4 In fact,the recent US dietary guidelines has taken off the ceiling limits of dietary cholesterol.5
In the Japanese population, SFAs intake was inversely associated with deep intraparenchymal haemorrhage and lacunar infarction and positively associated with myocardial infarction.6
Not all saturated fats are the same: short-chain saturated fatty acids (present in milk, ghee) can be readily utilized without mitochondrial beta oxidation and hence will not be a contributor to oxidative stress that would damage the myocardium. Milk, ghee, and unhydrogenated coconut oil have been used in India safely for centuries, and India had the lowest incidence of heart disease. After the switch to vegetable oils (particularly refined ones), the incidence has only been on the rise.7
Reverting back to a traditional low-fat cereal-based predominantly lactovegetarian diet,high in fibre content supplemented by omega 3 fat and devoid of fatty, fried, refined, preserved, and processed food, as consumed by our ancestors for centuries, has stood the test- of- time and is the best for health.
References:
1. BMJ 2015;351:h3978
2.Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, Franch HA, Franklin B, Kris-Etherton P, Harris WS, Howard B, Karanja N, Lefevre M, Rudel L, Sacks F, Van Horn L, Winston M, Wylie-Rosett J. Diet and Lifestyle Recommendations Revision 2006: a Scientific Statement From the American Heart Association Nutrition Committee. Circulation 2006;114:82-96.
3.Mente A, de Koning L, Shannon H, Anand S. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 2009;169:659-669.
4.Siri-Tarino P, Sun Q, Hu F, Krauss R. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 2010;91:535-546.
5. http://www.health.gov/dietaryguidelines/2015-scientific-report/PDFs/Scie...
6.Yamagishi K, Iso H, Kubobo Y etal. (2013) Dietary intake of saturated fatty acids and incident stroke and coronary heart diseases in Japanese communities:the JPHC study DOI:http//dx.doi.org/ID,1093/eurheratj/eht 043 1225-1232
7.Talim M (2007), Tradidional Diet : Hope for our children. DOI : http/dx/doi.org/10.1093/eurheartj/ehl516638
Competing interests: No competing interests
I read with interest this systematic review and meta-analysis which concluded that saturated fats are not associated with all-cause mortality, cardiovascular disease (CVD) mortality, ischemic stroke, or type 2 diabetes.
Today, social media, the Web, and newspapers are full with pro-saturated-fat articles. Medical professionals are also calling upon the nutrition experts who wrote the guidelines to reevaluate the recommendations on fatty acids and CVD on the basis of this mounting evidence that saturated fat is not the culprit! 1 With a persistent flood of misleading nutrition claims in the media, it is not surprising that the public is confused and dubious about the real opinion on the relative risks of fat, salt, cholesterol, and sugar! Five decades of controversy surrounding basic dietary guidelines and nutrition recommendations is a public acknowledgement of a failed research paradigm.2 However, the call by nutrition experts to restrict dietary saturated fat continues with the recently released U.S. Department of Agriculture (USDA) proposed 2015 Dietary Guidelines for Americans.3 Archer et al 2 criticized this report as being primarily informed by memory-based dietary assessment methods (M-BMs) (eg, interviews and surveys) despite decades of unequivocal evidence that M-BM data bear little relation to actual energy and nutrient consumption.
In another systematic review and meta-analysis, Chowdhury et al found no association between total saturated fatty acid consumption and coronary risk.4 The British Heart Foundation’s associate medical director, Jeremy Pearson, commented on Chowdhury’s findings and stated that large scale clinical studies are needed, as these researchers recommend, before making a conclusive judgement.5 Besides, further investigation on the effect of monounsaturated fat on the CVD risk is warranted.
The effect of a specific food (e.g., meat and dairy products) on risk of CVD cannot be determined simply on the basis of the fatty-acid profile of a food. The USDA Dietary Guidelines for Americans did note the need for future research on “. . . the effects of saturated fat from different sources, including butter, lard, plant (palm vs coconut oil), and production systems (e.g., refined, deodorized, and bleached vs virgin coconut oil) on blood lipids and cardiovascular disease risk.”3
So where do we go from here? And what should we tell our patients when they face us with all this astronomical information in the media?
We should continue to treat the basic disease process of atherosclerosis by changing the natural history of the disease, which we may be able to do with modification of risk factors.6 We should continue emphasizing the importance of eating less, avoiding obesity, exercising more and avoiding smoking. We need to talk less about nutrients and more about whole foods, eating patterns, and healthful cooking techniques, while limiting foods that are harmful, like sugar, trans-unsaturated fatty acids, and processed foods.1 Optimal intake for dietary fats is still unclear and clinical studies to define the safe lower and upper levels of consumption of dietary fats are warranted. The final advice would be :“Healthy living is the most powerful medicine of all. It requires no prescription, and all of the side effects are beneficial”.
References
1. Dildy T. Evidence For and Against Dietary Recommendations to Prevent Cardiovascular Disease. Tex Heart Inst J. 2015 Jun 1;42(3):234-6.
2. Archer E, Pavela G, Lavie CJ. The Inadmissibility of What We Eat in America and NHANES Dietary Data in Nutrition and Obesity Research and the Scientific Formulation of National Dietary Guidelines. Mayo Clin Proc. 2015 Jul;90(7):911-26.
3. Office of Disease Prevention and Health Promotion, U.S. Department of Health and Human Services. Scientific report of the 2015 dietary guidelines advisory committee [Internet].Available from: https://ods.od.nih.gov/About/2015_DGAC_Report.aspx
4. Chowdhury R, Warnakula S, Kunutsor S, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk. A Systematic Review and Meta-analysis. Ann Intern Med 2014;160:398-406
5. Wise J. Evidence does not support guidelines on saturated fat, researchers say. BMJ. 2014 Mar 19;348:g2238.
6. Chamsi-Pasha H. Cholesterol. How low should we go?(Review). Saudi Med J. 2005 Jan;26(1):11-8.
Hassan Chamsi-Pasha, FRCP, FACC. Cardiac department, King Fahd Armed Forces Hospital, Jeddah, Saudi-Arabia. (drhcpasha@hotmail.com)
Competing interests: No competing interests
I read with interest the thought-provoking recent article in BMJ. (1)
The concept: that trans-fatty acids are pernicious for health is well-proven beyond doubt.
The controversy among the fat group largely surrounded intake of saturated fats and cholesterol.
Enough data exist to prove that excessive intake of saturated fats produces/exacerbates atherosclerosis and lowering its intake leads to regression of atherosclerosis both in the experimental animals as well as in humans. Up to 10% of total calories can safely be derived from saturated fats for patients without any cardiovascular disease (CVD). In fact, clarified butter (Desi Ghee from cow's milk, commonly consumed for centuries in Indian culture) in Ayurveda has shown to have many salutary health benefits like improvement of immunity and prevention of certain cancers etc. Of course an excess of everything is bad.
Regarding cholesterol: Recent 2015 US dietary guidelines has removed the upper limit of cholesterol intake, as they could not find any appreciable relationship between dietary cholesterol and CVD. Yes they could find an association of red meat (high in cholesterol) with many diseases like CVD and certain cancers. Therefore red meat should not be consumed.(2)
References:
1. BMJ 2015;351:h3978
2. http://www.health.gov/dietaryguidelines/2015-scientific-report/PDFs/Scie...
Competing interests: No competing interests
In history research, where truth is often elusive, it’s legitimate to go back to data sources and make new interpretations. It’s different in natural science. After Galileo Galilei and colleagues established beyond reasonable doubt that the earth circles the sun, new generations of physicists do not open the case over and over again. This reminds me of the seemingly never ending set of meta-analyses on the health effects of saturated fats. Same sets of studies with their inherent weaknesses -- like adjusting factors in the pathogenetic pathway, or, not adjusting for eg. socioeconomic class or healthy user bias -- are put together to prove that saturated fats, after all, would not be not hazardous to our health.
Personally, I accepted the idea of harm from saturated fats through the following chain of reasoning: 1. saturated fat intake increases serum LDL cholesterol (proven repeatedly); 2. LDL cholesterol is a long-term risk factor for cardiovascular diseases (proven repeatedly); 3. lowering LDL cholesterol reduces cardiovascular events (also proven repeatedly). But like proponents of tobacco industry, some proponents of saturated fats are demanding more studies and direct proof in the same trial. This is practically impossible. Nowadays we cannot put people in control and diet groups for several years to directly prove that saturated fat intake increases cardiovascular events.
Once they could do it: in the 12-year, controlled Finnish mental hospital study (1) saturated fats were replaced with polyunsaturated fat and the results were compatible with the theory chain above: cholesterol was reduced with the experimental diet and cardiac events were reduced accordingly.
In the absence of new controlled trials, we are left with this endless series of meta-analyses from observational studies which cannot prove causality. And these studies also involve several potential biases: over- or underadjustment, inaccurate measurement of dietary intake moving results toward null (2) etc.
But why this research activity? An interesting explanation was recently proposed: In 2008 global dairy industry had a meeting, where it was decided that it is important to “neutralize the negative impact of milkfat by regulators and medical professionals” (http://www.nutritionaction.com/daily/fat-in-food/saturated-fats-link-hea...). It is appropriate to say that the study of de Souza et al does not report funding from dairy industry.
References
1. Miettinen M, Turpeinen O, Karvonen MJ, Elosuo R, Paavilainen E. Effect of cholesterol-lowering diet on mortality from coronary heart-disease and other causes. A twelve-year clinical trial in men and women. Lancet 1972;ii(7782):835-8
2. Archer E, Pavela G, Lavie CJ. The inadmissibility of what we eat in America and NHANES dietary data in nutrition and obesity research and the scientific formulation of national dietary guidelines. Mayo Clin Proc 2015;90:911-926
Competing interests: I have made research on lipids and was one author of a book on cholesterol in 2011 (very minor royalties).
This is an interesting research article [BMJ 2015;351:h3978].
This is the seventh systematic review and meta-analysis of observational studies published in the past 10 years [1], even then no clear consistent and conclusive results because evidence is heterogeneous with methodological limitations.
Authors rightly mentioned about strengths and weaknesses of the study; GRADE (Grading of recommendations assessment, development, and evaluation) approach was used to evaluate quality of evidence - the strength of the study. Limitations of the study - related to evidence synthesis and quality [1].
There’s good news and bad news about eggs. Yesterday egg was bad, today egg is good for health[2].
Butter, cheese and steak are not really bad [3]. is true that dietary cholesterol and egg yolks is not good for patients at risk of vascular disease[4].
Modern ‘Western diets’ diets can lead to poor immune functioning and increased risk of inflammatory conditions and allergy: Fast food fever [5].
This is very difficult to arrive at clear consistant and conclusive results for populations all over the world (populations with different genetic makeup, culture, life style and food habits).
References:
1. BMJ 2015;351:h3978
2.http://www.theglobeandmail.com/life/health-and-fitness/health/theres-goo...
3.http://www.wsj.com/articles/SB10001424052702303678404579533760760481486
4.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989358/
5. http://www.foodnavigator.com/Science/Fast-food-fever-Modern-diets-impact...
Competing interests: No competing interests
It is misleading to adjust away the cholesterol-raising effects of saturated fat if the focus of the study is to analyze the effects of saturated fat on adverse cardiovascular outcomes. Increased LDL is a predictable consequence of increasing intake of saturated fat; so subtracting that effect by adjusting the data will make saturated fat intake appear safe. However, this is analogous to contending that gun shot wounds are harmless if you adjust for blood loss, or cocaine use is benign if you adjust for blood pressure.
The fully adjusted data from this study are not very relevant to practical dietary applications, except of course if you add in statins to the equation. Atorvastatin for example can largely neutralize the cholesterol-raising effects of saturated fat. So, if one is willing to take a statin, and tolerate its side effects, then perhaps saturated fat can be largely ignored.
Competing interests: No competing interests
I disagree with the concept that saturated fats cause or do not cause mortality, heart disease, high cholesterol, etc. Surely, they are associated. So what? Because of the biochemical interchange inside the body of saturated fats with other fats, carbs and protein, the body concentrations of saturated fats are not determined by their intake, but primarily by the total intake of excessive calories, for which weight is a biomarker. Depending on how the study is designed, and what variables are measured, one may or may not find a statistically significant association between saturated fats and bad things. We need to remember that most studies use sample sizes over 100. The average of 100+ subjects of any two variables is highly unlikely to be mathematically identical within 5%. Conventional statistics will find such difference statistically significant. I consider them statistical flukes. Given the huge nature of normal variability, differences below 30% may be statistically significant but biologically irrelevant.
In clinical studies one can find that saturated fat prevents, treats or causes heart disease, depending on the study design. If we want to prove saturated fat causes heart disease, we provide a diet supplemented by a food like butter (very low in essential fats), maximize caloric intake. Over time, this diet depletes essential fats in the body. We can keep weight constant via exercise, so subjects can eat more fat. If we want to prove that saturated fat prevents or treats heart disease, we use a food high in saturated and essential fats, like egg yolks or soybean oil. If we want to prove that replacing saturated fats with other fats prevents disease, we replace butter with foods with cells rich in membranes. If we want to prove that saturated fats are better than carbs to prevent disease, we replace pure carbs from processed cereals (such as breads, pasta) with oil plus cells that contain both saturated and essential fats. According to my research, replacing foods rich in saturated fats and low in essential fats with food rich in essential fats, such as vegetables, will reduce the risk of cardiovascular disease.
Instead of spending huge amounts of time and money studying how saturated fat affects heart disease, and recommending we eat less or more, of some foods but not others, we should focus on weight. Overweight bad. Slim good. Following this simple advice, we can eliminate many treatments and research studies and save over $200B. We observe people and decide if the difference between their actual weight v. desirable ideal weight is statistically or substantially different. A scale and a measurement tape can quantify differences. We may find it is a better diagnostic test than CT scans or something else.
Dr. Ornish and I exchanged some letters in a professional journal and spoke several times about these issues. I don’t have the citation for his letters, but mine are listed below. I have seen and tasted some of Dr. Ornish foods, and spoke several times to his nutritionists. In general, I find his food recommendations are consistent with my nutrition recommendations. With regard to egg yolks, high in fat and cholesterol, I consider them desirable and I eat them frequently because they are rich in essential fats.
My opinion, based on my research, is that moderate intake of more cholesterol or more saturated fat (any type), are not the major factor in cardiovascular disease. Thus, recommendations to reduce intake of cholesterol or saturated fat are generally undesirable. Instead, weight (eating too many calories), inadequate intake of essential fats (from foods in their natural state, not necessarily supplements), and, to a minor extent, trans and isomers of fatty acids, are the major causes of cardiovascular disease. Treatments to lower cholesterol with drugs or eat fewer saturated fats or carbs or cholesterol miss the important causes.
Is it a coincidence that the US government created a national program to lower cholesterol, which can be accomplished with drugs, instead of a program to lose weight, which is difficult to accomplish with drugs? I spoke against the US National Cholesterol Program more than 15 years ago.
Worldwide focus to eliminate trans fats or lower fat in foods is neither efficient nor effective. Governments and corporations spend billions to replace one fat with another. This effort is unlikely to reduce overweight (and cardiovascular disease). Instead, they should focus on reducing weight and getting enough essential fats in their natural state. The important questions include: what is the purpose of lipoproteins? (I propose to carry non-water soluble nutrients like essential fats and some vitamins). When and why should we lower them and how much? Why does cholesterol go up or down? Was the US National Cholesterol Program a mistake? Were the policies of eating less saturated fats and cholesterol a mistake? Should governments shift massive amounts of tax dollars to reduce overweight, away from cholesterol treatment and fat avoidance? What are the implications for the dozens of billions currently spent on cholesterol treatment? Do we need to eat more essential fats?
Siguel E, Lerman RH. The Effects of Low-Fat Diet on Lipid Levels. JAMA, 1996; 275:759-60.
Siguel E, Lerman RH, MacBeath, B. Very Low-Fat Diets for Coronary Heart Disease: Perhaps, but Which One? JAMA, 1996; 275: 1402-03. Erratum in: JAMA 1996; 276(12):954 (let).
Competing interests: I conduct research, write books, and lecture about body biochemistry, behavioral changes, focusing on the types of fats to eat, including foods close to their natural state, exercise, stress management, social support, eating less, periodic fasting. I am writing about a new theory of lipid metabolism and the cause of cardiovascular disease. I intend to profit from my intellectual property (IP). My research involves fatty acids. I wrote a patent to measure fatty acids. I plan to write more patents on lipid metabolism and biomarkers. I analyze fatty acids and plan to earn income from these activities. I wrote one book on essential and trans fatty acids. I gave talks to corporations, conferences and trade shows, for which I was paid. I may receive compensation from food or other companies (none so far in 2014 or 2015). I plan to write several books and articles and earn income from IP (e.g., sales of books, ads, lectures, etc.). This comment is an extract of books and articles either written or in progress (authorized by the author, obviously cannot alter the original copyrights). This statement also applies to references cited. My opinions are influenced by my research and publications. I have exclusive data on fatty acid profiles of over 1,000 subjects. I worked with Pilgrim’s Pride (one of the largest producers of eggs and chicken). I suggested to the officers that they feed hens and chicken foods higher in essential fats. One outcome was an egg high in essential fats. Also spoke with other egg manufacturers and industry executives. I have not received compensation from them for more than 5 years.
De Souza and colleagues reported the results of a high quality meta-analysis examining saturated and trans fats in this week’s BMJ. Their findings are consistent with those of Chowdhury and colleagues (1) in 2014 showing that saturated fats did not appear to impact the risk for major health outcomes. Although both of these meta-analyses are well done, it is important to recognize that both studies extracted only adjusted risk ratios. If crude risk ratios were used instead, it is virtually assured that the pooled risk estimate for saturated fat would be highly suggestive of harm. Adjustment variables such as BMI and cholesterol typically drive risk estimates towards the null in these studies and it could be argued that their effects were not independent of saturated fat consumption.
1. Chowdhury, Rajiv, et al. "Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis." Annals of internal medicine 160.6 (2014): 398-406.
Competing interests: No competing interests
Understanding the association between different types of fatty acids (FA) and cardiovascular disease (CVD) or diabetes requires analysis of fat, energy intake and metabolism. We cannot study the effect of Saturated Fatty Acids (SFAs) or Trans FA (TFAs) separate from Essential Fats (=PUFAs of the w3 + w6 families, there are PUFAs of the w7, w9 families, a commonly overlooked issue), monounsaturated FAs (MUFAs) and caloric intake. The accumulation of SFA in the body does not depend on the intake of SFAs. It depends on the intake of total calories and their use. Storage of SFA ~ = Caloric intake – Calories used for metabolism, etc. = surplus calories. In general, surplus calories from any source (fat, carbs, protein) are stored as SFAs (with exceptions too lengthy to include here). It means that two isocaloric diets, one low fat diet high in carbohydrates, causes about the same body accumulation of SFAs, as a low carb high fat diet.
To study the effect of SFA on CVD or diabetes requires complex multivariate analysis involving caloric intake, exercise (calories “burned”), metabolism, etc. One alternative is to measure change in weight and change in fatty acid profiles (FAP) in plasma, cells and adipose tissue (accurately done, it takes hours for each measurement at a substantial cost, so I found it is rarely done accurately, read my papers and patent for methodological issues).
I found that TFA intake cannot be accurately measured from diet questionnaires or food intake. The formation of TFAs depends on a wide range of factors involved in food processing. Two apparently identical foods may have widely different TFA composition depending on food processing (e.g., cooking, storage). Further, some researchers focus only on TFAs. There are a wide range of other isomers that have effects similar to TFA (based on my preliminary data analysis where I measured many FA isomers). In general, advanced technology can separate and fairly accurately measure isomers up to 3 double bonds (e.g., linoleic and linolenic acid isomers). I rarely find it done accurately or reported. Isomers (and there are many) of longer chain FA with more double bonds (e.g., EPA, DHA, ARA) are almost impossible to measure with conventional technology (and they are very rarely reported, try to find them). It is likely that many foods, particularly supplements, high in long chain FA with more than 3 double bonds, contain substantial amounts of isomers. This is likely to be a problem because probably only one isomer has appropriate biological functions. The other isomers are probably “burned” for calories and thus replace calories from SFA or carbs or protein. A diet that appears to contain many essential fats (PUFAs) may not be so, and be biochemically equivalent to a diet low in PUFAs and high in SFAs. The relative importance of these issues is poorly known due to lack of adequate measurement technology and research data. It may be a reason that it is very difficult to profit from this research, and it is likely that some products may contain undesirable isomers (something not necessarily good for marketing, so ignorance may be bliss or blessed).
My research showed that CVD depends on body levels of essential fats and non-essential fats. Using TC/HDLC as a biomarker for the risk of CVD, the risk attributed to TFAs explains about 10% of the variance of TC/HDLC. Most of the variance is accounted for variations in essential fats and caloric intake. They are reflected in the formula I use, PUFA/NoPUFA (amount of PUFA over amount of FA that are not PUFA, including PUFAs of the w7 and w9). Further, when the body does not have enough essential fats, it makes more MUFAs. The body carefully regulates total MUFAs, so if we eat more, we probably make less MUFAs, but it is possible to increase body MUFA levels by following a diet very high in MUFAs (matters discussed in future papers based on my analysis of FAs in more than 1000 people).
The conclusion I make is that it is almost impossible to evaluate the effects of FA from diet on CVD without accurate FAP of the individuals involved. The analysis must concurrently evaluate all FAs via complex multivariate models with high predictive value (e.g., high R square). Without a high predictive value using all the relevant variables, I doubt it is possible to reach conclusions about the effects of any particular FA on CVD.
Lucky for patients, my recommendations are simple. Eat enough calories to achieve or maintain ideal weight. Eat foods rich in nutrients, because in Western societies exercise is limited (and so we must limit caloric intake), and one may not eat enough nutrients from highly processed food. Eat food close to their natural state, rich in cells with membranes. Of course, with moderation, we can eat toxic chemicals, cookies, desserts, and receive radiation. The key is the definition of moderation. With moderation, chemicals don’t hurt (i.e., limit toxic chemical exposure to one molecule per year, that would be moderation); one high energy photon or electron per year (radiation) is probably safe. Draw your conclusions for eating with moderation.
Other factors to consider. FAs are located in different parts of the molecules we eat (usually triglycerides or phospholipids). Their biological effects likely depend on their molecular configuration. Thus, two foods with equal amounts of w3 or w6 FAs but in different molecular configurations are likely to have very different biological effects. Soybean oil is relatively high in linolenic acid (an w3). Because of its usually optimal position on the triglyceride molecule, the body effects are more substantial than a food with higher quantity of w3s in the less desirable molecular configuration (but be careful, some modern soybean oil may be low in w3s). Food processing produces isomers; these isomers are usually not distinguished during FA measurements (it requires complex technology to accurately separate and measure them). Tables of FA composition are misleading to indicate actual intake of FAs (due to the formation of isomers during food processing).
Some References
Siguel E, Maclure, M. Relative Activity of Unsaturated Fatty Acid Metabolic Pathways in Humans. Metabolism, 1987; 36: 664-69.
Siguel, E. Method and Apparatus for Diagnosis of Fatty Acid or Lipid Abnormalities. U.S. Patent No. 5075101, Issue date 12/24/91.
Siguel E, Lerman, RH. Trans Fatty Acid Patterns in Patients with Angiographically Documented Coronary Artery Disease. Am. J. Cardiology, 1993; 71:916-20.
Siguel E, Lerman, RH. Altered Fatty Acid Metabolism in Patients With Angiographically Documented Coronary Artery Disease. Metabolism 1994; 43:982-93.
Siguel E. Essential and Trans Fatty Acid Metabolism in Health and Disease. Nutrition Issue. Comprehensive Therapy, 1994; 20(9):500-10 (Review).
Siguel E. Essential Fatty Acids in Health and Disease. 1994, P.O. Box 10187, Dept F, Gaithersburg, MD 20898 (book).
Siguel, E. A New Relationship between Total/HDL Cholesterol and Polyunsaturated Fatty Acids. Lipids, 1996; 31:S51-6.
Siguel, E. Identification and Quantification of Fatty Acids. J.Parent.Ent.Nutr. 1998; 22(6):401-02.
Siguel, E. Deficiencies and Abnormalities of Essential Fats in Gastrointestinal and Coronary Artery Disease. Journal of Clinical Ligand Assay 2000; 23:104–11.
Siguel, E. Clinical Impact of Methodological Issues in the Diagnosis of Deficiencies and Abnormalities of Essential Fats. Journal of Clinical Ligand Assay 2000; 23:112–21.
Competing interests: The author intends to profit from his intellectual property (IP). He conducts research on fatty acids (see references for examples). He wrote a patent to measure fatty acids. He plans to write more patents on lipid metabolism and biomarkers. He analyzes fatty acids and plans to earn income from these activities. He wrote one book on essential and trans fatty acids. He gave talks to conferences and trade shows, for which he was paid. He may receive compensation from food or other companies (none so far in 2014 or 2015). He plans to write several books and articles and earn income from IP (e.g., sales of books, ads, lectures, etc.). This comment is an extract of books and articles either written or in progress (authorized by the author, but obviously cannot alter the original copyrights). This statement also applies to references cited. His opinions are influenced by his research and his publications.
Re: 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
This debate is unlikely to be concluded soon. Everyone has a strong view either way and the usual suspects are wading into the debate with the usual dogma on both sides. What is of concern is that 50 years of dietary advice is under scrutiny despite thousands of articles all published under peer review. It is to some degree surprising that fat intake seems to have been isolated from food intake in general. Please correct me if I am wrong but isn't it the case that any excess carbohydrate is converted to triglyceride then sent round the body as LDL? And isn't the content of that triglyceride saturated fat? So is it sugar or fat? What is completely clear is that the dietary guidelines we have today are not leading to healthy outcomes judged by the incidence of obesity and diabetes. We need to forget about diets for all and concentrate on personalised care. The technology is available.
Competing interests: No competing interests