Low Carb Diets and Heart Disease – What Are We Afraid of?

I find it extraordinary how carbohydrate restriction is repeatedly rejected by the medical community as an alternative approach for obesity, metabolic syndrome and type 2 diabetes.

Obesity has reached epidemic proportions in many countries around the world. Diabetes and other obesity related disorders have become increasingly common.

Low Carb Diets and Heart Disease - What Are We Afraid of?

Public health organizations and medical societies usually advocate a low-fat, high-carbohydrate, energy-deficient diet to manage weight. Nonetheless, clinical experience and scientific studies indicate that other approaches may be more effective.

The main argument against carbohydrate-restricted, high-fat diets are concerns regarding their long-term safety. Most such diets encourage increased consumption of animal products and therefore they often contain high amounts of saturated fat and cholesterol. It has been suggested that this may cause unfavorable changes in blood lipids and thereby increase the risk of heart disease. Therefore, several professional organizations have cautioned against the use of low-carbohydrate, high-fat diets.

According to a statement from the American Heart Association AHA, updated January 2012, “eating large amounts of high-fat foods for a sustained period raises the risk of coronary heart disease, diabetes, stroke and several types of cancer.”

An older statement from the Heart and Stroke Foundation of Canada claims that ” low carbohydrate diets often lack vitamins and are low in fibre. A low fibre diet can result in constipation and can increase your risk of colon cancer. Low carbohydrate diets tend to replace carbohydrate with fat and protein. High intake of protein can result in large amounts of calcium in the urine, and loss of bone mass. High intake of fat, particularly saturated and trans fat, can lead to atherosclerosis, heart disease or stroke”.

These statements are based on observational data at best. Randomized clinical trials generally don’t support these conclusions. In fact, low carbohydrate diets have demonstrated their therapeutic value in numerous studies, and often outperform other diets when comparisons are made. Nonetheless, they are still ignored by governments and medical societies. Keep in mind though, that carbohydrate restriction is a matter of definition. Some diabetic associations have accepted moderate carbohydrate restriction as an alternative approach for weight loss in type 2 diabetes.

Doctors, cardiologists included, commonly recommend low-fat, high-carbohydrate diets to patients with heart disease, as well as for cardiovascular prevention. Limitation of saturated fats and cholesterol is advocated. This is what doctors are urged to do by clinical guidelines. The guidelines are written by specially selected experts and published by professional organizations.

Interestingly, there is often no mention of individual differences between patients. The low-fat, low saturated fat, low cholesterol, high-carbohydrate approach is recommended for all. It doesn’t matter whether you have high blood pressure, whether  you are obese or overweight, have the metabolic syndrome, or whether you have diabetes.

I have nothing against low fat diets. Look at the DASH diet for example. Extensive research indicates that this diet lowers blood pressure and cholesterol, and is associated with lower risk of several diseases, including heart disease. Furthermore, it was recently suggested that the DASH diet may be used for weight loss as well. I would be very satisfied if may patients would stick to the DASH diet. I usually urge them to do so. I am sure it benefits their health. The same thing can be said about plant based diets. Furthermore, I very often recommend a Mediterranean type diet to my patients. There is a lot of scientific date supporting the use of this diet for cardiovascular prevention as well as for patients with heart disease.

Low Carb, Obesity and Metabolic Syndrome

The role of diets takes on a different perspective when it comes to obese patients, and those with metabolic syndrome, where weight loss is a priority. For years I have struggled with the low-fat, high-carbohydrate, energy-deficient dietary approach to manage these conditions. Simply put, the results have been disappointing. Often weight loss is limited and not sustained, and there are very limited improvements in metabolic function. However, I might admit the lack of result is more often due to lack of compliance than something else. Maybe we provide instructions and recommendations that patients are unable to comply with, no matter how hard they try.

Low Carb Diets and Heart Disease - What Are We Afraid of?

 

I have found that people suffering from obesity or metabolic syndrome are much more likely to lose weight and improve their metabolic function on a low-carb, high-fat diet.

However, my clinical experience is that the effects of such a dietary approach on blood lipids are a bit hard to predict. Commonly there is an elevation of total cholesterol and LDL-cholesterol (“bad cholesterol”) which may be considered harmful. However, at the same time there is most often an elevation of HDL-cholesterol (“good cholesterol) and triglycerides are lowered.

So the question is; Should I not recommend a dietary approach that works in terms of weight loss and metabolic control, because there may be a slight elevation of LDL-cholesterol? According to the medical associations and the clinical guidelines, I should not.

Low Carb Diets and Heart Disease – The Scientific Studies

My purpose is not to go through all available scientific data on the issue of carbohydrate restriction and heart disease. However, I will try to convince you that the available data does not support the conclusion that low-carbohydrate diets are less safe than other dietary approaches for people who are obese, overweight or suffer from the metabolic syndrome.

The initial recommendations to avoid saturated fat and cholesterol were based on observations from epidemiological research. Some of this research was led by the famous American scientist, Ancel Keys. In a personal reflection from 1995

Keys wrote: “These observations led to our subsequent research in the Seven Countries Study, in which we demonstrated that saturated fat is the major dietary villain.” Keys observed that death rates were related positively to the average percentage of dietary energy from saturated fatty acids, but negatively to dietary energy percentage from monounsaturated fatty acids. In short; saturated fats seemed to increase risk, while monounsaturated fats appeared to lower risk.

Since then, an independent association of saturated fats with the risk of heart disease has not been consistently found in epidemiologic studies. Replacing saturated fats with carbohydrates has not been shown to be beneficial. In fact, replacement of saturated fats with refined carbohydrate can worsen blood lipids when insulin resistance is present, by increasing triglycerides, the number of small LDL particles, and by decreasing HDL-cholesterol. Some studies have indicated that replacing saturated fat with monounsaturated or polyunsaturated fat may be beneficial, although the latter was not supported by the recently published Sidney Diet Heart Study.

The relationship between the consumption of fat, saturated fat in particular was studied in the Swedish Malmö Diet and Cancer Study published in 2007. In this large prospective observational study, no trend towards higher cardiovascular event risk for women or men with higher total or saturated fat intakes, was observed. This study was later included in the much cited Siri-Tarino meta-analysis published 2010, showing no significant evidence for concluding that dietary saturated fat is associated with an increased risk of heart disease.

A number of randomized clinical trials have compared low-carbohydrate diets with other dietary approaches. In many of these studies, low carb diets have resulted in more short-term weight loss in healthy womenindividuals with severe obesity with high prevalence of the metabolic syndrome and type 2 diabetes, overweight adolescents, overweight individuals with hyperlipidemia, and  premenopausal women, compared with low-fat diets. Furthermore, negative effects on blood lipids with low-carbohydrate diets were not observed in these studies and markers of the metabolic syndrome were generally improved.

Most of these randomized trials are short term studies. Thus, the long-term effects of low-carbohydrate diets still remain to be clarified. Recently, it has been suggested that such diets may be harmful.

In a systematic review and meta-analysis of observational studies, published November last year, Noto and coworkers found that low-carbohydrate diets were associated with a significantly higher risk of all-cause mortality. However, they did not find an association between low-carb diets and the incidence of, and mortality from cardiovascular disease. The authors acknowledge that their analysis is based on limited observational studies, and that large-scale trials on the complex interactions between low-carbohydrate diets and long-term outcomes are needed. It is also necessary to point out that there was a substantial difference between studies, regarding both study design and definitions. Such heterogeneity may make meta-analysis problematic.

A Few Final Words

There are many different versions of low-carbohydrate, high-fat diets. Some promote the consumption of saturated fat, while others don’t. For a patient with heart disease or someone with elevated cholesterol, I usually recommend monounsaturated fat and polyunsaturated fats rich in omega-3. I find that using the Mediterranean approach, when selecting which fats to eat may be very helpful.

Although it does not comply with guidelines, I commonly recommend individuals who are obese or suffer from the metabolic syndrome to cut down on carbohydrates and increase fats. In most instances, I find these recommendations very useful. I don’t recommend my patients to stay in ketosis for long periods of time. However, if they choose to do so, if they feel well, and if their health is improving, I find no reason to tell them not to.

If an obese person with metabolic problems manages to achieve weight loss and improve his or her metabolic function on a low carbohydrate diet, it is hard to understand how such an achievement may be harmful.

I look forward to the day when low-carb, high-fat diets are accepted by public health representatives and medical associations for the treatment of obesity, metabolic syndrome and type 2 diabetes.

The medical community, which I am a part of, accepts that drugs that lower cholesterol, and slightly reduce the risk of heart disease (although having considerable side effects, among them increased risk of diabetes) are given to 25 percent of adults in many countries around the world.

I find it a bit hard to accept that the same medical community does not accept and recommend a dietary approach for obesity and the metabolic syndrome, that causes weight loss, increases wellbeing and improves metabolic function, and indeed appears to outperform other diets in this respect.





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83 thoughts on “Low Carb Diets and Heart Disease – What Are We Afraid of?”

  1. Thanks for the great article. One diet for everyone type of thinking should be dumped and patients should be treated as individuals. Especially if type 2 diabetics can avoid/reduce insulin treatment due the diet, it’s even better. There seems to be growing amount of evidence that insulin treatment has lots of unwanted “side” effects(https://jcem.endojournals.org/content/early/2013/01/31/jc.2012-3042.abstract).

    I’ve enjoyed reading your blog which seems to be free of bias 🙂

    Reply
    • Thanks for the encouragement “Someone”. You are right. Prevention is most important. Like someone said: “Medicine is not healthcare. Food is healthcare. Medicine is sickcare.”

      Reply
      • Hi Doc, I am totally convinced. i have Heterozygous Familial Hypercholesterolemia. So do my sons and I fear for them. My total cholesterol, especially trigs, plunged dramatically on a LCHF (and I really mean high fat – like they do with kids with epilepsy) – I KNOW in my knower that I can never go off this diet again. We cannot tolerate statins – we get rhabdomyolises within a week. This diet is a lifeline for us-wise, but I cannot find a single person with this disease in cyberspace who has gone for this diet – they are scared to death. I did it because I needed to see and my Doc was astounded. He said my results looked like they didn’t belong in my file. BUT, I cannot find a single cardiologist in South Africa who will support us. I refuse to fight it out with these learned people but I also refuse to opt for their high carb, low fat option. I once went onto a vegan diet for a whole month and my cholesterol went so high that my GP told me that I was now an emergency. I thought I would surprise them and I got the shock of my life. But the HIGH FAT scenario – now that DID surprise them. BUT, our type need a cardiologist once a year – can’t find one. thanx for your opinions.

  2. Fantastic article, Dr. Sigurdsson. My favorite line: “I look forward to the day when low-carb, high-fat diets are accepted by public health representatives and medical associations for the treatment of obesity, metabolic syndrome and type 2 diabetes.” This is something I’ve said repeatedly. Keep up the good work!

    Reply
  3. The question of whether saturated fats are healthy or not probably would have been settled decades ago had the United States Government not put a end to scientific debate by declaring saturated fats the cause of clogged arteries because they raise cholesterol and omega-6 industrial seed oils the cure because they lower cholesterol. Excerpt:

    “The point so far is that in order to gauge our current prospects for improving public health, we need to answer two questions: (1) Which approach to health and nutrition is the right approach? and (2) Which approach currently enjoys widespread acceptance? If we get two different answers (that is, if an incorrect approach enjoys widespread acceptance), then we have a problem. But this result would seem unlikely, because once we begin to make any progress regarding (1), that progress should influenc the answer to (2). In other words, if some approach has become more mainstream than the others, that’s probably because it’s the most correct approach. This is what we should see happen as a result of fair and honest scientific debate: the best ideas will (eventually) emerge victorious from the battlefield of ideas and win widespread acceptance. But this process may not play out like this if non-scientific intervening forces get involved and influence which approach ends up winning widespread acceptance. The “non-scientific intervening force” that I have in mind here is, of course, government. The U.S. federal government, in many of its actions, has prematurely taken a non-neutral stance on the scientific debate about what constitutes a healthy and nutritious diet. In doing so, it has helped one approach become entrenched dogma. Once the government got involved, there ceased to be free or fair marketplace of ideas about health and nutrition (and there hasn’t been for a very long time). And this is an important reason that the answers to the above questions (1) and (2) might be (and probably are) different. https://freepressonline.net/content/what-has-government-done-our-health

    Reply
  4. I read this post with interest — even looking hopefully for some explanation of the notion why it would not be recommended that your patients stay in ketosis for long periods of time. I do apologize if this comes across as rude — but I am growing frustrated with the number of times I see such statements without explanation of WHY long term ketosis is or would be a problem.
    I have been in stable ketosis since May of last year (approx 10months) and the difference in the weight loss pattern (MUCH smoother), mood swings, sugar crashes, cravings and general wellbeing is vastly improved since going into ketosis. The weight loss journey started in June 2011 and has resulted in a total 134 pounds melted off to date. The key to this in my case was/has been to restrict carbs to 50g daily, although I am now tweaking the system to consume NET of fibre carbs at 50g daily, so far with impunity.
    Overall I feel much better, due in large part to less weight, but sleeping better AND much less inflammation as demonstrated by smaller knuckes (and ability to wear old jewelry now) and very very few skin blemishes or pimples any more. I take no prescription medications of any sort (am pre-diabetic though). So ….. quite frankly I am confused by the statements that long-term ketosis is a poor idea. It has not been for me, unless 10 months is not considered a long time.
    Thank you.
    Meghann

    Reply
    • @Meghann
      Thanks for your comment Meghann. Maybe I should have spoken clearer on this issue. I don´t consider ketosis to be a problem, and in most cases I don´t tell people to avoid it. Indeed, I think it can be very helpful for many people. What I was implying is that it does not have to be a target in itself for everyone. You can get results with low carb although you don´t stay in ketosis. People have a choice on how hard they want to go.
      Congratulations on those fantastic results on improving your health 🙂

      Reply
  5. Our friends in Sweden have already accepted moderately low carb diet for the treatment of diabetes among other diets 🙂 See: https://www.socialstyrelsen.se/lists/artikelkatalog/attachments/18471/2011-11-7.pdf . They did approve low carb diet after comprehensive review of the literature.

    Also, ADA Position Statement: Standards of Medical Care -2012. ” For weight loss, either low-carbohydrate, low-fat calorie-restricted, or Mediterranean diets may be effective in the short-term (up to 2 years). (A)”

    ” The mix of carbohydrate, protein, and fat may be adjusted to meet the metabolic goals and individual preferences of the person with diabetes.”

    For me, this sounds like a cautious step forward. A low carb diet favouring fish, white meat, dairy and nuts as protein sources and vegetable oils as primary added fats may indeed be good for many with metabolic syndrome.

    Reply
  6. The DASH diet looks pretty much like the Standard American Diet – high in grains and fructose and low in fat – I think it sounds like the same disastrous dietary advice that has taken us to the epidemic levels of obesity, heart-disease and diabetes that we have around the world today.

    I tried the low fat, high carb, high fibre, calorie restricted diet for many years and though I could lose weight on it, I was always hungry, always irritable, always thinking about food and never able to sustain it for any length of time and as soon as I gave in and ate more the weight would pile back on, also my blood pressure was creeping up and up.

    I have been following a very low carb, high fat diet for 3 years now. I have lost 35 lbs in weight, got rid of sugar crashes, mood swings, energy crashes and acne. I have never felt better and I know I can easily sustain this lifestyle for the rest of my life. The fats I eat are – coconut oil, butter, ghee and olive oil and cod liver oil supplements. I also don’t trim the fat off my meat. I have no fear of saturated fats as there is no evidence that they are harmful. I do avoid all industrial seed oils such as canola, sunflower and vegetable oils.

    I have had all my blood work checked by my GP and my blood pressure, cholesterol, triglycerides and blood sugar levels are all perfect – her advice – whatever you are doing – keep on doing it!

    Reply
    • Thanks for sharing your thoughts Diane. This is exactly what so many others have experienced. Good luck and hope you will sustain your good health.

      Reply
      • First, canola is rapeseed. Second, inflammation is not the only issue of concern[1]. Third, what constitutes a realistic consumption scenario? Fourth, the government and most health organizations continue to recommend that polyunsaturated seed oils replace saturated (animal) fats[2]. Fifth, the public is rarely if ever advised to reduce the absolute amount of omega-6 intake to pre-industrial levels[3].

        References
        1. https://evilcyber.com/nutrition/disrobing-dogma-polyunsaturated-fat-and-health/
        2. https://www.hsph.harvard.edu/news/press-releases/saturated-fat-polyunsaturated-fat-cut-heart-disease-risk/
        3. https://www.asbmb.org/asbmbtoday/asbmbtoday_article.aspx?id=18

      • “Second, inflammation is not the only issue of concern[1].”

        No, but neither are the issues mentioned in the article you linked. A collection of studies without statistical significance & attempts to “force out” the evils of n-6 from the data available (Ramsden 2011); selected animal studies & short term studies limited to very narrow scenarios etc. etc. With enough attempt, virtually anything can be made to seem harmful. Scare-mongering, nothing more since NONE of the meta-analyses of either prospective cohorts nor RCTs that I’m aware of has shown statistical significance in the supposed detrimental effects of pufa/n-6, Especially when consumed to the extent it is consumed now. E.g. Ramsden had to go the levels TWICE than those currently consumed by the average American.

        Relevance? Virtually none.

        “Third, what constitutes a realistic consumption scenario?”

        How about the amount of pufa consumed in western countries at the moment? Connect that with the recommendable sources of pufa (olive, fish, rapeseed) and what do you get? One part of a healthy diet, e.g. Mediterranean.

        “Fourth, the government and most health organizations continue to recommend that polyunsaturated seed oils replace saturated (animal) fats[2].”

        Since e.g. Mente et al (2009) and Hooper et al (2011) hint that this indeed seems reasonable – as part of healthy diet pattern such as e.g. Mediterranean – I see no problems with this. Safa offers no health benefits as such, with the possible exception of that over refined carbs in CVD prevention.

        “Fifth, the public is rarely if ever advised to reduce the absolute amount of omega-6 intake to pre-industrial levels[3].”

        Perhaps due to the fact that there’s limited evidence of this? A better way would be to increase the consumption of n-3 fatty acids.

      • Both US and European populations get less 7 % of total energy from PUFA (NHANES 2009; FINRISK 2007 etc.) and therefore omega-6 intake is less than 6 % of total energy. This is the big picture, a realistic scenario. No harm showed at this level. Here in Nordic contries oils rich in omega-6 oils are not recommended. New Nordic recommendations endorse canola, flaxseed or olive oil. US may be different due to argicultural and food politics. Don’t know.

  7. David, still promoting that n-6 -scare? No reason to, since adverse effects seem to occur only when the amount of pufa is SEVERAL times that of what we Westeners get now. Not very realistic.

    Reply
    • @Meghann.
      Thanks for providing the dailytelegraph link. It appears they are referring to the meta-analysis performed by Hiroshi Noto and coworkers which I also cited in my article. This is a systematic review of studies lasting for more than one year. They did not find any randomized clinical trial that fulfilled their selection criteria. So, only observational studies were included in their meta-analysis. Such a meta-analysis is difficult to perform because of methodological differences between studies. Selection bias does also have to be taken into account. Although adjustments were made for some of the risk factors, there may be differences between the groups, other than differences in carbohydrate consumption. Also remember that such an analysis of observational studies does not prove a causative relationship between low carb diets and mortality.

      Large studies, like the Nurse´s Health Study, which included almost 83.000 women did not show an increased risk of heart disease with low carb, higher protein and fat diets. Indeed, when vegetable sources of fat and protein were chosen, these diets appeared to moderately reduce the risk of heart disease.

      So, for the time being we have to live with the fact that the long term effects of low carb, high fat diets compared to other diets have not been clearly defined and will continue to be debated. However, I guess we all agree on the negative effects of refined sugars and its role for the obesity epidemic. If somebody suffers from obesity or metabolic dysfunction related to overweight, and does not get results with the traditional advice, it is hard to understand why we should not recommend the low carb, high fat approach which has helped so many.

      Reply
      • “Large studies, like the Nurse´s Health Study, which included almost 83.000 women did not show an increased risk of heart disease with low carb, higher protein and fat diets.”

        Neither did the meta-analysis by Sato et al. However, there was a statistically significant increase in all-cause mortality. Cancer, anyone?

      • Mie. Increased cancer risk was my first thought as well. However, the risk of cancer by low carb diets was found to be non-significant in Hiroshi Noto´s meta-analysis. So, if it´s not cardiovascular disease and not cancer, what is it then?. Their study cannot really explain what causes the difference in overall mortality. Personally, I think a meta-analysis of observational studies may be problematic. There is no intervention. Moreover, there is often heterogeneity between studies, and different definitions are used. The concept of meta-analysis was initially intended for the aggregation of similar studies.

      • Low carb diet pattern in these kind of cohort studies reflect diet rich in red and processed meat and marginally lower in carbohydrates. Red and processed meat is the biggest source of animal protein and fat in western diets. In Finland we consume more than 1 kilo red and processed per week (compared 300 grams fish and 400 grams poultry).

        So, I suspect that what we really see in the meta-analysis of Noto is the effect of high red meat consumption. This notion is supported by multiple meta-analyses on red and processed meat in many devastating diseases. Those who are described as low carb dieters, are not truly following healthy low carb diet.

      • Thanks Reijo. I definitively agree and I think you make a very important point here. Red meat might indeed play an important role here. A low carb diet is not just a low carb diet. There are both unhealthy and healthy ones. So, if you chose low carb, you should really strive to make it as healthy as possible, for example by being careful with processed meat products etc.

      • “However, there was a statistically significant increase in all-cause mortality. ” – as this could be traffic accidents or a myriad other things I don’t think it sheds any light at all.

  8. @ Mie, I’m not promoting a scare. But it’s scary that almost the entire world is now consuming excessive amounts of omega-6.

    What one consumes in terms of fat intake gets incorporated into cell membranes and fat stores. One of the most frightening aspects of the matter is that during the third trimester of a pregnancy, fatty acids stored in fat tissues are used to construct brain tissue. Excerpt:

    Because the first neurons evolved in an environment high in the n−3 (omega-3) fatty acid docosahexaenoic acid (DHA), this fatty acid became a major component of neural structure and function and makes up 10% of the dry weight of the human brain. Since n−3 fatty acids must come from the diet, this suggests a possible positive role for dietary n−3 fatty acids in cognition and a possible negative role for n−6 fatty acids, which compete with n−3 for access to critical enzymes. Because human females must provide DHA for the growth of the unusually large brains of their offspring from maternal fat stored during childhood, their need for DHA is especially great. We used stepwise regression to determine whether particular dietary fatty acids and other nutrients were related to cognitive performance in over 4000 American children aged 6–16 from the Third National Health and Nutrition Examination Survey; a variety of possible biological, social, and environmental
    risk factors were statistically controlled. In this context the only dietary factors related to cognitive performance were n−3 and n−6 fatty acids. Dietary n−3 fatty acids were positively related to cognitive test scores in male and female children, while n−6 showed the reverse relationship, significantly so in females. In female children the positive effects of n−3 intake were twice as strong as in males and exceeded the negative effects of lead exposure. This suggests that increasing dietary intake of n−3 and decreasing n−6 fatty
    acids may have cognitive benefits in children, especially in females. https://www.ncbi.nlm.nih.gov/pubmed/22065957
    Also: https://www.deepdyve.com/lp/elsevier/different-fatty-acid-pattern-in-breast-milk-of-obese-compared-to-NFxfyxkrxz

    Another excerpt:
    An absolute and relative change of omega-6/omega-3 in the food supply of Western societies has occurred over the last 150 years. A balance existed between omega-6 and omega-3 for millions of years during the long evolutionary history of the genus Homo, and genetic changes occurred partly in response to these dietary influences. During evolution, omega-3 fatty acids were found in all foods consumed: meat, wild plants, eggs, fish, nuts and berries. Studies by Cordain et al. on wild animals confirm the original observations of Crawford and Sinclair et al. However, rapid dietary changes over short periods of time as have occurred over the past 100–150 yr is a totally new phenomenon in human evolution. https://ebm.rsmjournals.com/content/233/6/674.long

    Excerpt from a PLEFA letter to the editor:
    What really has changed during the last half of the 20th century is the quality of the fat, with an increased use of vegetable oils to exchange the diary fat and reduce the intake of saturated fat. Most of these oils have a very high content of omega-6 fatty acids, although the variation is large, being more than 100-fold between sunflower oil and rape seed oil. Simultaneously the intake of fish has decreased, thus resulting in a lower intake of long chain omega-3 fatty acids, all together resulting in a much higher ratio of omega-6/omega-3 in food and fodder globally. This is clearly documented in breast milk…All results in humans and animals challenge the present recommendations, and indicate that we have to decrease the omega-6 intake instead of extending the use of extra supply of omega-3 fatty acids.

    The research if taking place but it is not being widely publicized. One needs to dig into the scientific literature for details is one wants to truly understand how industrialization of the food supply affects various aspects of human health. The above is just a small sampling of what’s out there.

    Reply
    • “Mie, I’m not promoting a scare. But it’s scary that almost the entire world is now consuming excessive amounts of omega-6.”

      Err, try and put that into less subjective terms. I’ll quote myself from an earlier post concerning the issue of n-6 and CVD:

      “According to NHANES 2009-10, a regular American gets about 6,5% of total energy intake from n-6 fatty acids. If we compare this to e.g. Sydney Diet Heart (which, according to some, offered further proof of the detrimental effects of n-6 fatty acids) where the amount of n-6 was about 12+ % of total energy intake, you’ll see that there’s little reason to be alarmed. Even less reason if we consider that current dietary recommendations argue for adequate n-3 intake.”

      Then, something about the case of cognitive performance. The study was based on samples from older NHANES, which isn’t really ideal and certainly far from being able to establish causal relations. If you know of any quality trials which examine the role of n-6 fatty acids independently, please let me know.

      And the protective effect of n-3 fatty acids isn’t on very solid ground either. Riediker et al. (2009) reviewed three small RCTs in which the effects were small. After this, Quinn et al. 2011 and Yurko-Mauro et al. 2010) – both of which had hundreds of participants – but the results weren’t that “hot” either. At best, it seems that the effect is kinda small & it doesn’t appear in all groups who could be expected to benefit from n-3 supplementation.

      Reply
      • It’s, “try to put that into less subjective terms.” Excerpts from a September 2003 article by global obesity expert Barry Popkin:

        “The world’s nutrition problems have changed dramatically in recent years in a way most Americans probably have difficulty fathoming: In most of the developing world, obesity is now a larger problem than malnutrition. Here’s why.

        If you lived in a village or urban-slum area in China or Mexico or Egypt 25 years ago, you were unlikely to have electricity or pumped water. You certainly did not know what television was; you walked to work or rode a cart linked to an animal; and your work was physically very strenuous. Your diet was monotonous and was based on rice or wheat products with possibly a few vegetables and/or beans, and few condiments and NO COOKING OIL (emphasis mine). If you go back to those same villages or slum areas today, people have electricity and television, their transportation is often via a bus or gas-powered vehicle, and their work utilizes some type of gas-powered engine. And THEIR DIET INCLUDES A LOT OF VEGETABLE OIL (emphasis mine) and some processed-food products that contain added sugar. Some animal-source foods — be they chicken, beef, pork, goat or fish products — are consumed, as well.

        Worldwide today, the number of obese people far exceeds the number of undernourished ones. This is a startling development that requires some explanation. What is happening to the diets of the world? Again, imagine how bland and healthful the diets of Mexicans might have been. When at their best, rice, beans, tortillas and a little citrus juice produce a well-balanced diet that is LOW IN OIL (emphasis mine) and sugar and high in fiber and many critical nutrients. But the modern food-processing industry and added consumer income, urbanization, improved transportation, TV, food advertising and other changes have led to DIETS THAT ARE MUCH HIGHER IN FAT (emphasis mine) and added sugar.

        Healthful fruits and vegetables are not increasing much in people’s diets, while they are more likely to consume sugared water in some soft drinks or fruit drinks and ADD A LOT OF VEGETABLE OIL TO THEIR DISHES (emphasis mine). And they consume more meat.

        A revolution has occurred. For instance, in the early 1980s, no adults in China consumed what we call a high-fat diet with more than 30 percent of their calories from fat. Today, over half of Chinese adults consume such a diet. In China, dietary shifts are very quickly occurring. Rice and flour intake is down, and animal-source foods such as pork and poultry and fish are way up, and THE STEEPEST INCREASE IS IN THE USE OF EDIBLE VEGETABLE OILS FOR COOKING (emphasis mine)…THE EDIBLE-OIL INCREASE IS FOUND THROUGHOUT ASIA AND AFRICA AND THE MIDDLE EASE AS A MAJOR SOURCE OF CHANGE (emphasis mine).”
        https://articles.orlandosentinel.com/2003-09-28/news/0309270148_1_overweight-or-obese-women-were-overweight-south-africa?pagewanted=all

      • David

        “It’s, “try to put that into less subjective terms.””

        Oh my God! The fact that I used a colloquial expression typical of American English totally demolished all the points I had. Dave, you rule! 🙂

        Seriously, Dave. By “less subjective” I didn’t mean “copypaste parts of an article & capitalize whatever you think might be relevant”. No, no and no. You need to define “excessive amounts” by providing evidence from research literature.

        Please try. For once, I’d like to believe that this isn’t just another case of silly low carb/paleo dogmas that have spread like wildfire.

      • I try to say exactly what I mean when I write about nutritional issues and controversies. When someone responds with sarcasm or exaggeration (totally demolished all the points…Dave, you rule), or ridicules my attempts to communicate information about the omega-6 hazard(silly..dogmas), I don’t know what to think. I don’t take it personally because, if someone wants to use that style of communication to defend a belief, that is the person’s prerogative.

        Mie wrote, “…a regular American gets about 6,5% of total energy intake from n-6 fatty acids.”

        An estimate, is it not? But what of those who consume far more than 6.5%? For many years the sugar interests insisted that high sugar intake was not related to obesity because, on average, skinny people consume more sugar than fat people. That’s likely true as far as it goes. But people vary in their response to nutrients according to how their metabolism’s are configured. For example, “Five healthy students were found to maintain their serum lipid levels within the normal range despite relatively high sugar content of their home diet. The students did not develop significant hyperlipemia even after their average dietary sugar content was raised to 285-300 g/per day for three weeks. This amount if dietary sugar constituted about 30-40% of their daily caloric intake…Feeding experiments suggested that it was necessary to raise the dietary carbohydrate to 85-90% of the total calories, and to supply the major proportion of it as sugars, before significant degrees of hyperglyceridemia could be induced in subjects who did not have disturbances in carbohydrate and glyceride metabolism.” https://ajcn.nutrition.org/content/20/2/116.abstract

        Another question arises. Is a percentage of total energy intake important or is it the absolute amount of omega-6 consumed that is causing the damage? Quote from a scientific article authored by William Lands:

        “Dietary n-3 and n-6 fatty acids compete in the desaturation, elongation, acyltransferase, and hydrolysis events that maintain tissue HUFA levels [5••]. The competitive metabolism is more visible when dietary supplies of n-3 and n-6 are similar and near 1% of food energy, but it is always present[48]. Current intakes of the n-6 linoleate in United States are much higher now than a century ago, and a controlled experiment showed that an accumulated n-3 HUFA, eicosapentaenoic acid (20:5n-3), was lower when dietary linoleate was 10.5% of food energy rather than 3.8% [49]. The result illustrates the merits of direct HRA monitoring of tissue status rather than attempting to manage uncertainties about competing interactions among nutrients.”
        https://www.ncbi.nlm.nih.gov/pubmed/19500490

        A bit more evidence from research literature:
        Abstract
        Several sources of information suggest that human beings evolved on a diet with a ratio of omega-6 to omega-3 essential fatty acids (EFA) of ~1 whereas in Western diets the ratio is 15/1–16.7/1. Western diets are deficient in omega-3 fatty acids, and have excessive amounts of omega-6 fatty acids compared with the diet on which human beings evolved and their genetic patterns were established. Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today’s Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 PUFA (a lower omega-6/omega-3 ratio), exert suppressive effects. In the secondary prevention of cardiovascular disease, a ratio of 4/1 was associated with a 70% decrease in total mortality. A ratio of 2.5/1 reduced rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4/1 with the same amount of omega-3 PUFA had no effect. The lower omega-6/omega-3 ratio in women with breast cancer was associated with decreased risk. A ratio of 2–3/1 suppressed inflammation in patients with rheumatoid arthritis, and a ratio of 5/1 had a beneficial effect on patients with asthma, whereas a ratio of 10/1 had adverse consequences. These studies indicate that the optimal ratio may vary with the disease under consideration. This is consistent with the fact that chronic diseases are multigenic and multifactorial. Therefore, it is quite possible that the therapeutic dose of omega-3 fatty acids will depend on the degree of severity of disease resulting from the genetic predisposition. A lower ratio of omega-6/omega-3 fatty acids is more desirable in reducing the risk of many of the chronic diseases of high prevalence in Western societies, as well as in the developing countries.https://ebm.rsmjournals.com/content/233/6/674.long

        Excerpt from a Letter to the Editor published in Prostaglandins, Leukotrienes, and Essential Fatty Acids 85 (2011) 405-406
        In the paper of Guesnet et al. [1] in the present issue, the interaction between omega-6 and omega-3 fatty acids are illustrated in a thought-provoking way. It adds to the increasing evidence of a relation between the changes of this ratio in human and animal diets and the global epidemics of increases of metabolic complications as obesity, diabetes and neurological diseases. A recent paper analyzing the plurality of the obesity epidemics, Klimentidis et al. [2] express their concern about that also primates, domestic and feral animals are developing obesity and furthermore that a similar trend is observed in laboratory animals. The interesting fact is that neither the fat content of the chow or the fat intake of the human population has increased over the latest decades [3], so other environmental causes are probably involved. In the humans special interest has been focused on less physical activity depending on the technical development worldwide, but this alone cannot explain the obesity epidemics, which also involve infants and the population in developing countries [2]. It is certainly less likely in laboratory animals, whose living conditions have been rather the same for many decades.

        What really has changed during the last half of the 20th century is the quality of the fat, with an increased use of vegetable oils to exchange the diary fat and reduce the intake of saturated fat. Most of these oils have a very high content of omega-6 fatty acids, although the variation is large, being more than 100-fold between sunflower oil and rape seed oil. Simultaneously the intake of fish has decreased, thus resulting in a lower intake of long chain omega-3 fatty acids, all together resulting in a much higher ratio of omega-6/omega-3 in food and fodder globally [4,5]. This is clearly documented in breast milk [6].

      • Here in South Africa we have a Dr. Tim Noakes – a sports scientist and he has just written a recipe book called “the real meal revolution”. It’s what people like Dr. Peter Attia, Dr. Michael Eades, Dr Donald Miller (thoracic surgeon), and others suggest. It’s definitely NOT high protein – one of the major newspapers here, had to publish an apology last Sunday for calling Tim Noakes’ book a high protein diet. It is Low Carb, HIGH fat and moderate protein (I eat duck, goose, eggs, a tablespoon of extra virg cold pressed coconut oil everyday (must admit ygh ygh ygh – but will endure) plus double cream, only butter, extre virg Olive oil (TONS of it – i refrigerate it in large jars just to be safe), and lots and lots of mackerel, sardines and salmon and green veggies and now and then some other veg. Look, I could really do with a lovely Doughnut right now, but I just don’t. I am very thin (naturally) – for me it’s about cholesterol, period. I just WISH I could find a cardiologist who doesn’t fight me on this. I go for those profusions and thus far I have clean arteries – I am 58. Sorry about the much writ. Cheers

  9. I have been on the Atkins diet for one year now. I lots 35 lbs. in the first 6 mo. and have been maintaining since. I have increased my good carbs since the induction stage and figured out about how many I can have without gaining. I have an egg and sausage for breakfst every morning but for the most part have mono and polyunsaturated fats in the rest of my daily routine and do not eat white flour, pasta, root vegetables or refined foods. My cholesterol has been elevated but my ratio is excellent.. The AMA has it all wrong and our nation will continue to be sick and obese until we are educated about the success of low carb diets…

    Reply
  10. Without a doubt my best research is my body…and I encourage others to listen to what theirs is telling them especially when it comes to food choices. By choice my diet is very clean…gluten, dairy, sugar & yeast free. I don’t eat any grains, processed or packaged food or those awful refined vegetable oils…just coconut, olive & sesame oil for me. So its mainly carbs & protein from vegetables, salads, lamb, fish, chicken, nuts…you know like we used to eat years ago. For the last 6 weeks I have cut out all fruit as my body felt better without it…and I found that the fructose in fruit was creating cravings to want to eat more. Since stopping fruit I don’t really snack and feel satisfied after meals. And why do I choose this way to eat you may ask? Because I listen to my body & what it needs & I feel so much more vital and energised. I feel what to eat…not eat what I feel. All this mumbo jumbo about low carb diets being dangerous is just silly…anybody can come up with research to confirm whatever it is they have decided is truth for them! Thank god for free will & choice…

    Reply
    • “l this mumbo jumbo about low carb diets being dangerous is just silly…anybody can come up with research to confirm whatever it is they have decided is truth for them!”

      But in that case the research won’t stand up to scrutiny.

      Reply
      • But the question is who has the guts to challenge consensus opinions?

        If you look at the paper I’ve linked to below you can see just how long it’s taken before someone has taken the trouble to go back to the original research concerning saturated fats and check on the original classification of those saturated fats and the courage to state the obvious.

        How many researchers actually are prepared to put their jobs, careers and financial security on the line to support research that is contrary to the consensus?

      • Yes Ted. It´s admirable. I found the paper extremely interesting. The whole thing is a bit scary. If the initial definitions from the SCS were wrong, the whole conclusion is out of order. I was thinking about writing a blog post focusing on the paper. Hope I can find a time to do it soon. Again, thanks for drawing my attention to it.

      • What is this “conclusion” that you referring to? The role of safa in nutrition? The current scientific opinion on the issue has virtually nothing to do whatsoever with SCS: yes, it was a starting point, but its value nowadays is purely historical. You might as well argue that the fact that Newtonian physics is outdated would somehow indicate that our current knowledge of e.g. the universe is inherently false.

      • Ted, I’m not too enthusiastic about this “who dares challenge the consensus” thing which I consider to be one-sided and mostly irrelevant. Once again, let’s take the safa issue as an example: during the past 3+ years, we’ve seen a number of meta-analyses challenging the role of safa in CVD. I fail to see any “scare” or “blacklisting” in the scientific community in connection with these issues.

        In addition, about the consensus: you do know that one well-known example of publication bias is the fact the studies reporting outcomes different to the current opinion are more LIKELY to get published than x amount of studies confirming the current opinion?

  11. Dave:

    “But what of those who consume far more than 6.5%?”

    Well yes, what of those?

    Dave, please try to understand that copypastying something you’ve come across on the Internet does not constitute a proper argument. None of the studies you referenced actually demonstrates the dangers of this alleged “excessive” intake of n-6. What you have listed is, at best, SUGGESTIVE. There is virtually no evidence from studies looking at e.g. cancer of CVD endpoints that would prove that current intakes of n-6 are are problem. The best we’ve got on e.g. the latter is Ramsden et al, and there the intake of n-6 had to be TWICE the current intake before problems started to occur.

    Reply
    • “There is virtually no evidence from studies looking at e.g. cancer of CVD endpoints that would prove that current intakes of n-6 are are problem.”

      Isn’t that backwards? Studies do not PROVE anything. Studies are the sort of science that is only suggestive. It’s experimental biochemical research that furnishes confirmation. Currently, that sort of research involving omega-6s is being ignored. Sometimes scientists even have trouble getting it published. For example:

      “Our hypothesis is that levels of omega 6 are so high in our bodies that any more unsaturated fatty acid — even omega 3, despite its health benefits — will actually contribute to the negative effects omega 6 PUFA have on the heart and gut,” said Ghosh. “When there is too much [polyunsaturated fatty acid], the body doesn’t know what to do with it.”

      This is not the first time that Ghosh has produced findings that turned popular notions about nutrition and health on their head.

      As a graduate student Ghosh discovered by accident that so-called “heart healthy” oils rich in Omega-6 polyunsaturated fatty acids inflicted damage to the hearts of rats and neo-natal pigs.
      The result was so shocking that Ghosh was turned down for publication by all the major scientific journals. https://life.nationalpost.com/2013/01/23/excessive-omega-fatty-acids-may-make-heart-health-worse-not-better-b-c-researchers/

      Also:

      “Southampton researchers have demonstrated that mothers who have higher levels of n-6 polyunsaturated fatty acids (PUFAs), which are found in cooking oils and nuts, during pregnancy have fatter children.”
      https://www.southampton.ac.uk/mediacentre/news/2013/jan/13_06.shtml

      Finally, I don’t just come across things on the internet that I copy and paste. I am simply furnishing excerpts from articles you can read if you’ve a mind to click on the links I provide. Currently, the scientific consensus is that omega-6s are not a problem. In a 2003 speech delivered to the California Institute of Technology, Michael Crichton said, “I regard consensus science as an extremely pernicious development that ought to be stopped cold in its tracks. Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you’re being had. Let’s be clear: the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world. In science consensus is irrelevant. What is relevant is reproducible results. The greatest scientists in history are great precisely because they broke with the consensus. There is no such thing as consensus science. If it’s consensus, it isn’t science. If it’s science, it isn’t consensus. Period.” https://www.cfa.harvard.edu/~scranmer/SPD/crichton.html

      Reply
  12. Dave:

    “Isn’t that backwards? Studies do not PROVE anything. Studies are the sort of science that is only suggestive.”

    And here I was, thinking that the whole idea behind a randomized controlled trial was to confirm causal relationships. Oh well, I guess someone better notify e.g. the “Big Pharma” …

    C’mon Dave, seriously!

    “It’s experimental biochemical research that furnishes confirmation.”

    Errr, not really. Here’s the fundamental problem with biochemists vs nutritionists: the former can’t often see the forest for the trees. The fact that there’s a mechanism doesn’t tell whether that mechanism will actually a have perceivable, meaningful effect in REAL life or not. Let’s take saturated fat as an example. Yes, there’s solid evidence from metabolic ward studies that it indeed raises LDL levels in humans. But is the case really THAT simple in real life where people don’t spend their time in metabolic wards? Both cohort and RCT evidence teels a different story.

    So, back to n-6: the evidence from RCTs tells us that the potential inflammatory effects of n-6 fatty acids really don’t constitute that much of a problem in real life setting. See this systematic review of linoleic acid & inflammation markers:

    https://www.andjrnl.org/article/S2212-2672(12)00464-9/abstract

    And n-6 fatty acids also have anti-inflammatory qualities, see e.g. this

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2217562/

    If you wish to challenge these findings Dave, you’d better come up with either a) a recent meta-analysis of RCTs telling otherwise or b) a large recent RCT showing the anti-inflammatory effects of n-6 & either risk marker data or CVD end point data. So …?

    And a word of advice: irrelevant nonsense from Crichton will get you nowhere.

    Reply
    • “So, back to n-6: the evidence from RCTs tells us that the potential inflammatory effects of n-6 fatty acids really don’t constitute that much of a problem in real life setting.”

      RCTs wherein n-6 is increased above average levels of intake to study it’s inflammatory effects tell us nothing about what happens when n-6 is decreased below pre industrial levels. It’s sort of like forcing someone, drowning in eight feet of water, into 12 feet of water to see what happens in terms of distress level. The World is currently drowning in industrial seed oils.

      “If you wish to challenge these findings Dave, you’d better come up with either a) a recent meta-analysis of RCTs telling otherwise or b) a large recent RCT showing the anti-inflammatory effects of n-6 & either risk marker data or CVD end point data. So …?”

      Google – PDF Dietary Fat Quality and Coronary Heart Disease. Excerpt:

      “The only long-term trial that reduced n-6 LA intake to resemble a traditional Mediterranean diet (but still higher than preindustrial LA intake) reduced CHD events and mortality by 70% [31]. Although this does not prove that LA intake has adverse consequences, it clearly indicates that high LA intake is not necessary for profound CHD risk reduction.”

      “And a word of advice: irrelevant nonsense from Crichton will get you nowhere.”

      Dr. Crichton’s comment about consensus science would, indeed, be “irrelevant nonsense” if consensus were the proper test for the validity of opinions. But here’s the thing. Dr. Sigurdsson wrote this blog post precisely because the long-standing, widely accepted doctrine that saturated fats clog arteries is now being widely challenged and vigorously debated. So if consensus swings to the opposite side (I’ve been wondering, for more than three decades, when this would happen), how can anyone maintain that it is irresponsible to go against consensus of opinion? Quotes from this video: https://video.au.msn.com/watch/video/is-saturated-fat-good-for-you/x4goj61

      Christine: “The vilification of fat is the biggest health mistake we’ve made in history. That’s my belief.”

      Dietitian: “I actually think that’s really irresponsible because there have been decades of research and tens of thousands of studies done to show that saturated fat is linked to heart disease, dementia, some forms of cancer It’s not OK for that kind of message to be getting out there.”

      Christine: “Everyone’s following conventional diets, but the problem’s not going away; it’s getting worse.

      Dietitian: “If that was the case, then the Heart Foundation, the World Health Organization, all big medical bodies around the World would be saying saturated fat is what we should be eating and that’s not happening.”

      So what does consensus science accomplish? Nothing good as far as Dr. Laura Corr is concerned. Excerpt:

      Ask almost member of the general public about a diet which would reduce their chance of heart disease and the reply is the same: ‘a low fat diet’. On closer questioning, this means a diet with a reduction in cholesterol and saturated ‘animal’ fats, i.e. less meat, butter, milk and cheese. Most national and international recommendations for the prevention of heart disease, whether for primary prevention of or for patients who have developed the clinical manifestations of coronary heart disease, have made dietary restriction of total and saturated fats and of cholesterol the primary advice and often the sine qua non in relation to all other forms of management. To this extent they are to be congratulated that the message seems to be so universally accepted. Unfortunately, the available trials provide little support for such recommendations and it may be that far more valuable messages for the dietary and non-dietary prevention of coronary heart disease are getting lost in the immoderate support of the low fat diet.” https://www.omen.com/corr.html

      That was 1997. Not much change in consensus as yet.

      Reply
      • “RCTs wherein n-6 is increased above average levels of intake to study it’s inflammatory effects tell us nothing about what happens when n-6 is decreased below pre industrial levels.”

        Well then, show me some RCTs where such a reduction is achieved.

        But darn it, you can’t! Such trials don’t exist!

        So instead of this, form a SOLID argument why such a thing would be beneficial – with reference to trials indicating this.

        But darn it, again! You can’t because the evidence from trials doesn’t support this either!

        “The only long-term trial that reduced n-6 LA intake to resemble a traditional Mediterranean diet (but still higher than preindustrial LA intake) reduced CHD events and mortality by 70% [31]. Although this does not prove that LA intake has adverse consequences, it clearly indicates that high LA intake is not necessary for profound CHD risk reduction.”

        Dave, you do realize that this refers to Lyon Heart Study, which was a multi-factorial trial? Heck, there’s a very clear reason why the authors CLEARLY state that this doesn’t prove their/your argument!

        “Dr. Crichton’s comment about consensus science would, indeed, be “irrelevant nonsense” if consensus were the proper test for the validity of opinions. But here’s the thing. Dr. Sigurdsson wrote this blog post precisely because the long-standing, widely accepted doctrine that saturated fats clog arteries is now being widely challenged and vigorously debated. So if consensus swings to the opposite side (I’ve been wondering, for more than three decades, when this would happen), how can anyone maintain that it is irresponsible to go against consensus of opinion?”

        Dave, you’re going for a strawman argument here. No one’s suggesting that going against the current scientific opinion is irresposible or bad. What I’m arguing is that an argument or opinion isn’t valid JUST because it goes against the current opinion.

        Furthermore, I’m saying that the whole “boohoo, bad consensus” thing is a silly way of approaching the matter. The focus should be on scientific evidence, not secondary school level philosophy of science. So pretty please with sugar on top: could we just focus on the REAL ISSUE?

        About which: am I to conclude that you have nothing relevant to back up your position on n-6 fatty acids? Ramsden et al (the PDF which you mentioned) points out – despite the fact that the authors try their best to make it seem otherwise by referring to ecological/historical data – that there is currently no experimental (RCT) evidence indicating that the amount of n-6 fatty acids in current western diet is problematic as such. Period. So what you got is ecological data and (to some extent cherry-picked) historical data from a selected group of our ancestors – which of course is hopelessly inadequate in this sense.

      • “Well then, show me some RCTs where such a reduction is achieved.”

        I thought I made it clear that there aren’t any RTCs in which n-6 was deliberately reduced. That being the case, how can health authorities be certain that increasing omega-6 intake, which is already overly high, will reduce heart attack risk?

        “So instead of this, form a SOLID argument why such a thing would be beneficial – with reference to trials indicating this.”

        RCTs, it would seem, are the only kind of science you seem willing to pay attention to. Too bad because there’s this:

        “In 1938, a biochemist William Brown volunteered to go six months eating an extremely low-fat diet. He consumed a diet of defatted milk and cottage cheese, sucrose, potato starch, orange juice and some vitamin and mineral supplements. His blood lipids became more saturated and their concentrations of linoleic and arachidonic acids were cut in half. He experienced an absence of fatigue, his high blood pressure returned to normal, and migraines he had suffered from since childhood vanished, his metabolic rate increased and he lost weight, his respiratory quotient increased suggesting greater carbohydrate oxidation, lower respiratory quotients are associated with diabetes. The diet produced no deficiency, and likely corrected a PUFA excess. Six months on a specially prepared laboratory diet, no deficiency, if these fats are essential they’re essential in such tiny amounts that its almost meaningless to call them essential.”
        https://pranarupa.wordpress.com/2012/12/25/pufa-because-this-wouldnt-be-a-ray-peat-themed-blog-without-at-least-one-post-on-pufa/

      • “RCTs, it would seem, are the only kind of science you seem willing to pay attention to.”

        Err, no. However, they are the BEST kind of science to offer insight into matters like this.

        “Too bad because there’s this:”

        N = 1? And a website which claims that pufa is toxic despite the fact that we just established that there is NO evidence to back up such a ridiculous claim?

        Dave, are you trying to terminate our discussion by constantly reaching for new lows? 🙂

  13. I’m going to play devils advocate on this one and think with my R.D. brain. The problem with most of these studies is that they are not defining “Low Carb” or “High FatProtein” they are saying lower carb and higher fat/protein. You lose weight by cutting calories we all know calories in vs. calories out. The DASH and TLC are essentially this diet. If you are truly on a low carb, high fat diet you would essentially be eating only meat, nuts, and vegetables. However, since most of the said diets above also include sweet potatoes, milk, beans, peanuts, fruit— which are ALL sources of Carb then they are not necessary “Low Carb” but they are “Lower Carb”– 2 g/kg/day body weight (IBW if obese or LBM if you’ve been able to test for that with bod pod or other methods). The problem here is processed food, inflammation, limited physical activity and hypercaloric feeds. This is what we are trying to educate the public on. If you want to follow your Atkins diet and eat 4,000 kcals of meat, butter, and veggies all day long then go ahead but you will not lose weight permanently based on macronutrient distribution– it has been studied over and over. Calories in vs. Calories out. If someone finds that if they cut out certain foods (i.e. dairy or grains or whatever it may be) will help then lose weight and they can stick to that diet and it works for them then that’s great and the weight loss is what will make most of the difference in their overall health. I also know people that eat high fat dairy and meat and loads of Carb but they work out several hours a day and are in excellent health because of it (great vitals, lipid panel, bmi etc…). Just food for thought here. Happy National Nutrition Month!

    Reply
    • “If you want to follow your Atkins diet and eat 4,000 kcals of meat, butter, and veggies all day long then go ahead but you will not lose weight permanently based on macronutrient distribution– it has been studied over and over.”

      It’s well established that “calories count.” It’s also true that metabolism counts, hormone balance counts, and appetite counts.

      The point of carbohydrate restriction is that, if done properly, it heals the metabolism, balances hormonal action, and normalizes appetite. However, if a carbohydrate restricted diet is high in omega-6, among other deleterious effects there can be problems with chronic pain and appetite dis-regulation. https://sciencenordic.com/vegetable-oils-promote-obesity

      Reply
      • Agreed. I wish more cardiologists and nutritionists would read Gary Taubes’ excellent book,”Why We Get Fat.” It’s a clear, scientific, logical look at the past 100 years of research into obesity and nutrition.

    • “If you are truly on a low carb, high fat diet you would essentially be eating only meat, nuts, and vegetables. ”

      That’s not true — not at all. If you are TRULY on a low-carb diet such as Atkins, you are eating meat, sure — but you are also eating also turkey, salmon, shrimp, chicken, tuna salad, pork, eggs, bacon, shrimp, scallops, lamb, lobster, and cheese. And of course salad, green peppers, asparagus, zucchini, mushrooms, broccoli, cauliflower and other low-carb veggies. Even blueberries and strawberries occasionally. Doesn’t that sound like a really, really healthy diet?

      People who have never been on a healthy, low-carb diet — one that includes low-carb salads and vegetables — have been using “scare tactics” for decades to try to convince us that low-carb eating is dangerous. I don’t understand this at all — not when study after study is showing that everything we believed about fat and carbs may have been twisted by scientists with agendas, and of course the food and pharma lobbies.

      It’s good news that thousands of cardiologists are finally starting to speak up and tell the truth: the low carb way of eating is safe and healthy. Since eliminating sugar, wheat, corn and high-sugar fruits from my diet, I have become slim, strong and healthy. I eat wonderful salads, berries with whipped cream, shrimp casserole with asparagus, omelets, even chicken fajitas with avocado in low-carb wraps. This way of eating is DELICIOUS. You can enjoy food, you are never hungry, you are full of energy and YOU DON’T GET OBESE. Oh and yes, my cholesterol is normal, my blood sugar is normal, and my weight is ideal.

      Reply
  14. RCTs “are the BEST kind of science to offer insight into matters like this.”

    From Wickipedia: “RCTs are considered by most to be the most reliable form of scientific evidence in the hierarchy of evidence that influences healthcare policy and practice because RCTs reduce spurious causality and bias.” https://en.wikipedia.org/wiki/Randomized_controlled_trial

    There’s that consensus of opinion again. I’m not clear on what is meant by the phrase “matters like this.” You’re talking about the efficacy of medical or nutritional interventions, right? One would think that five decades of public health policy based on the notion that saturated fats clog arteries along with “thousands of studies” would produce some definitive results. In other words, if the actual cause of heart disease could be verified by RCTs, one would think that public health policy would have reduced the incidence of heart disease by now. But no. Heart disease is spreading along with the proliferation of omega-6 industrial seed oils. Meanwhile, scientists are still trying to blame saturated fats. Excerpt:

    “The ingestion of excessive amounts of saturated fatty acids (SFAs) and transfatty acids (TFAs) is considered to be a risk factor for cardiovascular diseases, insulin resistance, dyslipidemia, and obesity. The focus of this paper was to elucidate the influence of dietary SFA and TFA intake on the promotion of lipotoxicity to the liver and cardiovascular, endothelial, and gut microbiota systems, as well as on insulin resistance and endoplasmic reticulum stress. The saturated and transfatty acids favor a proinflammatory state leading to insulin resistance. These fatty acids can be involved in several inflammatory pathways, contributing to disease progression in chronic inflammation, autoimmunity, allergy, cancer, atherosclerosis, hypertension, and heart hypertrophy as well as other metabolic and degenerative diseases.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572653/

    I refer you to “The Modern Nutritional Diseases: And How to Prevent Them” by Fred and Alice Ottoboni. Excerpt from the 2002 edition of the book:

    “The current relentless pressure to convert the entire population to a low-fat, high carbohydrate dietary regime seems to be driven by a curious set of circumstances. It began with an idea aimed at inducing
    the public to buy and eat foods that are profitable to the agricultural and food industries as opposed to foods that man was designed to eat. With judicious use of public relations, advertising, pseudo science, and political prowess, this idea has grown into a sophisticated and powerful movement that is changing eating habits throughout the world. Concurrently, the national priority aimed at the treatment of the modern nutritional diseases, rather than their prevention, has focused medical research on patentable new drugs rather than on preventive methods…The consequences are sobering. Older adults suffer premature
    disabilities and shortened life spans; younger adults, and even children, are increasingly affected by early signs of atherosclerosis, obesity, and type-2 diabetes. Enormous prescription drug and medical care costs have nearly reached the point of overwhelming the national budget. And tragically, a growing body of evidence suggests that the bizarre and increasingly common behavioral problems among young children and teen-agers are related to the combined effects of high sugar intakes and the virtual absence of omega-3 essential fatty acids in the American diet.”
    https://www.amazon.com/The-Modern-Nutritional-Diseases-Diabetes/dp/091524103X

    Abstract from a 2012 article:
    Given the large social impact of dietary advice, it is important that the advice have a solid scientific basis. Evidence-based dietary advice should be built on results from all studies available, according to a given methodology. Conclusions should be a valid representation of the summarized results. The association between saturated fat intake and cardiovascular disease was examined. Results from three reports of
    leading U.S. and European advisory committees were compared with results as they were presented in the articles referred to. Findings were put into perspective with results not included in these reports. Different lines of evidence were included in the different reports. No overlap whatsoever was found in the articles included. Most results from the scientific literature were lacking for most different lines of evidence in all reports. All three reports included the effect of saturated fat on low-density lipoprotein cholesterol in the evidence linking saturated fat to cardiovascular disease, but the effect on high-density lipoprotein cholesterol was systematically ignored. Both U.S. reports failed to correctly describe the results from the prospective studies. Results and conclusions about saturated fat intake in relation to cardiovascular disease, from leading advisory committees, do not reflect the available scientific literature. https://www.nutritionjrnl.com/article/S0899-9007%2811%2900314-5/abstract

    “N = 1? And a website which claims that pufa is toxic despite the fact that we just established that there is NO evidence to back up such a ridiculous claim?”

    I fail to see where WE established anything beyond the fact that we are in substantial disagreement regarding the toxic effects of omega-6s. Excerpt:

    Omega-6 fat intake has sky-rocketed in the last century, so it would seem that we should see a dramatic lowering of heart disease in the USA, yes? No. The incidence of cardiovascular disease has increased in parallel with the increase in linoleic acid intakes in many countries. Linoleic acid is the most commonly eaten omega-6 fatty acid. Notably, people who have died from heart disease have higher blood levels of the omega-6 fat, arachidonic acid.
    https://omega-6-omega-3-balance.omegaoptimize.com/2009/01/30/the-american-heart-associations-agendait-sure-aint-science-or-public-health.aspx

    “Dave, are you trying to terminate our discussion by constantly reaching for new lows?”

    Heavens, no. I’ve been researching these matters for decades. I still have an enormous amount of material I’d like to share.

    Now, a word of advice. When I first began writing essays about nutritional issues and controversies about 30 years ago, I asked an older, more experienced friend to critique one of my early efforts. I can still hear these words in my mind. He said, “Never insult your audience.” So whether I’m writing for an audience of one or a thousand, I try to be respectful, kind, honest, and fair. My goal is never to persuade others to agree with me through argument, but rather to share information.

    Reply
    • “There’s that consensus of opinion again.”

      And once again (for the last time, though, since this conversation isn’t really worth continuing): so what? If you had any REAL criticism against the validity of a randomized controlled trial setting in investigating causality – apart from that “boohoo,consensus” stuff – shouldn’t you have shown it already?

      “In other words, if the actual cause of heart disease could be verified by RCTs, one would think that public health policy would have reduced the incidence of heart disease by now.”

      Dave, please. We do know of several risk factors, but mere knowledge doesn’t really help if the main problems (overweight, crappy diet, too much alcohol etc. etc.) cannot be eradicated.

      In addition Dave, CVD mortality (and CVD incidence, in general) has dropped substantially in many European countries.

      “But no. Heart disease is spreading along with the proliferation of omega-6 industrial seed oils.”

      Correlation equals causation? Please. We’ve just established that there is neither epidemiological nor RCT evidence to support the claim that n-6 fatty acids (in the amount currently consumed by the average Westener) are to blame. Just because you keep repeating something doesn’t make it trye.

      “My goal is never to persuade others to agree with me through argument, but rather to share information.”

      But evidently your goal isn’t to learn from information presented to you nor from criticism which you’ve been unable to counter.

      Anyway, enjoy the rest of your Good Friday. Cheers.

      Reply
      • “But evidently your goal isn’t to learn from information presented to you nor from criticism which you’ve been unable to counter.”

        What criticism? Ridicule isn’t criticism. And sarcasm adds nothing of value to any serious discussion.

        I long ago familiarized myself with the arguments you presented. And like South African physician Timothy Noakes, I don’t think the mainstream view that saturated fats are bad and omega-6 are good has any merit whatsoever. Excerpt:

        “I concluded that the cause of the global epidemic of obesity and diabetes is simple; both conditions occur in those who are genetically carbohydrate-resistant but who persist in eating the high-carbohydrate diet according to the US Dietary Guidelines. This interpretation is not novel – it was the standard teaching in most medical schools in Europe and North America, but disappeared when the fallacious diet/heart hypothesis took hold in the 1970s.

        But if obesity and diabetes are due to the overconsumption specifically of carbohydrates in those who are carbohydrate-resistant, then their prevention and cure require only that those who are the most severely affected eat a high-fat and -protein diet to which carbohydrates contribute less than 60 g per day. Yet as long as these conditions present massive commercial opportunities to the pharmaceutical and food industries, there will be no appetite for such a simple solution. Our sole recourse is to change the behaviours of those at risk, one meal at a time.

        The evidence is tenuous for the related diet/heart hypothesis, which holds that a diet full of ‘artery-clogging saturated fat causes an elevation of blood lipid concentrations, thus promoting coronary atherosclerosis and ultimately heart attack. I argue that the evidence is essentially non-existent.

        Opposing this is that coronary heart disease (CHD) is, like obesity and diabetes, an inflammatory disorder caused by abnormal carbohydrate metabolism in those eating a diet low in omega-3 polyunsaturated fats and high in trans fatty acids and omega-6 polyunsaturated fats.” https://www.samj.org.za/index.php/samj/article/view/5627/4216

    • So merely switching from full-fat milk to skim milk doesn’t help to fight weight gain. Sounds … well, obvious. Doesn’t it?

      Reply
  15. I wonder if US and Canadian authorities would have an easier time if they didn’t include Fiber (sic) in their Carbohydrates figure on nutritional labels. In the UK / EU we measure carbohydrates, rather than calculating by difference, and do not include fibre in the figure – it’s a separate line.

    So in the UK you can eat 15g of carbohydrates and 25g of fibre per day which makes it less controversial than over the pond where “reducing carbs” can be taken to mean inadequate fibre intake.

    Reply
  16. Thank you for an unbiased, well-researched and documented article. I have 100 pounds to lose and tried the Atkins Diet, which, in my opinion, was the healthiest I’ve eaten in a long time: lean meats, veggies, fruits, fish, nuts, etc. I also never felt better in my life, with increased energy levels and elevated moods. I quit the diet, though, after reading negative reviews. Now, after reading this article, I think I’ll resume the diet and listen to what my body told me while I was on it – that I felt great and was never hungry. My mother has just been diagnosed with congestive heart failure, mirroring her sister and father (who died in his 50s of a heart attack). I have a lot of work ahead of me to not go down the same road, and I think this diet is a place to start.

    Reply
  17. Thanx for a very interesting article. My wife & I got quite a bit motivated by the LCHF diet recently. We are 50+, I am on Statin to control high Cholesterol and my wife is on medication to control her Hypertension. We are not obese but would be keen on getting rid of about 5-6 kgs. We have been on low fat moderate Carb high fibre diet for long time, but still we have been slowly getting heavier, bigger around the waist. Our concern is with HF part of the LCHF diet. What do you think?

    Reply
  18. Judit, my 55 yr. old husband has heart disease. It hurts to type that. He had a heart attack 2 weeks ago; 99% blockage in one main artery, and 50% blockage in the other. A stent in the almost totally blocked one was placed, and while no damage to the heart was done, we are obviously not out of the woods. I am devastated.
    His father and all of his brothers have high cholesterol; particularly high LDL. I am learning that there is more testing we could do, but it doesn’t seem to be easily had. Caridologists here follow the standard protocol for testing, diet and so on. One size fits all.
    I was following a high fat low carb diet, but am scared now to have him follow it. I am interested in your story.
    I don’t believe that a low fat, low cholesterol diet is necessary, but since he has heart disease and has had a heart attack, I am nervous about what diet to have him follow.

    Reply
  19. I am so grateful whenever I see a serious, thoughtful physician taking the time to really analyze the pros and cons of low-fat and low-carb regimes. I’ve been on a low-carb regime for three years now and my test results are (to quote my doctor, who has no clue about how I eat) “terrific.” Meanwhile I have lost weight, increased muscle, and improved my athletic capacity. Living without sugar, flour, grains, corn, and sweet fruits is a way of life for me now. But since I get to eat eggs, cheese, steak, salads, shrimp, chicken, veggies and whipped cream with strawberries, it’s a pretty nice life. I only wish the medical establishment would pay attention to all the clinical trials showing that low-carb diets are healthy and effective for weight loss and for overall health.

    Reply
  20. Doc,

    I am a Functional Medicine Certified Provider and a Chiropractor. I re-post many of your articles on a regular basis and am not a big fan of statin drugs. In the US, it is difficult. The docs have tremendous time constraints and are not able to spend the time necessary to start producing behavioral changes.

    Secondly, standard of care requires that they prescribe statin drugs, regardless of their best instincts. Litigation in the US is a tremendous burden on the health care system.

    But the population of the US has a tremendous hunger for Dr.s offering alternative approaches like Carb restriction, metabolic assessments and the ability to spend time with them and make a connection. If you add to that, the time lag between research results and changes in standard of care, reliance on continuing education produced by pharmaceutical corporations, and the ego’s inability to admit error, we end up with the present system. Like many things in the world these days, we need a revival of a desire to do what is right, and not what is popular.

    Reply
  21. I just want to follow up and say that since my preschooler has begun the ketogenic diet for epilepsy, we have noticed HUGE gains in speech and cognition. Seizure control is moderate, but we are encouraged to continue the diet based on his improvements alone. Granted, the ketogenic diet is extremely low carb and is a medical diet, but I cannot dispute the positive correlation we have observed.

    Reply
  22. “If you add to that, the time lag between research results and changes in standard of care, reliance on continuing education produced by pharmaceutical corporations, and the ego’s inability to admit error, we end up with the present system. Like many things in the world these days, we need a revival of a desire to do what is right, and not what is popular.”

    This is a huge problem with the NHS in the UK. I have a relative who is in hospital with depression, and who would undoubtedly benefit from dietary supplements but the tests aren’t done and nobody seems to know about the latest research between diet/nutrition and mental health.

    Reply
  23. I found this article very interesting. My husband and I have followed a low carb diet for a while and both lost some weight and felt better. However my husband this week has had a mild heart attack. He has had an angioplasty and been recommended to follow a low fat diet. We are at a loss,I don’t want to go against medical advice, but we both feel strongly that low carb, rather than low fat is the way to go, but on the other hand we keep reading how fruits,oats and legumes are heart healthy. We really don’t know what to eat.

    Reply
    • Hi Siobhan

      Of course your husband should follow his doctors’ advice. It would be irresponsible of anyone commenting here to recommend anything else.

      Just to add to the general discussion I can say that following a heart attack most patients are put on statin therapy. This usually takes care of their LDL cholesterol (it drops) and likely has some other beneficial effects. There is very little evidence (maybe none) that a low-fat diet will provide further benefit. However, there’s evidence that a Mediterranean type diet is of benefit for those who already have cardiovascular disease or are at high risk.

      In my practice I often recommend carbohydrate restriction to patients with coronary heart disease if they also have metabolic syndrome, that is if they’re overweight, have high blood pressure, high levels of triglycerides and low HDL-cholesterol. As I said, one usually doesn’t have to worry much about LDL cholesterol if the patient is already on statins.

      Reply
      • Trouble with statins is that there is still no evidence that cholesterol or even controlling LDL helps prevent heart attacks. From what I’ve read, the overall mortality is the same with more people having strokes as a result than heart attacks. Cardiologists also say that cholesterol levels of their heart attack patients are all over the place, high, low, normal…

        Dr Malcolm Kendrick’s blog on ‘what causes heart disease’ (which has now run into 40-something instalments) is very enlightening and well worth reading because it isn’t what we’ve been led to believe…

  24. I was happy to find your informative article this morning. My husband and I started a LCHF diet on January 2nd, and as of February 1st, I’ve lost 15.5 lb. (gotta mention that extra .5), I feel more energetic already, have had no sugar cravings to speak of, and am very happy with our progress. I did visit my doctor when we embarked on this plan, and to my great surprise, she was 100% in favor of it, knew the research, and said “go for it.” So I feel great having that support. And the food is excellent and very satisfying. I have been seriously overweight for so many years that I’m sick to death of dieting, losing that 15 or 30 lb. and then gaining it back again, on the low-fat or extremely low cal vegetarian diet plan. LCHF may not be for everyone, but it surely is for me. Keep spreading the word!

    Reply
  25. hi Doc,

    I am khendy from indonesia, I am on LCHF diet for 2 months and loss my weight over 12 kg , I am strict in carb and almost very low carb. 2 day ago I checked my lipid profile and the result was cholesterol total = 251, Trygliceride = 111, LDL Cholesterol =181, HDL Cholesterol=47 all in mg/dL

    please could you help me is it good or bad for me to continue my diet on LCHF?, honestly I really happy I can loss my weight 12 kg and I can control my appetite not feel hungry everytime. thank you Doc

    Reply
    • Alien
      Maybe I wasn’t clear enough on this point. I think you can benefit from carbohydrate restriction without long-term ketosis. But, as I said, If people prefer very strict low carb and continuous ketosis it’s fine with me as long as they feel well and metabolic markers are in order. So, I don’t recommend against ketosis, but metabolic benefits can be achieved without it.

      Reply
  26. “The initial recommendations to avoid saturated fat and cholesterol were
    based on observational from epidemiological research. Some of this
    research was led by the famous American scientist, Ancel Keys”

    Well, gee, did you know what kind of saturated fats that ol Ancel was feeding people in his studies? Most people think butter, or animal fat. NOPE! He was feeding them Crisco and Margarine, which are chock full of trans fats. Gee, I wonder why those people were “dropping like flies” compared to people eating a “low fat diet”?!?!

    To even mention the 7 countries study is bad joke, because of how CHERRY PICKED the data from that study was (what happened to the OTHER 22 COUNTRIES?)

    The whole “cholesterol = bad” model of heart disease is wrong to begin with, and it has been found in recent studies that lowering cholesterol has VERY little over all affect on preventing death by CVD/Stroke.

    I know that the low fat / high carb fan boys will start throwing epidemiological studies, cohort and dietary questionnaire types of studies that imply that low fat is the only sane diet to prevent heart disease, obesity, and/or diabetes. Well, show me an RTC study (that’s been done properly). YOU CAN’T, because there ISN’T ONE!

    But there has been a VERY LARGE “unofficial experiment” that has been going on since the early 80’s. This is when we were all first told to eat a low fat high carb diet. If you look at the statistics our intake of fat has gone down, and our intake of carbohydrates have gone up since then. And since then look at what has happened to our rate of obesity, diabetes, and CVD rates. The rates of CVD and diabetes have skyrocketed since the early 80’s (even though smoking rates have gone down dramatically), to the point that 1 in 3 people in the US are diabetic, and it is estimated that AT LEAST another 1/3 of the population are either pre-diabetic or just undiagnosed full blown diabetics.

    When a recent study looked at [70] heart disease victims, it was found that upwards of 85% of were ultimately found to be diabetics (only 1/3rd were known to be diabetics before they “double checked” the rest). BTW, they didn’t actually check the other 15%, so that number could be even higher….

    Reply
  27. Some people have a predisposition for heart disease and have a family history of early heart attacks. The culprit in these individuals is lp(a). Lipoprotein (a) is the killer in these individuals. I suggest you have your doctor measure this lipoprotein because many doctors don’t know about this.

    Reply

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