Low Carb Diet Best for Obesity According to Swedish Health Authorities

Low carb diet best for obesitySix months ago I wrote a blog post named “Low Carb Diets and Heart Disease. What Are We Afraid of? One of the concluding remarks of my article was: “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“.

Well, this day may actually have arrived sooner than I expected because today Swedish health authorities published a report (Dietary Approach for Obesity. A Systematic Review of the Literature) concluding that carbohydrate restriction is the best short term dietary approach to lose weight for people with obesity. Furthermore, they concluded that the current scientific literature does not indicate that such an approach has any harmful effects on health as so many have suggested.

SBU (Swedish Council on Health Technology Assessment) is a group of experts appointed by Swedish authorities, whose role is to update health care professionals on the best available diagnostic and treatment options for diverse medical conditions. SBU’s reports are based on systematic reviews of the available medical literature. Their approach is standardized and well tested. SBU has been performing systematic reviews since 1987, and they consider themselves to be one of the oldest and best established Health Technology Assessment Organization in the world.

Today SBU published their systematic analysis of currently available scientific studies on different dietary approaches for the treatment of obesity. Their review deals with studies on individuals with a BMI higher than 30 kg/m, generally defined as obesity. A total of 16.000 published scientific papers were analyzed.

Low carb diet best for obesity

SBU concludes that during short term (less than 6 months), dietary advice emphasizing moderate or strict carbohydrate restriction is more effective in terms of weight loss, than advice emphasizing a low fat diet. During long term, there are no differences in weight loss between moderate or strict carbohydrate restriction, low fat diets, high protein diets, a Mediterranean diet, a low GI-diet, or a diet rich in monounsaturated fatty acids. Advice to increase the consumption of dairy products (milk in particular) or reduce the amount of sugary beverages may induce weight loss as well.

The Swedish experts conclude that available scientific evidence does not support that advising moderate or strict carbohydrate restriction will increase the risk of heart disease. Even low carb diets containing high amounts of saturated fat have not been shown to increase risk. However, they emphasize that because of the lack of reliable studies, it would be rational to limit the amount of saturated fat under these circumstances : “…it’s not possible to draw any conclusions about the relationship between a low-carbohydrate diet – regardless of fat content – and cardiovascular disease. Here we could apply the precautionary principle, and advise some restraint on saturated fat intake, as long as the documentation of the long-term effects are inadequate.”

Jonas Lindblom, who lead the group of experts that wrote the report says that the results should encourage health professionals to inform individuals with obesity about the efficacy of carbohydrate restriction. “We did not find any scientific support for the conclusion that carbohydrate restriction may increase the risk of heart disease or increase mortality”, he said.

The SBU report also contains data indicating that low carb diets lead to better blood sugar levels than low fat diets among individuals with obesity and diabetes.

D-Day for LCHF

In my blog post six months ago I wrote: “I find it extraordinary how carbohydrate restriction is repeatedly rejected by the medical community as an alternative approach for obesity, the 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. 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”.

By their systematic review, health authorities in the Sweden are among the first in the world to acknowledge the huge potential of carbohydrate restriction to treat conditions such as obesity, metabolic syndrome and type 2 diabetes. I do hope this is only the beginning and that health authorities elsewhere will follow in their footsteps. There is very much at stake because obesity and its metabolic and cardiovascular consequences are becoming very serious health issues of pandemic proportions.  We should not accept that effective weapons to fight these disorders are left unused.


17 thoughts on “Low Carb Diet Best for Obesity According to Swedish Health Authorities”

  1. it’s not possible to draw any conclusions about the relationship between a low-carbohydrate diet – regardless of fat content – and cardiovascular disease. Here we could apply the precautionary principle, and advise some restraint on saturated fat intake, as long as the documentation of the long-term effects are inadequate.

    How much restraint on saturated fat?

  2. According to SBU, there’s no evidence that LCHF diet elevates serum cholesterol. Phew…..they have should have asked you, Doc. You’ve actually treated patients. This was an expert group without the experts.

    Many of LCHF studies promoted and sponsored by the Atkins foundation do not even report LDL cholesterol (see the papers by Shai et al) . Hernandez et al indeed did indeed report LDL and it didn’t look too nice; the participants in the LCHF group lost 6 kg’s and despite of this weight loss the LDL went up by 10%. “Low-fat”-group dropped weight as much as the LCHF -group did and managed to drop their LDL cholesterol by 6%. Moreover, it’s good keep in mind that in many of the studies that have tested LCHF (this includes PREDIMED and Lyon as well) the intervention group is on statins, diuretics and plenty of other drugs to a high extent.

    Bantning med lågkolhydratdiet kan sätta fart på aterosklerosprocessen: Kolhydratfattig kost ökar fria fettsyror och LDL-kolesterol

    • Still playing your disingenuous games with “LDL cholesterol” Richard? You don’t really think that a calculated LDL “volume” is all that matters do you?

      How many balls does it take to fill a garbage sack Richard? Do you think the answer might depend on what kind of balls these are? Would you rather be hit you over the head with a bag full of beach balls, or golf balls Richard? Same “volume ” in both… right?!?

      Perhaps the Atkins funded studies do not report this magic number because it is largely meaningless in terms of predicting long-term health.

      Let’s talk about HDL cholesterol (higher is better and it is higher with LCHF), Triglycerides (lower is better — again LCHF wins out) and if you, must LDL particle size and count where larger particle size and lower particle count is considered by many to be safer. But surely larger LDL particles would INCREASE the volume that you constantly harp on about… eh Richard?!?

      • https://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf

        Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB and an inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation: please see Ira Tabas, Kevin Jon Williams, Jan Borén. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis Update and Therapeutic Implications Circulation. 2007;116:1832-44.

        So, should the people who have this increased LDL-C and LDL-P response to a low carb or ketotic diet be worried? Have they simply gone from one type of CV risk to another. Usually the diet drives weight loss and improves many markers of insulin resistance (TG, glucose, insulin, etc). Some have proposed based on anecdotal experience that rise in LDL-P may be transient and take several months to return to normal theorizing there is confusion on the part of the body as to where and from what substrate to generate ATP. The big question right now really is: Are there persons who do not get atherosclerosis with apoB-cholesterol/lipoprotein levels greater than the above posted concentrations who do not get atherosclerosis? Can a human last long with atherogenic lipid concentrations above the 80th percentile population cut point? It seems for a small percentage of people that is true, but using existing trial evidence (which looked at folks on no specific diets or standard AHA low fat, low cholesterol type diets) they are rare exceptions, not the rule. Maybe one day someone will do a mega trial enrolling tens of thousands of low-carbers or paleo diet enthusiasts and follow them over many years to determine what happens to morbidity and mortality. But let’s not hold our breath on that one? Could some sort of atherosclerosis trial utilizing imaging be done – i.e. carotid intimal thickening or coronary calcium? Before we use in them to advise a therapy is working or not working a trial relating positive or negative changes in those images to CV events has to be done. As of 2013, neither of those imaging techniques has shown in an empowered clinical trial that changes (good or bad) in response related to a given therapy are related to CV outcomes and no national CV guideline advices them to be used in that fashion. Right now CAC and IMT should only be used for risk assessment and even there coronary calcium is especially poor in risk assessment in women unless they are rather elderly and CIMT is only of value for screening when done by very competent professionals.

      • Charles. Thanks for quoting Dr. Thomas Dayspring. Nobdy can beat him when it comes to explaining these issues. The first paragraph underlines the importance of understanding that both cholesterol and inflammation play a role in atherosclerosis, it´s not one or the other. The second paragraph deals with the extreme elevation of LDL-C and LDL-P sometimes seen among people on a ketogenic diet consuming a high amount of saturated fat. We still don´t know what this means in terms of risk.

      • So – would it not be more responsible for the SBU to give some guidelines on % of saturated fat to be consumed?

      • Charles. SBU´s role is not write guidelines or give recommendations. Their role is to perform systematic analyses and summarize results on currently available scientific evidence in different areas of medicine.

      • I agree with these points Charles… all of which goes to underline my intention which is that: a focus only on the LDL-C “level” (which is really a calculated volume) by itself, is not very helpful and can be downright misleading — which I believe was Richard’s intention.

      • FrankG,

        the Atkins crew love the HDL-C and triglyceride sales pitch. It’s their thing. These markers have little to do with diet composition as such and they respond favorable to weight loss independent of the mechanism used (See Stamler 2010). Amphetamines and chemotherapy all work as well on these biomarkers. So, let’s get not get blinded! The LDL story is fundamentally different!

        Fat is the new gospel at the moment, and the SBU went along this fad. However, fiber is gradually making a comeback from the 1990s. Soon we are asking whether this new fat craze went a bit too far. Cholesterol levels are on the surge in Norway, Sweden and Finland. Fiber and complex starch is the solution.

      • Richard. The SBU does not write guidelines or give recommendations on which therapy to use or not. They have not chosen to follow one fad or another. Their results are based on systematic analysis of 16.000 scientific papers. It´s not cherry picking. Their work cannot be ignored. Although you have other beliefs, it may be irresponsible and unrational to just look in a different direction. At least such an attitude does not reflect belief in scientific methodology.

        Furthermore, it´s important to keep in mind that SBU´s report only deals with dietary tretament of obesity. The results cannot be extrapolated to other groups of individuals.

      • Doc,

        are you serious? The only way to make LCHF look good is to compare it to a strawman diet composed of cookies, soda, etc, the “the 15g/d fiber diet”. Weight loss is not a synonym with health. There are very quick ways to loose lot of weight very rapidly (and enhance triglycerides and HDL-C cholesterol) without any adverse effects on LDL; these are acquiring food poisoning, chemotherapy, amphetamines, etc.

        Why did you enunciate me being a cherry-picker? We both agree that LCHF elevates serum cholesterol, the SBU disagreed, according to them they found no evidence of LCHF and adverse effects to blood lipids. Did any of the members in this panel had any history in diet and/or atherosclerosis research?

      • Richard, you’re talking baloney here:

        1) In many studies low carb diets have indeed been compared to the standard Western diet, yes. Just like low fat vegan diets. Hmm? Catch my point?

        2) Not in all, however. E.g. this one


        or this one


        both of compared Atkins and Ornish, among other diets. Of course, if you wish to argue that Ornish is a strawman diet, be my guest.

        And while weight loss is not necessarily a synonym for health, it is usually a synonym for improved lipid profile, glucose tolerance etc.

  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751676/

    Longitudinal analysis of short-term high-fat diet on endothelial senescence in baboons

    “…our results clearly established that 1) even a short-term exposure (7 weeks) to a high-fat diet can have devastating pathological effects on vascular endothelial cells, and 2) physiological responses during the first 3 weeks of high-fat diet may have lasting effects that are manifested in endothelial cells at a later time. These conclusions significantly impact the traditional perception that a high-fat diet is detrimental only if exposure to it is of long duration. They also have important implications for the design of experiments aimed at understanding the progression of events that lead to diet-induced atherogenesis. Assessment of physiological effects of diet after 3 weeks of exposure may be essential to understanding mechanisms of atherogenesis as well as individual variation in extent and severity of atherosclerosis years after the initiation of the dietary challenge.”

  4. https://circ.ahajournals.org/content/116/16/1832.full

    Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis

    The key initiating process in atherogenesis is the subendothelial retention of apolipoprotein B–containing lipoproteins. Local biological responses to these retained lipoproteins, including a chronic and maladaptive macrophage- and T-cell–dominated inflammatory response, promote subsequent lesion development. The most effective therapy against atherothrombotic cardiovascular disease to date—low density lipoprotein–lowering drugs—is based on the principle that decreasing circulating apolipoprotein B lipoproteins decreases the probability that they will enter and be retained in the subendothelium.

  5. I am a novice at all the talk of diets and way of eating plans. I can say I just finished a low fat low carb (vegetarian) way of eating and had a lipid test after four months. HDL rose slightly to 37, TG fell from 211 to 92 and total dropped to 156. I was taking a low dose 10mg statin irregularly meaning not every day as the doctor prescribed. When I did take it every day that is when the LDL was 82. My wife recently went from vegetarian to LCHF and enjoys this way of eating over the previous. I, too, went back to meat and some higher fat such as real cream and Kerrygold butter, however, still have my veggies and usually one or two fruits per day. Very little carbs for me except for Uncle Sam cereal in the morning and what I get from the veggies. Uncle Sam has the following: Whole wheat kernels, whole flaxseed, salt, barley malt. 38 carbs and 10 grams of fiber. Only 1 gram of sugar. Prior to my changes my LDL was around 180 plus and my HDL was low around 32 and sometimes lower. Any thoughts on what I am eating?

    • After thought …. my LDL was 100 on the lipid test with irregular use of the 10mg statin and being on a vegetarian diet.


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