The ongoing low-carb vs. low-fat debate continues to dominate many nutritional discussions, just last week we saw the headlines were in a frenzy about carbs and our health! These discussions can be very heated and polarising, so I love this guest blog by Alan Flanagan (A.K.A. The Nutritional Advocate) which takes a close look at the evidence as to whether low-carb diets are helpful or harmful for population health.
Alan is a lawyer and nutritionist based in Dublin, Ireland. In addition to his legal practice, Alan has finished a Masters in Nutritional Medicine at the University of Surrey. Alan combines an investigative and logical approach to nutrition with advocacy skills to translate the often complicated world of nutrition science, and is dedicated to guiding healthcare professionals in evidence-based nutrition.
Recently, a narrative has emerged which places dietary carbohydrate and sugars as Public Enemy No.1 for the epidemic of diet-related chronic lifestyle diseases – in particular obesity and type-2 diabetes – currently facing public health. This has not just been in the realm of social media, but has emerged within medicine. In 2016, the National Obesity Forum Report published in association with the low-carbohydrate advocacy group, the Public Health Collaboration, entitled ‘Eat Fat, Cut the Carbs, and Avoid Snacking to Reverse Obesity and Type 2 Diabetes’, made several statements in favour of low-carb, high-fat [LCHF] diets, including:
1. That LCHF diets are superior to low-fat diets for weight loss;
2. That refined carbohydrate and dietary sugars are uniquely responsible for chronic lifestyle diseases;
3. That public health guidelines should recommend a LCHF diet (1).
A number of issues arise from these positions, not least in that they are often presented in dogmatic manner, and create an extreme and polarizing view of nutrition and public health. Let’s look at each in turn.
1. Are LCHF Diets Superior to Low-Fat Diets for Weight Loss?
This contention has been subject to a level of scrutiny that not many areas of nutrition science have. The hypothesis that LCHF diets are superior to low-fat diets [LFD] was generated largely from earlier trials showing significantly greater weight loss from LCHF diets over short-term periods of 12-weeks to 12-months (2).
However, many of these trials did not compare like with like, by failing to match dietary protein intake between diets (3-4).
This is important, as when people undertake low-carb diets, this is usually replaced with protein, yet protein is the most satiating macronutrient and induces significant diet-induced thermogenesis (i.e. a quarter of all protein intake is burned off as heat in the process of digestion) (2). This adds a significant metabolic advantage, which has underscored the suggestion of superiority of LCHF diets. For example, in two meta-analysis which appeared to find superiority of LCHF diets, the average protein intake in the LCHF groups was 30-35% of energy, compared to 15-18% in the LFD groups (3-4).
In recognition of this significant confounder, more recent evidence has compared LCHF to LFD with protein intake matched between diets, finding no difference in weight loss (5-10).
In fact many of the metabolic benefits are related to the increase in dietary protein, not the lowering of carbohydrate per se (8).
A recent comprehensive meta-analysis of controlled feedings studies comparing the effects of diets containing equal calories protein, but differing in the ratio of carbohydrate to fat, appears to have determined this issue (6). With total energy and protein matched between diets, even extreme variance in the balance of carbohydrate to fat made no difference to weight loss (6). While these were metabolic ward studies, and arguably lack real-world relevance, the recent DIETFITS study confirmed these findings. In this randomized controlled trial in free-living subjects counselled to either a lower carbohydrate or lower fat diet, with protein intake averaging 20% between groups, there was no significant difference in weight loss (5). Of particular note, diet quality was a major emphasis in both intervention diets, with a focus on minimally processed whole food choices in both diet patterns (5).
While a reduction in overall carbohydrate quantity is important if the diet is defined by refined intake and added sugars, this can be achieved by addressing diet quality as wholegrain and high-fibre carbohydrates have substantial evidence of benefit to health, including improving blood lipids, and increasing insulin sensitivity (11-15). And this is a particularly important point, as many low-carb advocates advocate intakes in the range of <15% energy (16).
However low-carb diets can cause high-fibre, wholegrains, and unrefined complex carbohydrates to be displaced from the diet.
Therefore a low-carb diet can often become high in animal fat and low in micronutrients and antioxidants (17-18). The question thus begs, why restrict carbohydrate intake in such an extreme way? The proposed model behind the diets superiority, the “carbohydrate-insulin” model of obesity, has been tested and disproven (6, 9-10). The reported superiority ‘in the field’ compared to LFD is also an oversimplification as a wide variety of response to either diet pattern is evidence from the literature, and a more flexible LFD may be just as effective (5, 19).
Graph representing differences in weight loss on a LCHF or LFD from the DIETFITS Study (Gardner). The mirror-image contrast is striking, indicating both inter-individual differences in response to diet, and lack of superiority of one diet over the other.
Therefore, emphasizing superiority of LCHF diets not only misleads healthcare professionals but creates a barrier to the effective counselling of patients towards improved diet quality. And given that diet quality can be a driver of diet quantity (17), this is problematic.
Summary: When protein intake is matched, studies have found no significant difference in weight loss when low-carb high fat diets (LCHF) are compared with low fat diets. There is good evidence that improving carbohydrate quality is important for our health, this can be done by reducing the intake of sugar and increasing the intake of wholegrains. But LCHF diets can often cause an unhealthy balance which is low in fibre, high in fat and low in vitamins and minerals.
2. Are Refined Carbohydrates and Sugar Responsible for Chronic Lifestyle Diseases?
Before looking at the role of refined carbohydrate [hereafter simply ‘sugar(s)’ for ease of reference], it can be helpful to understand the mechanisms through which cardiometabolic risk is increased in response to sugar intake. Primarily, sugars increase circulating triglycerides, an effect noted from high sugar intake in both the fasting state and after a meal (20). This increase in circulating triglycerides influences, and is in turn influenced by, the accumulation of liver fat, which causes insulin resistance in the liver and an overproduction of VLDL-cholesterol (21). After a meal, insulin resistance in the liver and in adipose tissue leads to increased circulating levels of free fatty acids, which in turn upregulates the synthesis of new triglycerides, and causes impaired clearance (22;23).
Therefore, sugar intake can cause an increase in triglyceride levels after a meal due to increasing triglyceride synthesis in the liver, and impairing triglyceride clearance, both of which are strongly influenced by a fatty liver.
This is central to the cardiometabolic risk of dietary sugars, as impaired triglyceride metabolism is a primary risk factor for cardiovascular disease through driving alterations in blood cholesterol, in particular small, dense LDL subparticles (21).
However, this is merely the mechanistic understanding of how sugars may increase risk – the relevant question is to what degree these effects occur through the habitual diet.
To answer this, we need to look at controlled feeding studies and then compare them to population levels of consumption. In a trial which compared diets containing either 25% energy from fructose or 25% from glucose, the fructose diet increased visceral fat deposition and abnormal lipid levels in the blood, but this was not observed in the glucose diet despite similar weight gain between the groups (24). A further study by the same group comparing 145g fructose, 79g high-fructose corn syrup [HFCS], and 145g glucose found significant increases in cardiometabolic risk factors from HFSC and fructose-sweetened beverages, but no effect from glucose-sweetened beverages (25).
These studies have pointed to a uniquely problematic health effect of fructose and refined sugars, however, let’s take a pause and question the real-world validity of the findings. The first thing to note is that pure fructose does not exist in the UK food supply [nor does HFCS], sucrose is the primary added sugar used in the food supply, and sucrose is a disaccharide made up of 50:50 fructose and glucose. Studies using the pure monosaccharide fructose in feeding trials show a dose-response to adverse effects on blood cholesterol levels, with 50g per day increasing triglyceride levels after a meal, while 100g per day increases plasma circulating triglycerides (26). Given sucrose is a disaccharide, to achieve these levels of pure fructose intake would require consumption of either 100g or 200g, respectively, of sucrose per day, and the fact of the matter is that these levels of free sugar intake are simply not reflected in current average population levels of consumption (27-28). There are extreme examples within the population consuming >20% calories from added sugar (27-30).
However the most recent National Diet and Nutrition Survey [NDNS] in the UK shows average free sugar consumption in adults of 11.1% for men and 11.2% for women (27-28, 30).
A recent systematic review of fructose-feeding trials found that the amount of fructose used in trials where sugar was added to the diet was 187.3 g per day on average [i.e. you’d have to consume 374g sucrose to reach that dose, which is almost 94 teaspoons of sugar!], and thus completely failed to reflect average population levels of intake (31).
Therefore the real-world relevance of studies which use extremes sugar intakes that are not representative of the typical diet is questionable – beyond illustrating mechanistic pathways.
The fact that sugar is added to the diet in the aforementioned studies is of particular relevance.
As studies find no adverse effect on cardiometabolic risk when fructose is substituted for other types of sugar, if the calorie content of the sugar swap is kept the same (32).
A controlled trial comparing low calorie weight-loss diets matched for energy intake with 10% energy from either HFSC or sucrose, found improvements in plasma lipids and TGs, illustrating that the presence of 10% energy from free sugars did not negate the beneficial effects of weight loss on improving cardiometabolic risk (33).
Numerous systematic reviews and meta-analyses have found that the increase in cardiometabolic risk from dietary sugars is due to excess energy intake, which in turn drives weight gain (31 – 35).
This salient point has been conveniently misplaced by the LCHF movement, who continue to advocate that sugars drive weight gain independent of calories. But this is wholly unsupported from any scientific line of inquiry.
Summary: Excess sugar intake can damage triglyceride metabolism, which is a risk factor for heart disease. Studies which test the effect of fructose and high fructose corn syrup on weight are often irrelevant to real life as the amounts of fructose used are unrealistically high. Many good quality studies have found that the increase risk of heart disease and diabetes related to sugars intake is due to weight gain caused by excess calorie intake.
3. Should Dietary Guidelines Advocate a LCHF Diet?
Current NDNS data also shows average population carbohydrate consumption is 45-50% depending in the age group in question, and the average dietary fat intake at 32-35% (30).
This carbohydrate and fat intake in the UK is in fact in line with dietary recommendations, yet obesity has risen from 15% in 1993 to 26% in 2014 (36).
This suggests that the primary driver is not any single isolated macronutrient, but an overall increase in energy availability in the food supply and increased dietary energy-density (37-38). Substantial evidence exists in support of a greater effect of energy-density on total energy intake than macronutrient variations, and independent of macronutrient composition, chronic surplus energy intake will increase adiposity (27, 39).
We know from tightly controlled overfeeding studies that weight gain is identical regardless of whether participants are overfed by either carbohydrate or fat, where energy is matched (40).
In this respect, we can see the fallacy behind the LCHF narrative, which looks at diet and health through the lens of one single macronutrient. When you actually look at the foods in the typical adult Western diet – based on both US and UK adult data – you’ll see that the most significant contributors to calories in the diet are refined flour and potato-based products, cereals, animal fats and added vegetable oil fats (28, 30, 41).
More specifically, we can look at actual food, beverage and environmental factors which caused an increase in calories from the 1970’s to the 2000’s (40 – 42):
- Potato chips
- Sugar-sweetened beverages
- French fries
- Processed animal meats
- Refined grain products
- Sweets and desserts
- Calories consumed away from the home
- Increased calories coming from snacks
This shows that the typical Western diet is high in calories, not “it’s all carbs” as the LCHF narrative portrays.
This was recently confirmed by study showing that up to 50% of daily energy in the UK diet comes from ultra-processed foods [i.e., foods made entirely from fats, refined starch and sugar, and additives] (43). Where exactly do we start to identify one, single nutrient amidst that diet pattern to blame for cardiometabolic disease?
While it is compelling in its simplicity, blaming one single nutrient lacks any scientific or logical validity.
The primary goal for public health is thus a reduction in overall dietary energy density across the population, which has not been achieved to date.
But broadly recommending a low-carb diet may not be an optimal way to reduce disease burden on a population level as many studies have found a higher risk of death and poor heart health related to low-carb diets (44 – 48).
Recall that where carbohydrates are excluded from the diet, the primary replacement food groups are typically animal proteins and fats (17). Further research differentiating between low-carb diets where more energy comes from plant proteins and fats, compared to low-carb diets with a more animal fats, found that in fact the greater proportion of plant-based foods in a low-carb diet was protective (44 – 59).
However, low-carb diets with predominantly animal-based food replacements show a significant increase in all-cause and cardiovascular disease mortality (44 – 47).
This is largely attributed to the significant increase in saturated fat intake associated with animal-based low-carb diet patterns (44 – 47). And this is crucial in relation to the LCHF narrative, which in the same breath as demonizing carbohydrate asserts that “saturated fats do not clog the arteries” (50). No one ever said they did, the effects of saturated fat on heart disease have always been indirect, mediated by the harmful impact on blood lipids. And let’s be clear on this issue, both the World Health Organization and SACN both, independently of each other, confirmed that the population target for saturated fat intake of 10% remains valid, as the threshold at which the greatest reductions in cardiovascular events is found (51 – 52).
Since inception of UK dietary guidelines in 1983, recommendations have included reducing sugar intake, increasing fibre, vegetables and wholegrain carbohydrates (53). In the interim, sugar has increased, refined carbohydrates predominate in the diet and fibre and vegetable intake has declined (35, 53). Given that data, it would be seriously misguided to recommend a LCHF diet to the population, as there is no evidence to support that there would be an increase in plant-based foods in that diet pattern, and the risk of a population shift to an animal-based LCHF diet would be a legitimate concern to long-term population health.
The LCHF narrative blames national dietary guidelines for the increase in cardiometabolic disease, which is a misnomer given they were never complied with.
Summary: Although the overall intake of carbohydrate and fat in the UK is in-line with government recommendations, sugar intake is high and the intake of wholegrains and vegetables is low. The Western diet is high in calories, which we know leads to weight gain regardless of fat or carbohydrate intake. Following a low-carb diet runs the risk of reducing the intake of wholegrains and vegetables further, which can increase the risk of heart problems and early death.
Nutrition science is currently evolving to a ‘food-first’ paradigm, and the study of diet patterns as a whole.
There is no longer any scientific validity to single-nutrient hypotheses in the context of the overall diet pattern which is problematic for cardiometabolic disease.
Singling out sugar is misconceived. Singling out fat is simplistic. The goal for public health is to address the outstanding problem: the high intake of calories which exists across the population.
The LCHF narrative decrying dietary carbohydrate and attempting to absolve saturated fat of any role in cardiometabolic disease is not only lacking evidence, it is dangerous. The foothold of this movement within conventional medicine is as worrying as the implementation of such diets by doctors, in the absence of any professional nutrition oversight. What is the likelihood that patients are in practice simply cutting out all carbohydrate and replacing with increased animal meats and fat consumption? Based on a cursory representation of low-carb on social media, I would say quite likely. And that is cause for concern for anyone within evidence-based nutrition.
Unfortunately, the hardest challenge of combating the LCHF alarmism for evidence-based nutrition professionals is in clarifying these issues without becoming apologists for a food industry and food environment that has so clearly precipitated diet-induced disease.
Summary: It is the overall dietary pattern which impacts health risk, looking at single nutrients such as fat or carbohydrates is overly-simplistic, misleading and often damaging. To improve public health calorie intake needs to be reduced across the board, which can be impacted by many environmental factors.
For more information on low-carb diets, check out:
- National Obesity Forum. Eat Fat, Cut the Carbs, and Avoid Snacking to Reverse Obesity and Type 2 Diabetes. National Obesity Forum in association with Public Health Collaboration; 2016.
- Schoeller D, Buchholz A. Energetics of Obesity and Weight Control: Does Diet Composition Matter?. Journal of the American Dietetic Association. 2005;105(5):24-28.
- Hu T, Mills K, Yao L, Demanelis K, Eloustaz M, Yancy W et al. Effects of Low-Carbohydrate Diets Versus Low-Fat Diets on Metabolic Risk Factors: A Meta-Analysis of Randomized Controlled Clinical Trials. American Journal of Epidemiology. 2012;176(suppl 7):S44-S54.
- Mansoor N, Vinknes K, Veierød M, Retterstøl K. Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials. British Journal of Nutrition. 2015;115(03):466-479.
- Gardner C, Trepanowski J, Del Gobbo L, Hauser M, Rigdon J, Ioannidis J et al. Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion. JAMA. 2018;319(7):667.
- Hall K, Guo J. Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition. Gastroenterology. 2017;.
- Hill A, Harris Jackson K, Roussell M, West S, Kris-Etherton P. Type and amount of dietary protein in the treatment of metabolic syndrome: a randomized controlled trial. The American Journal of Clinical Nutrition. 2015;102(4):757-770.
- Soenen S, Bonomi A, Lemmens S, Scholte J, Thijssen M, van Berkum F et al. Relatively high-protein or ‘low-carb’ energy-restricted diets for body weight loss and body weight maintenance?. Physiology & Behavior. 2012;107(3):374-380.
- Hall K, Chen K, Guo J, Lam Y, Leibel R, Mayer L et al. Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men. American Journal of Clinical Nutrition. 2016;104(2):324-333.
- Hall K, Bemis T, Brychta R, Chen K, Courville A, Crayner E et al. Calorie for Calorie, Dietary Fat Restriction Results in More Body Fat Loss than Carbohydrate Restriction in People with Obesity. Cell Metabolism. 2015;22(3):531.
- Flight I, Clifton P. Cereal grains and legumes in the prevention of coronary heart disease and stroke: a review of the literature. European Journal of Clinical Nutrition. 2006;60(10):1145-1159.
- Pereira M, Jacobs D, Pins J, Raatz S, Gross M, Slavin J et al. Effect of whole grains on insulin sensitivity in overweight hyperinsulinemic adults. The American Journal of Clinical Nutrition. 2002;75(5):848-855.
- Kirwan J, Malin S, Scelsi A, Kullman E, Navaneethan S, Pagadala M et al. A Whole-Grain Diet Reduces Cardiovascular Risk Factors in Overweight and Obese Adults: A Randomized Controlled Trial. The Journal of Nutrition. 2016;146(11):2244-2251.
- Kaczmarczyk MM, Miller MJ, Freund GG. The health benefits of dietary fiber: beyond the usual suspects of type 2 diabetes, cardiovascular disease and colon cancer. Metabolism, 2012 Aug; 61(8):1058-1066
- Tosh SM. Review of human studies investigating the post-prandial blood-glucose lowering ability of oat and barley food products. Eur J Clin Nutr. 2013 Apr;67(4):310-7.
- Feinman R, Fine E. Thermodynamics and Metabolic Advantage of Weight Loss Diets. Metabolic Syndrome and Related Disorders. 2003;1(3):209-219.
- Mozaffarian D. Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity. Circulation. 2016;133(2):187-225.
- Tapsell L, Neale E, Satija A, Hu F. Foods, Nutrients, and Dietary Patterns: Interconnections and Implications for Dietary Guidelines. Advances in Nutrition. 2016;7(3):445-454.
- Astrup A, Grunwald G, Melanson E, Saris W, Hill J. The role of low-fat diets in body weight control: a meta-analysis of ad libitum dietary intervention studies. International Journal of Obesity. 2000;24(12):1545-1552.
- Parks, E. (2002). Changes in fat synthesis influenced by dietary macronutrient content. Proceedings of the Nutrition Society, 61(02), pp.281-286.
- Kotronen, A. and Yki-Jarvinen, H. (2007). Fatty Liver: A Novel Component of the Metabolic Syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology, 28(1), pp.27-38.
- Larsen, L. (2002). The role of de novo lipogenesis in development of obesity in man. British Journal of Nutrition, 88(03), p.331.
- Griffin B.A., & Cunnane S.C. (2009). Nutrition and metabolism of lipids. In M.J. Gibney, S.A. Lanham-New, A. Cassidy, H.H. Vorster (Eds). Introduction to Human Nutrition. West Sussex, UK: Wiley-Blackwell.
- Stanhope, K., Schwarz, J., Keim, N., Griffen, S., Bremer, A., Graham, J., Hatcher, B., Cox, C., Dyachenko, A., Zhang, W., McGahan, J., Seibert, A., Krauss, R., Chiu, S., Schaefer, E., Ai, M., Otokozawa, S., Nakajima, K., Nakano, T., Beysen, C., Hellerstein, M., Berglund, L. and Havel, P. (2009). Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation, 119(5), pp.1322-1334.
- Stanhope, K., Bremer, A., Medici, V., Nakajima, K., Ito, Y., Nakano, T., Chen, G., Fong, T., Lee, V., Menorca, R., Keim, N. and Havel, P. (2011). Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. The Journal of Clinical Endocrinology & Metabolism, 96(10), pp.E1596-E1605.
- Livesey, G. and Taylor, R. (2008). Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. The American Journal of Clinical Nutrition, 88, pp.1419-37.
- Centers for Disease Control and Prevention: National Center for Health Statistics (2017). National Health and Nutrition Examination Survey Data. Hyattsville, MD: U.S. Department of Health and Human Services.
- Department of Health (2015). The Scientific Advisory Committee on Nutrition recommendations on carbohydrates, including sugars and fibre. London: Public Health England.
- Yang, Q., Zhang, Z., Gregg, E., Flanders, W., Merritt, R. and Hu, F. (2014). Added Sugar Intake and Cardiovascular Diseases Mortality Among US Adults. JAMA Internal Medicine, 174(4), p.516.
- Results of the National Diet and Nutrition Survey (NDNS) rolling programme for 2014 to 2015 and 2015 to 2016 [accessed August 2018 via: https://www.gov.uk/government/statistics/ndns-results-from-years-7-and-8-combined].
- Choo, V. and Sievenpiper, J. (2015). The Ecologic Validity of Fructose Feeding Trials: Supraphysiological Feeding of Fructose in Human Trials Requires Careful Consideration When Drawing Conclusions on Cardiometabolic Risk. Frontiers in Nutrition, 2.
- Khan, T. and Sievenpiper, J. (2016). Controversies about sugars: results from systematic reviews and meta-analyses on obesity, cardiometabolic disease and diabetes. European Journal of Nutrition, 55(S2), pp.25-43.
- Lowndes, J., Kawiecki, D., Pardo, S., Nguyen, V., Melanson, K., Yu, Z. and Rippe, J. (2012). The effects of four hypocaloric diets containing different levels of sucrose or high fructose corn syrup on weight loss and related parameters. Nutrition Journal, 11(1).
- Te Morenga, L., Mallard, S. and Mann, J. (2012). Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ, 346(jan15 3), pp.e7492-e7492.
- Rippe, J. and Angelopoulos, T. (2016). Sugars, obesity, and cardiovascular disease: results from recent randomized control trials. European Journal of Nutrition, 55(S2), pp.45-53.
- HSCIC. Statistics on Obesity, Physical Activity and Diet. Health and Social Care Information Centre; 2016.
- Swinburn B, Sacks G, Ravussin E. Increased food energy supply is more than sufficient to explain the US epidemic of obesity. American Journal of Clinical Nutrition. 2009;90(6):1453-1456.
- Rolls B. The relationship between dietary energy density and energy intake. Physiology & Behavior. 2009;97(5):609-615.
- Lammert, O., Grunnet, N., Faber, P., Bjørnsbo, K., Dich, J., Larsen, L., . . . Quistorff, B. (2000). Effects of isoenergetic overfeeding of either carbohydrate or fat in young men. British Journal of Nutrition, 84(2), 233-245.
- Mozaffarian, D., Hao, T., Rimm, E., Willett, W. and Hu, F. (2011). Changes in Diet and Lifestyle and Long-Term Weight Gain in Women and Men. New England Journal of Medicine, 364(25), pp.2392-2404.
- Nielsen S, Siega-Riz A, Popkin B. Trends in Energy Intake in U.S. between 1977 and 1996: Similar Shifts Seen across Age Groups. Obesity Research. 2002;10(5):370-378.
- Nielsen S, Popkin B. Patterns and Trends in Food Portion Sizes, 1977-1998. JAMA. 2003;289(4):450.
- Monteiro C, Moubarac J, Levy R, Canella D, Louzada M, Cannon G. Household availability of ultra-processed foods and obesity in nineteen European countries. Public Health Nutrition. 2017;21(01):18-26.
- Fung T. Low-Carbohydrate Diets and All-Cause and Cause-Specific Mortality. Annals of Internal Medicine. 2010;153(5):289.
- de Koning L, Fung T, Liao X, Chiuve S, Rimm E, Willett W et al. Low-carbohydrate diet scores and risk of type 2 diabetes in men. The American Journal of Clinical Nutrition. 2011;93(4):844-850.
- Seidelmann et al. Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis. The Lancet. 2018.
- Noto H, Goto A, Tsujimoto T, Noda M. Low-Carbohydrate Diets and All-Cause Mortality: A Systematic Review and Meta-Analysis of Observational Studies. PLoS ONE. 2013;8(1):e55030.
- Lagiou P, Sandin S, Lof M, Trichopoulos D, Adami H, Weiderpass E. Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study. BMJ. 2012;344(jun26 3):e4026-e4026.
- Trichopoulou A, Psaltopoulou T, Orfanos P, Hsieh C, Trichopoulos D. Low-carbohydrate–high-protein diet and long-term survival in a general population cohort. European Journal of Clinical Nutrition. 2006;61(5):575-581.
- Malhotra A. Saturated fat is not the major issue. BMJ. 2013;347
- World Health Organisation. Guidelines: Saturated fatty acid and trans-fatty acid intake for adults and children. WHO; 2018.
- Scientific Advisory Committee on Nutrition. Saturated fats and health. Public Health England; 2018.
- Foster R, Lunn J. 40th Anniversary Briefing Paper: Food availability and our changing diet. Nutrition Bulletin. 2007;32(3):187-249.