(Photo by Brooke Lark)
Ahh, the FAT dilemma… Are low-fat or low-carb diets better for weight loss and overall health? It never stops to amaze me how nutritional information can be so conflicting and confusing, with opposing parties both claiming their rights based on the scientific evidence…
Well, let’s separate the grains from the chaff, shall we?
The old dogma based on poor science
Beginning in the 1970s major professional nutrition organizations recommended that individuals eat a low-fat/high-carbohydrate diet, launching arguably the largest public health experiment in history.
Based on pre-clinical and poor quality – no doubt industry founded studies it was concluded that the higher energy per gram containing fats do not increase satiety, but being rather palatable, they increase food intake. The glycogenostatic model held that low body stores of glycogen (stored sugar) drive food intake— whereas fat intake was not, providing another reason that high-fat/low-carbohydrate diets might lead to overconsumption. Primarily for these reasons, the prevailing notion emerged that “it was difficult, if not virtually impossible, to overeat on a high-carbohydrate diet” and that replacing fat with carbohydrate – even added sugars, would facilitate weight control.3,4
In 1992 the Food Guide Pyramid was born with high emphasis on bread, cereal, and other processed grain products; the government called for thousands of new reduced-fat processed foods; marketing schemes involving industry, nutrition societies, and government officials promoted low-fat food products of exceedingly low quality. The food industry followed suit, systematically replacing fat in food products with starch and sugar.
Throughout the ensuing 40 years, the prevalence of obesity and diabetes increased several-fold, even as the proportion of fat in the diet decreased by 25%. According to Dr David S. Ludwig of New Balance Foundation Obesity Prevention Center, Boston Children’s Hospital and Harvard Medical School “a comprehensive examination of this massive public health failure has not been conducted. Consequently, significant harms persist, with the low-fat diet remaining entrenched in public consciousness and food policy.” 1
The reality in light of the real evidence
As a result of the above efforts, dietary fat decreased to near the recommended limit of 30% total energy. But contrary to prediction, total calorie intake increased substantially, the prevalence of obesity tripled, the incidence of type 2 diabetes and heart disease increased many-fold, despite greater use of preventive drugs. Recent high quality prospective research suggests that dietary fat reduction has directly contributed to this growing burden of chronic disease.6-9
In fact, the major low-fat diet studies, such as the Women’s Health Initiative clinical trial and Look Ahead, failed to reduce risk. The PREDIMED study was terminated early when cardiovascular disease incidence decreased more rapidly than expected in the higher-fat diet groups compared with the low-fat control. Consistent with these findings, men and women adhering to low-fat/high-carbohydrate diets had higher, not lower, rates of premature death, although the type of dietary fats consumed importantly modified risk.7
One reason for the apparent failure of low-fat diets is that they may elicit biological adaptations—increasing hunger, slowing metabolic rate, and other hallmarks of the starvation response—that antagonize ongoing weight loss. Preliminary studies suggest that the reduced insulin secretion with low-carbohydrate and low-glycaemic-index diets may attenuate these adaptations, facilitating long-term weight-loss maintenance and reducing diseases associated with hyperinsulinemia.8
According to a recent report regarding the sugar industry, the adverse cardiovascular effects of added sugar remain largely underrecognized because of an industry-sponsored research program in the 1960s and 1970s “that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in heart disease”.2
New research highlighted that enterochromaffin cells in our intestines that produce most of our happy hormone; serotonin, are also responsible for nutrient sensing, gastric emptying, pancreatic enzyme secretion and regulating appetite controlling hormone secretions, such as CCK, glucagon, PYY, GIP, and somatostatin. Upon fat ingestion they increase a hormone called leptin, thus increasing satiety.10,11
A new combined analysis of all earlier studies shows that a Mediterranean diet with unlimited amounts of fat may reduce the risk of developing cardiovascular disease, obesity, breast cancer and type 2 diabetes, and now considered the gold standard of healthy eating.12 Dr Aseem Malhotra, one of Britain’s top cardiologists who is also one of the most outspoken voices for the anti-sugar campaign recently researched and published a book about the health benefits of the low-carb high-fat Pioppi diet – Challenging the mainstream advice he said “It is high time we in the UK moved towards food based guidelines and lift restrictions on dietary fat from nutritious foods.”13
Conclusion
All calories are not alike, and our metabolic responses to foods greatly differ depending on the quality of macro and micronutrients found within them. Nutritional science is particularly complex because of numerous, interacting components of diet, changing composition of the food supply, and important biological differences among individuals, affecting response. A tailor-made individual meal plan taking into account your genetics, health status, lifestyle and taste is the only way to achieve a health-promoting and sustainable diet.
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References:
1, Ludwig DS. 2016. Lowering the Bar on the Low-Fat Diet. JAMA. ;316(20):2087–2088. doi:10.1001/jama.2016.15473
2, Kearns CE, Schmidt LA. & Glantz SA. 2016. Sugar industry and coronary heart disease research: a historical analysis of internal industry documents. JAMA
Intern Med. Published online September 12. doi:10.1001/jamainternmed.2016.5394
3, Blundell JE. & MacDiarmid JI. 1997. Fat as a risk factor for overconsumption: satiation, satiety, and patterns of eating. J Am Diet Assoc.; 97(7)(suppl):S63-S69.
4, Stubbs RJ, Mazlan N. & Whybrow S. 2001. Carbohydrates, appetite and feeding behavior in humans. J Nutr.;131(10):2775S-2781S.
5, Hill JO. & Prentice AM. 1995. Sugar and body weight regulation. Am J Clin Nutr.; 62(1)(suppl):264S273S.
6, Mansoor N, Vinknes KJ, Veierød MB, 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. Br J Nutr. 2016;115(3):466-479.
7, Wang DD, Li Y, Chiuve SE, et al. Association of specific dietary fats with total and cause-specific mortality.JAMA Intern Med. 2016;176(8):1134-1145.
8, Ludwig DS. & Friedman MI. 2014. Increasing adiposity: consequence or cause of overeating? JAMA.; 311(21):2167-2168.
9, Mozaffarian D. et al. 2011. Changes in diet and lifestyle and long-term weight gain in women and men. N Engl J Med.; 364(25):2392-2404.
10, Diwakarla, S. et al. 2017. Heterogeneity of enterochromaffin cells within the gastrointestinal tract. Neurogastroenterol Motil; 29(6). doi: 10.1111/nmo.13101
11, Martin AM. et al. 2017. The Diverse Metabolic Roles of Peripheral Serotonin. Endocrinology; 158(5):1049-1063. doi: 10.1210/en.2016-1839.
12, Bloomfield HE. et al. 2016. Effects on Health Outcomes of a Mediterranean Diet With No Restriction on Fat Intake: A Systematic Review and Meta-analysis. Ann Intern Med.; 165:491–500. doi: 10.7326/M16-0361
13, Dr Malhotra,A. & O’Neill, D. 2017. The Pioppi Diet. Penguin Books Ltd. ISBN10 1405932635
