Low Fat Diet – StatPearls

Definition/Introduction

There is a consensus among all clinical specialties that the fat content of the average diet should be lowered to decrease the risk of cardiovascular morbidity and mortality. Low-fat diets are food where 30% or less of the calories come from fat. Multiple correlational studies have related a country’s cardiovascular mortality to the food consumption of its population.[1]

A general rule is that if a provides 100 calories and it has 3 grams or less of fat, then it is a low-fat food. Common examples include vegetables, fruits, whole grain cereals, egg whites, chicken and turkey breast without skin, beans, lentils, peas, seafood, and low-fat dairy, among others.

Fats are essential to us, but we need to consume them in a limited amount. The main four types of dietary fats include polyunsaturated, monounsaturated, trans, and saturated fats. These four varieties of fats differ in their physical and chemical structures. The saturated and trans fats are considered solid at room temperature, whereas the mono and polyunsaturated fats are liquid at room temperature. Regardless of their physical and chemical properties, these all different forms of fat provide nine calories for every gram consumed, which is much higher than the amount of energy supplied per gram of carbohydrates or proteins. The saturated and trans fats raise the low-density lipoproteins (LDL) and are considered unhealthy, whereas the monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), which lower LDL, are considered beneficial.

Current National Cholesterol Education Program (NCEP) guidelines for adults based on ATP III (Adult Treatment Panel III) recommends reducing intake of saturated fats to less than 7 % of the total calories and cholesterol to less than 200 mg/day. Guidelines also recommend that polyunsaturated fat constitutes up to 10% of total calories, and monounsaturated fats constitute up to 20% of total calories. [2]

There is abundant literature to suggest that a decrease or modification of serum cholesterol is a possible way to prevent atherosclerosis. Decreasing the amount of fat intake is an effective means of lowering the serum cholesterol concentration. Hence, a low-fat diet has been widely advocated by clinicians for reducing the cardiovascular-related morbidity and mortality of their patients.

Issues of Concern

There have been multiple issues of concern and controversies around the concept of a low-fat diet. The biggest concern with the promotion of the low-fat diet has been that manufacturing companies are touting products labeled as low-fat products, where they are replacing the fat with large amounts of refined carbohydrates, which increase the risk of metabolic disorders and hypertriglyceridemia. Studies are also reporting that diets rich in carbohydrates, and low in unsaturated fat, can also negatively impact lipoprotein risk factors and increase cardiovascular risks. [3] There is also a proposed theory that refined carbohydrates decrease the cardioprotective action of HDL by altering its metabolic functions.[4] There has undoubtedly been a focus on replacing the carbohydrates for fats, but the specificities of the replaced carbohydrates remain poorly defined.[5] These concerns have led to the development of alternative dietary approaches.[6]

Studies have also raised concern over the potential of lowering HDL cholesterol, raising triglycerides, and cause unfavorable postprandial lipemic changes.[7][8] So much so that the “2013 AHA/ACC Guideline on Lifestyle Management to Reduce Cardiovascular Risk” did not state any recommendations for dietary cholesterol and indicated a lack of sufficient evidence to show that lowering of dietary cholesterol reduces LDL-C (low-density lipoprotein cholesterol) or not.[9]

The 2015 Dietary Guidelines Advisory Committee did not endorse limiting dietary cholesterol to less than 300 mg/dL as presented in their prior editions. The committee made recommendations with a focus on dietary patterns rather than on the macronutrients.[10]

Clinical Significance

Association with
Cardiovascular Disease

There has been a direct relationship between dietary fat intake and cardiovascular disease (CVD).[11] Besides, dietary cholesterol has been a focus of considerable attention due to a direct connection between diet and blood cholesterol levels and the subsequent risk for coronary artery disease.[12] The level of LDL particles is the best predictor of cardiovascular risk.[13][14] Studies have concluded that saturated fatty acids raised blood cholesterol levels, whereas PUFA’s reduced serum cholesterol levels and MUFA’s were neutral.[15] Studies have also found myristic and palmitic acid to have cholesterol elevating effects, whereas stearic acid did not affect the levels.[16] Trans fatty acids are similar to saturated fatty acids in raising cholesterol, as well.[17] The level of saturated fats, trans-fatty acids should be low, and the levels of polyunsaturated fatty acids should be high. [15] The results from the Nurses’ Health Study, in which the women who consumed diets low in saturated and trans fatty acids and relatively high in unhydrogenated mono- and polyunsaturated fatty acids had the least risk for cardiovascular outcomes.[18]

Recent studies have reported that in men, the reduction of total fat and saturated fatty acids from 36% and 12% of energy to 27% and 8% of energy, respectively, resulted in a substantial decline in the total and LDL cholesterol levels.[19][20]. Over the years, although there has been some decline in the percentage of fat intake, there has been a paradoxical increase in the total amount of fat intake, suggesting that the total energy intake has increased. A large part of the U.S. population still consume diets that contain more total and saturated fatty acids than recommended in dietary guidelines, which is an area of concern.

Association with Cancer

The association between dietary fat and the risk of cancer development has had consistent support through multiple studies. There is epidemiologic evidence demonstrating associations between dietary fat intake and breast, prostate, colon, and even lung cancers in humans.[21]

Of those cancers, dietary fat intake has been the most extensively linked with breast cancer.[22] Various mechanisms have been suggested, including conversion of essential fatty acids to short-lived hormone-like lipids, the production of reactive oxygen species that carry the potential to induce changes in the genomic DNA changes, leading to alterations in gene expression.[23] Other potential mechanisms include modifications in the hypothalamus-pituitary axis leading to alterations in hormone levels, the effect on enzyme functions affecting the estrogen, changes in the structure and functioning of the cells, and changes in immune function.[24] Studies have also suggested a positive effect of polyunsaturated fatty acids, especially the omega -3 fatty acids, to have a protective effect against the development of cancers and high animal fat to have the strongest positive correlation for developing these cancers.

One potential mechanism for the relationship between fat intake and prostate cancer include altered levels of sex hormones.[25] Studies have shown that mortality data from colorectal cancer correlated with the consumption of animal fat. Potential mechanisms for a diet and colon cancer link are primarily related to bile acid secretion or intestinal metabolism.[26] Populations that consume foods containing olive oil or oils derived from marine animals and fish have a significantly lower likelihood of developing colon cancer, suggesting again that fat quality is much more important than the type of dietary fat.[27]

Association with Obesity

Obesity is a chronic disease associated with a plethora of comorbidities like diabetes mellitus, dyslipidemia, hypertension, fatty liver, and obstructive sleep apnea, to name a few.[28][29][30] It has multiple external and internal influences. Among the many environmental impacts, dietary fat intake is thought to have the strongest association. Energy imbalances result from excessive nutritional intakes along with low levels of physical activity. If we use BMI as the criterion to define obesity, more than one-third of adults in the United States are categorized as overweight or obese.[31] The rate at which obesity is increasing in this country and throughout the world is alarming. The relationship between diet composition and body weight has been studied in various epidemiological studies, including ecologic, cross-sectional, and prospective studies.[32] Most of the cross-sectional studies show that obese patients have a higher intake of energy from fat than people with a healthy BMI.[33] Fat being an energy-dense food contributes to excess calorie ingestion as compared to other foods. There has also been a hypothesis that obese subjects have difficulty oxidizing fat and maybe under oxidizing it compared to their leaner counterparts.[34]  Recent data suggest that for a reduction in absolute amounts of fat consumed and a decline in the percentage of total dietary intake at the population level, a concomitant decrease in body weight has not occurred. [35]

Nursing, Allied Health, and Interprofessional Team Interventions

As an interprofessional health care team taking care of patients, practitioners must work in unison to provide the best dietary care practices. Recent recommendations have focused more on advocating proper dietary patterns rather than laying emphasis on macronutrients. Commensurate with the above approach focuses on a lifestyle approach, also called the Therapeutic Lifestyle Changes (TLC). It is the lifestyle component of the third report of the NCEP Adult Treatment Panel (ATP) III guidelines and is currently advocated by various health organizations, including the American Diabetes Association, American Heart Association, and The Obesity Society. It is currently a recommended therapeutic strategy for metabolic and cardiovascular health benefits.

The providers must develop tools to educate their team members, including nursing and allied health personnel, about this concept. This approach will help in forming a comprehensive team approach to propagate this strategy among the patient population. The team members need to comprehend the benefits of such a diet, which are not limited to improving the risk of developing metabolic syndrome, diabetes, hypertension, hyperlipidemia, obesity, and cardiovascular risk factors.

Patients should receive advice to follow a dietary pattern with emphasizes increased intake of vegetables, fruits, whole grains, low-fat dairy, poultry, fish, legumes, nontropical vegetables and oils, and limits consumption of sweets, sugar-sweetened beverages, and red meats. It also emphasizes the DASH dietary pattern along with lower sodium intake. Adults should also engage in aerobic physical activity to reduce LDL cholesterol and non -HDL cholesterol to counter the obesity epidemic and its various co-morbidities. The team of primary care providers, nurse practitioners, dietitians, and internists must be aware of the perils of high-fat content in the diet and form a multidisciplinary approach to manage the patient. A shared decision-making process with the patient is imperative to initiate this dietary change.

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

1.

Mann J. Complex carbohydrates: replacement energy for fat or useful in their own right? Am J Clin Nutr. 1987 May;45(5 Suppl):1202-6. [PubMed: 3554968]

2.

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001 May 16;285(19):2486-97. [PubMed: 11368702]

3.

Sacks FM, Lichtenstein AH, Wu JHY, Appel LJ, Creager MA, Kris-Etherton PM, Miller M, Rimm EB, Rudel LL, Robinson JG, Stone NJ, Van Horn LV., American Heart Association. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. Circulation. 2017 Jul 18;136(3):e1-e23. [PubMed: 28620111]

4.

Andraski AB, Singh SA, Lee LH, Higashi H, Smith N, Zhang B, Aikawa M, Sacks FM. Effects of Replacing Dietary Monounsaturated Fat With Carbohydrate on HDL (High-Density Lipoprotein) Protein Metabolism and Proteome Composition in Humans. Arterioscler Thromb Vasc Biol. 2019 Nov;39(11):2411-2430. [PMC free article: PMC6874109] [PubMed: 31554421]

5.

Berglund L, Lefevre M, Ginsberg HN, Kris-Etherton PM, Elmer PJ, Stewart PW, Ershow A, Pearson TA, Dennis BH, Roheim PS, Ramakrishnan R, Reed R, Stewart K, Phillips KM., DELTA Investigators. Comparison of monounsaturated fat with carbohydrates as a replacement for saturated fat in subjects with a high metabolic risk profile: studies in the fasting and postprandial states. Am J Clin Nutr. 2007 Dec;86(6):1611-20. [PubMed: 18065577]

6.

Bolla AM, Caretto A, Laurenzi A, Scavini M, Piemonti L. Low-Carb and Ketogenic Diets in Type 1 and Type 2 Diabetes. Nutrients. 2019 Apr 26;11(5) [PMC free article: PMC6566854] [PubMed: 31035514]

7.

Ginsberg HN, Kris-Etherton P, Dennis B, Elmer PJ, Ershow A, Lefevre M, Pearson T, Roheim P, Ramakrishnan R, Reed R, Stewart K, Stewart P, Phillips K, Anderson N. Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: the DELTA Study, protocol 1. Arterioscler Thromb Vasc Biol. 1998 Mar;18(3):441-9. [PubMed: 9514413]

8.

Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb. 1992 Aug;12(8):911-9. [PubMed: 1386252]

9.

Eckel RH, Jakicic JM, Ard JD, de Jesus JM, Houston Miller N, Hubbard VS, Lee IM, Lichtenstein AH, Loria CM, Millen BE, Nonas CA, Sacks FM, Smith SC, Svetkey LP, Wadden TA, Yanovski SZ., American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Jul 01;63(25 Pt B):2960-84. [PubMed: 24239922]

10.

Jahns L, Davis-Shaw W, Lichtenstein AH, Murphy SP, Conrad Z, Nielsen F. The History and Future of Dietary Guidance in America. Adv Nutr. 2018 Mar 01;9(2):136-147. [PMC free article: PMC5916427] [PubMed: 29659693]

11.

Nettleton JA, Brouwer IA, Geleijnse JM, Hornstra G. Saturated Fat Consumption and Risk of Coronary Heart Disease and Ischemic Stroke: A Science Update. Ann Nutr Metab. 2017;70(1):26-33. [PMC free article: PMC5475232] [PubMed: 28125802]

12.

Tsoupras A, Lordan R, Zabetakis I. Inflammation, not Cholesterol, Is a Cause of Chronic Disease. Nutrients. 2018 May 12;10(5) [PMC free article: PMC5986484] [PubMed: 29757226]

13.

Upadhyay RK. Emerging risk biomarkers in cardiovascular diseases and disorders. J Lipids. 2015;2015:971453. [PMC free article: PMC4407625] [PubMed: 25949827]

14.

Cromwell WC, Otvos JD, Keyes MJ, Pencina MJ, Sullivan L, Vasan RS, Wilson PW, D’Agostino RB. LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study – Implications for LDL Management. J Clin Lipidol. 2007 Dec;1(6):583-92. [PMC free article: PMC2720529] [PubMed: 19657464]

15.

Siri-Tarino PW, Chiu S, Bergeron N, Krauss RM. Saturated Fats Versus Polyunsaturated Fats Versus Carbohydrates for Cardiovascular Disease Prevention and Treatment. Annu Rev Nutr. 2015;35:517-43. [PMC free article: PMC4744652] [PubMed: 26185980]

16.

Tholstrup T, Vessby B, Sandstrom B. Difference in effect of myristic and stearic acid on plasma HDL cholesterol within 24 h in young men. Eur J Clin Nutr. 2003 Jun;57(6):735-42. [PubMed: 12792657]

17.

Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients. Curr Atheroscler Rep. 2010 Nov;12(6):384-90. [PMC free article: PMC2943062] [PubMed: 20711693]

18.

Dhaka V, Gulia N, Ahlawat KS, Khatkar BS. Trans fats-sources, health risks and alternative approach – A review. J Food Sci Technol. 2011 Oct;48(5):534-41. [PMC free article: PMC3551118] [PubMed: 23572785]

19.

Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):502-9. [PMC free article: PMC2824150] [PubMed: 20089734]

20.

Briggs MA, Petersen KS, Kris-Etherton PM. Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk. Healthcare (Basel). 2017 Jun 21;5(2) [PMC free article: PMC5492032] [PubMed: 28635680]

21.

Donaldson MS. Nutrition and cancer: a review of the evidence for an anti-cancer diet. Nutr J. 2004 Oct 20;3:19. [PMC free article: PMC526387] [PubMed: 15496224]

22.

Holmes MD, Willett WC. Does diet affect breast cancer risk? Breast Cancer Res. 2004;6(4):170-8. [PMC free article: PMC468678] [PubMed: 15217490]

23.

Ayala A, Muñoz MF, Argüelles S. Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal. Oxid Med Cell Longev. 2014;2014:360438. [PMC free article: PMC4066722] [PubMed: 24999379]

24.

Herman JP, McKlveen JM, Ghosal S, Kopp B, Wulsin A, Makinson R, Scheimann J, Myers B. Regulation of the Hypothalamic-Pituitary-Adrenocortical Stress Response. Compr Physiol. 2016 Mar 15;6(2):603-21. [PMC free article: PMC4867107] [PubMed: 27065163]

25.

Di Sebastiano KM, Mourtzakis M. The role of dietary fat throughout the prostate cancer trajectory. Nutrients. 2014 Dec 22;6(12):6095-109. [PMC free article: PMC4277017] [PubMed: 25533015]

26.

Ocvirk S, O’Keefe SJ. Influence of Bile Acids on Colorectal Cancer Risk: Potential Mechanisms Mediated by Diet – Gut Microbiota Interactions. Curr Nutr Rep. 2017 Dec;6(4):315-322. [PMC free article: PMC5802424] [PubMed: 29430336]

27.

Liu AG, Ford NA, Hu FB, Zelman KM, Mozaffarian D, Kris-Etherton PM. A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion. Nutr J. 2017 Aug 30;16(1):53. [PMC free article: PMC5577766] [PubMed: 28854932]

28.

Engin A. The Definition and Prevalence of Obesity and Metabolic Syndrome. Adv Exp Med Biol. 2017;960:1-17. [PubMed: 28585193]

29.

Lavie CJ, De Schutter A, Parto P, Jahangir E, Kokkinos P, Ortega FB, Arena R, Milani RV. Obesity and Prevalence of Cardiovascular Diseases and Prognosis-The Obesity Paradox Updated. Prog Cardiovasc Dis. 2016 Mar-Apr;58(5):537-47. [PubMed: 26826295]

30.

Meldrum DR, Morris MA, Gambone JC. Obesity pandemic: causes, consequences, and solutions-but do we have the will? Fertil Steril. 2017 Apr;107(4):833-839. [PubMed: 28292617]

31.

Cetin D, Lessig BA, Nasr E. Comprehensive Evaluation for Obesity: Beyond Body Mass Index. J Am Osteopath Assoc. 2016 Jun 01;116(6):376-82. [PubMed: 27214774]

32.

Satija A, Yu E, Willett WC, Hu FB. Understanding nutritional epidemiology and its role in policy. Adv Nutr. 2015 Jan;6(1):5-18. [PMC free article: PMC4288279] [PubMed: 25593140]

33.

Galgani J, Ravussin E. Energy metabolism, fuel selection and body weight regulation. Int J Obes (Lond). 2008 Dec;32 Suppl 7(Suppl 7):S109-19. [PMC free article: PMC2897177] [PubMed: 19136979]

34.

Bergouignan A, Kealey EH, Schmidt SL, Jackman MR, Bessesen DH. Twenty-four hour total and dietary fat oxidation in lean, obese and reduced-obese adults with and without a bout of exercise. PLoS One. 2014;9(4):e94181. [PMC free article: PMC3979741] [PubMed: 24714529]

35.

Lichtenstein AH, Kennedy E, Barrier P, Danford D, Ernst ND, Grundy SM, Leveille GA, Van Horn L, Williams CL, Booth SL. Dietary fat consumption and health. Nutr Rev. 1998 May;56(5 Pt 2):S3-19; discussion S19-28. [PubMed: 9624878]

Disclosure: Priyanka Bhandari declares no relevant financial relationships with ineligible companies.

Disclosure: Amit Sapra declares no relevant financial relationships with ineligible companies.

Low Fat Diet – StatPearls

Definition/Introduction

There is a consensus among all clinical specialties that the fat content of the average diet should be lowered to decrease the risk of cardiovascular morbidity and mortality. Low-fat diets are food where 30% or less of the calories come from fat. Multiple correlational studies have related a country’s cardiovascular mortality to the food consumption of its population.[1]

A general rule is that if a provides 100 calories and it has 3 grams or less of fat, then it is a low-fat food. Common examples include vegetables, fruits, whole grain cereals, egg whites, chicken and turkey breast without skin, beans, lentils, peas, seafood, and low-fat dairy, among others.

Fats are essential to us, but we need to consume them in a limited amount. The main four types of dietary fats include polyunsaturated, monounsaturated, trans, and saturated fats. These four varieties of fats differ in their physical and chemical structures. The saturated and trans fats are considered solid at room temperature, whereas the mono and polyunsaturated fats are liquid at room temperature. Regardless of their physical and chemical properties, these all different forms of fat provide nine calories for every gram consumed, which is much higher than the amount of energy supplied per gram of carbohydrates or proteins. The saturated and trans fats raise the low-density lipoproteins (LDL) and are considered unhealthy, whereas the monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), which lower LDL, are considered beneficial.

Current National Cholesterol Education Program (NCEP) guidelines for adults based on ATP III (Adult Treatment Panel III) recommends reducing intake of saturated fats to less than 7 % of the total calories and cholesterol to less than 200 mg/day. Guidelines also recommend that polyunsaturated fat constitutes up to 10% of total calories, and monounsaturated fats constitute up to 20% of total calories.[2]

There is abundant literature to suggest that a decrease or modification of serum cholesterol is a possible way to prevent atherosclerosis. Decreasing the amount of fat intake is an effective means of lowering the serum cholesterol concentration. Hence, a low-fat diet has been widely advocated by clinicians for reducing the cardiovascular-related morbidity and mortality of their patients.

Issues of Concern

There have been multiple issues of concern and controversies around the concept of a low-fat diet. The biggest concern with the promotion of the low-fat diet has been that manufacturing companies are touting products labeled as low-fat products, where they are replacing the fat with large amounts of refined carbohydrates, which increase the risk of metabolic disorders and hypertriglyceridemia. Studies are also reporting that diets rich in carbohydrates, and low in unsaturated fat, can also negatively impact lipoprotein risk factors and increase cardiovascular risks. [3] There is also a proposed theory that refined carbohydrates decrease the cardioprotective action of HDL by altering its metabolic functions.[4] There has undoubtedly been a focus on replacing the carbohydrates for fats, but the specificities of the replaced carbohydrates remain poorly defined.[5] These concerns have led to the development of alternative dietary approaches.[6]

Studies have also raised concern over the potential of lowering HDL cholesterol, raising triglycerides, and cause unfavorable postprandial lipemic changes.[7][8] So much so that the “2013 AHA/ACC Guideline on Lifestyle Management to Reduce Cardiovascular Risk” did not state any recommendations for dietary cholesterol and indicated a lack of sufficient evidence to show that lowering of dietary cholesterol reduces LDL-C (low-density lipoprotein cholesterol) or not.[9]

The 2015 Dietary Guidelines Advisory Committee did not endorse limiting dietary cholesterol to less than 300 mg/dL as presented in their prior editions. The committee made recommendations with a focus on dietary patterns rather than on the macronutrients.[10]

Clinical Significance

Association with
Cardiovascular Disease

There has been a direct relationship between dietary fat intake and cardiovascular disease (CVD).[11] Besides, dietary cholesterol has been a focus of considerable attention due to a direct connection between diet and blood cholesterol levels and the subsequent risk for coronary artery disease.[12] The level of LDL particles is the best predictor of cardiovascular risk.[13][14] Studies have concluded that saturated fatty acids raised blood cholesterol levels, whereas PUFA’s reduced serum cholesterol levels and MUFA’s were neutral.[15] Studies have also found myristic and palmitic acid to have cholesterol elevating effects, whereas stearic acid did not affect the levels.[16] Trans fatty acids are similar to saturated fatty acids in raising cholesterol, as well.[17] The level of saturated fats, trans-fatty acids should be low, and the levels of polyunsaturated fatty acids should be high. [15] The results from the Nurses’ Health Study, in which the women who consumed diets low in saturated and trans fatty acids and relatively high in unhydrogenated mono- and polyunsaturated fatty acids had the least risk for cardiovascular outcomes.[18]

Recent studies have reported that in men, the reduction of total fat and saturated fatty acids from 36% and 12% of energy to 27% and 8% of energy, respectively, resulted in a substantial decline in the total and LDL cholesterol levels.[19][20]. Over the years, although there has been some decline in the percentage of fat intake, there has been a paradoxical increase in the total amount of fat intake, suggesting that the total energy intake has increased. A large part of the U.S. population still consume diets that contain more total and saturated fatty acids than recommended in dietary guidelines, which is an area of concern.

Association with Cancer

The association between dietary fat and the risk of cancer development has had consistent support through multiple studies. There is epidemiologic evidence demonstrating associations between dietary fat intake and breast, prostate, colon, and even lung cancers in humans.[21]

Of those cancers, dietary fat intake has been the most extensively linked with breast cancer.[22] Various mechanisms have been suggested, including conversion of essential fatty acids to short-lived hormone-like lipids, the production of reactive oxygen species that carry the potential to induce changes in the genomic DNA changes, leading to alterations in gene expression.[23] Other potential mechanisms include modifications in the hypothalamus-pituitary axis leading to alterations in hormone levels, the effect on enzyme functions affecting the estrogen, changes in the structure and functioning of the cells, and changes in immune function.[24] Studies have also suggested a positive effect of polyunsaturated fatty acids, especially the omega -3 fatty acids, to have a protective effect against the development of cancers and high animal fat to have the strongest positive correlation for developing these cancers.

One potential mechanism for the relationship between fat intake and prostate cancer include altered levels of sex hormones.[25] Studies have shown that mortality data from colorectal cancer correlated with the consumption of animal fat. Potential mechanisms for a diet and colon cancer link are primarily related to bile acid secretion or intestinal metabolism.[26] Populations that consume foods containing olive oil or oils derived from marine animals and fish have a significantly lower likelihood of developing colon cancer, suggesting again that fat quality is much more important than the type of dietary fat.[27]

Association with Obesity

Obesity is a chronic disease associated with a plethora of comorbidities like diabetes mellitus, dyslipidemia, hypertension, fatty liver, and obstructive sleep apnea, to name a few.[28][29][30] It has multiple external and internal influences. Among the many environmental impacts, dietary fat intake is thought to have the strongest association. Energy imbalances result from excessive nutritional intakes along with low levels of physical activity. If we use BMI as the criterion to define obesity, more than one-third of adults in the United States are categorized as overweight or obese.[31] The rate at which obesity is increasing in this country and throughout the world is alarming. The relationship between diet composition and body weight has been studied in various epidemiological studies, including ecologic, cross-sectional, and prospective studies.[32] Most of the cross-sectional studies show that obese patients have a higher intake of energy from fat than people with a healthy BMI.[33] Fat being an energy-dense food contributes to excess calorie ingestion as compared to other foods. There has also been a hypothesis that obese subjects have difficulty oxidizing fat and maybe under oxidizing it compared to their leaner counterparts.[34]  Recent data suggest that for a reduction in absolute amounts of fat consumed and a decline in the percentage of total dietary intake at the population level, a concomitant decrease in body weight has not occurred. [35]

Nursing, Allied Health, and Interprofessional Team Interventions

As an interprofessional health care team taking care of patients, practitioners must work in unison to provide the best dietary care practices. Recent recommendations have focused more on advocating proper dietary patterns rather than laying emphasis on macronutrients. Commensurate with the above approach focuses on a lifestyle approach, also called the Therapeutic Lifestyle Changes (TLC). It is the lifestyle component of the third report of the NCEP Adult Treatment Panel (ATP) III guidelines and is currently advocated by various health organizations, including the American Diabetes Association, American Heart Association, and The Obesity Society. It is currently a recommended therapeutic strategy for metabolic and cardiovascular health benefits.

The providers must develop tools to educate their team members, including nursing and allied health personnel, about this concept. This approach will help in forming a comprehensive team approach to propagate this strategy among the patient population. The team members need to comprehend the benefits of such a diet, which are not limited to improving the risk of developing metabolic syndrome, diabetes, hypertension, hyperlipidemia, obesity, and cardiovascular risk factors.

Patients should receive advice to follow a dietary pattern with emphasizes increased intake of vegetables, fruits, whole grains, low-fat dairy, poultry, fish, legumes, nontropical vegetables and oils, and limits consumption of sweets, sugar-sweetened beverages, and red meats. It also emphasizes the DASH dietary pattern along with lower sodium intake. Adults should also engage in aerobic physical activity to reduce LDL cholesterol and non -HDL cholesterol to counter the obesity epidemic and its various co-morbidities. The team of primary care providers, nurse practitioners, dietitians, and internists must be aware of the perils of high-fat content in the diet and form a multidisciplinary approach to manage the patient. A shared decision-making process with the patient is imperative to initiate this dietary change.

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

1.

Mann J. Complex carbohydrates: replacement energy for fat or useful in their own right? Am J Clin Nutr. 1987 May;45(5 Suppl):1202-6. [PubMed: 3554968]

2.

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001 May 16;285(19):2486-97. [PubMed: 11368702]

3.

Sacks FM, Lichtenstein AH, Wu JHY, Appel LJ, Creager MA, Kris-Etherton PM, Miller M, Rimm EB, Rudel LL, Robinson JG, Stone NJ, Van Horn LV., American Heart Association. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. Circulation. 2017 Jul 18;136(3):e1-e23. [PubMed: 28620111]

4.

Andraski AB, Singh SA, Lee LH, Higashi H, Smith N, Zhang B, Aikawa M, Sacks FM. Effects of Replacing Dietary Monounsaturated Fat With Carbohydrate on HDL (High-Density Lipoprotein) Protein Metabolism and Proteome Composition in Humans. Arterioscler Thromb Vasc Biol. 2019 Nov;39(11):2411-2430. [PMC free article: PMC6874109] [PubMed: 31554421]

5.

Berglund L, Lefevre M, Ginsberg HN, Kris-Etherton PM, Elmer PJ, Stewart PW, Ershow A, Pearson TA, Dennis BH, Roheim PS, Ramakrishnan R, Reed R, Stewart K, Phillips KM., DELTA Investigators. Comparison of monounsaturated fat with carbohydrates as a replacement for saturated fat in subjects with a high metabolic risk profile: studies in the fasting and postprandial states. Am J Clin Nutr. 2007 Dec;86(6):1611-20. [PubMed: 18065577]

6.

Bolla AM, Caretto A, Laurenzi A, Scavini M, Piemonti L. Low-Carb and Ketogenic Diets in Type 1 and Type 2 Diabetes. Nutrients. 2019 Apr 26;11(5) [PMC free article: PMC6566854] [PubMed: 31035514]

7.

Ginsberg HN, Kris-Etherton P, Dennis B, Elmer PJ, Ershow A, Lefevre M, Pearson T, Roheim P, Ramakrishnan R, Reed R, Stewart K, Stewart P, Phillips K, Anderson N. Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: the DELTA Study, protocol 1. Arterioscler Thromb Vasc Biol. 1998 Mar;18(3):441-9. [PubMed: 9514413]

8.

Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb. 1992 Aug;12(8):911-9. [PubMed: 1386252]

9.

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Disclosure: Priyanka Bhandari declares no relevant financial relationships with ineligible companies.

Disclosure: Amit Sapra declares no relevant financial relationships with ineligible companies.

90,000 Who is eligible for a low-carb, high-fat diet?

Low-carbohydrate diets are now very popular for weight loss, and everyone who is not lazy “sits” on them. More precisely, those who have enough willpower and health to withstand this style of eating. How effective are such diets, and to whom are they shown?

How Reducing Carbohydrates Treats Epilepsy

In the 1920s, a low-carbohydrate, moderate-protein, high-fat diet was well established in the treatment of epilepsy. Scientists have noticed that with a lack of carbohydrates in the diet, the brain begins to use not glucose, but ketone bodies (metabolic products formed in the liver) as an energy source. At the same time, patients with epilepsy feel much better.

The diet has become known as the ketogenic diet, and numerous experiments have shown that it is actually effective. One study involved children under 2 years of age suffering from daily epilepsy attacks. On the background of the ketogenic diet, the number and severity of seizures decreased by 50%. Now the ketogenic diet is also successfully used in pediatrics for the treatment of neurological diseases.

An important point — Throughout the entire period of therapeutic nutrition, it is necessary to control the amount of ketone bodies in the urine and, if necessary, adjust the diet.

Dr. Atkins’ Low Carbohydrate Diet

More recently it has been discovered that the ketogenic diet leads to weight loss because ketone bodies are formed from fatty acids. In other words, when there is a lack of glucose in the body, the liver begins to process fat reserves.

In the 1970s, American cardiologist Robert Atkins adapted ketogenic nutrition into a weight loss diet, but it only became popular in the early 2000s. At that time, many Hollywood stars “hooked” on Atkins and achieved stunning results. Yes, and the author of the diet lost 28 kg on it. The essence of the diet is that you can not limit yourself in calories by eating proteins and fats, and minimize carbohydrates. So that the body does not suffer from a lack of vitamins and fiber, non-starchy vegetables are included in the diet. Agree, with cucumbers, tomatoes, peppers, zucchini, broccoli, leafy greens, you can make a completely normal menu. In addition, small amounts of fruits, berries and grains are sometimes allowed.

The Atkins Diet consists of four phases (induction, weight loss, transition, maintenance), and each phase has its own dietary recommendations, including the amount of carbohydrates. Compared to the classic keto diet, the Atkins diet has fewer restrictions, more proteins, and there is no need to control the level of ketones.

Modern low-carbohydrate diets

The classic keto diet, developed for the treatment of epilepsy, is the basis of many low-carbohydrate diets. For example, the LCHF (Low Carb High Fat) food system, developed by the Swedish nutritionist Andreas Enfeldt, is not very strict. You just try to eat fewer carbohydrates, the rest – at will. True, it is better to exclude harmful foods and fast food.

French physician Pierre Ducane created a low-carbohydrate diet, high in protein and low in fat and carbohydrates. This food system is tough, as the diet consists of only 100 products. Dukan, like Atkins, also has 4 stages – attack, cruise, consolidation and stabilization. This food system later had a Russian analogue – the “Kremlin” diet. Within the framework of the Kremlin, each product is assigned a price in conventional units, where 1 c.u. equals 1 g of carbohydrates. But if Dukan allows you to consume up to 20 g of carbohydrates per day, then the Kremlin diet is more sparing and allows up to 40 g of carbohydrates in the daily diet.

The German gastroenterologist Walter L. Wegtlin is considered to be the author of the paleo diet. The fact is that in the Paleolithic era there was no agriculture, and people ate what they could take from nature – meat, fish, nuts, fruits and plants, without specially growing them. In this system, there are no strict calculations of the norms of proteins, fats and carbohydrates, but it is recommended to eat in moderation and only when hunger appears. The paleo diet has two therapeutic varieties – epipaleo from the American neurosurgeon Jack Cruz for the treatment of leptin resistance and the autoimmune paleo diet (AIP) for the relief of autoimmune thyroiditis.

Dr. Berg’s Keto Diet

World-famous keto expert Dr. Eric Berg promotes “Healthy Keto”, believing that you first need to get healthy, and then the body will get rid of excess weight. In his nutrition system, losing weight is a nice bonus, the main thing is the restoration of proper metabolism and hormonal levels.

Dr. Berg advises to give preference to exclusively natural farm products, include in the diet a sufficient amount of healthy fats (organic butter, coconut, olive oil, avocado), eat as many non-starchy vegetables and greens as possible. The amount of carbohydrates is up to 50 g, which is more than on other low-carbohydrate diets, while vegetables and greens are not taken into account when calculating BJU. Berg recommends erythritol, xylitol, and stevia as natural sweeteners.

The doctor advises eating no more than two or three times a day, explaining that constant snacking leads to an increase in insulin levels, and this provokes the development of insulin resistance and diabetes. The diet, in accordance with Berg’s theory, should be selected according to the type of physique (there are four in total). You should also monitor the sufficient intake of vitamins and minerals in the body, get enough sleep and introduce physical activity into your life.

Low carbohydrate diet and diabetes

Whether a low-carbohydrate diet helps prevent type 2 diabetes is still a subject of debate. At the same time, they note that any diet within the framework of proper nutrition can give good results. A keto diet, even with carbohydrates up to 50 g per day, is quite difficult for long-term adherence, a diet with carbohydrates up to 150 g is much more practical. However, it is too early to talk about the benefits of low-carb diets for the prevention of diabetes due to the lack of data confirming their effectiveness.

It is believed that lower glucose levels and increased insulin sensitivity are due to weight loss, not carbohydrate reduction. What’s more, studies have shown that a balanced, high-carbohydrate, calorie-restricted diet leads to the same results in terms of insulin resistance as low-carbohydrate diets, only without the side effects of constipation due to a lack of fiber.

Low carb and sport

Many athletes go on low-carbohydrate diets, believing that they increase the body’s endurance and help them achieve high results. However, in the course of the experiments, it turned out that athletes who adhere to the keto diet do not show special sports records. Moreover, some of those who eat more carbohydrates are more effective during training and competition.

Celine Evans, a dietitian and nutrition coach at the Canadian company Lifesport Coaching, is wary of claims that the ketogenic diet has any positive effect on athletic performance. “In a recent review of eight different studies of the ketogenic diet in cyclists and runners, not only was there a very high rate of diet non-compliance (over 50% in some studies), but no improvement in athletic performance was found among those who were able to complete the study,” she said. she.

Are low carbohydrate diets beneficial?

Scientific studies have shown that low carbohydrate diets do not offer any specific weight loss benefits compared to other diets. At least an experiment with 609 overweight people who were on different diets during the year clearly demonstrated this. However, the undoubted advantage of “low carbohydrates” is the reduction in hunger, which leads to a decrease in the calorie content of the diet.

It is difficult to assess the benefits of such diets for the heart and blood vessels, since the trials have not been conducted for more than 3 years, and it is important to monitor the condition of patients in the long term. In addition, a low level of carbohydrates in the diet increases “bad” cholesterol, and this leads to atherosclerosis and other cardiovascular disorders. The experiment showed that after three weeks of a low-carbohydrate diet, the level of “bad” cholesterol in the subjects increased by 44%. In addition, diets with a predominance of protein (such as the Atkinsk, Dukan, “Kremlin” diets) are fraught with kidney problems, so you definitely shouldn’t eat like that for a long time. This is more of an option when you need to quickly lose weight for an important event.

At the end of the 20th century, scientists began to study ketogenic diets as an adjunct in the treatment of cancer. For experiments, mice with tumors were selected and put on a keto diet, and subsequently a significant decrease in oncological formations was noted. Observations were also made for cancer patients who ate in accordance with the principles of keto. A state of ketosis has been found to increase the sensitivity of certain cancer cells to chemotherapy.

Low carbohydrate diets are contraindicated in liver failure, pancreatitis and congenital disorders of fat metabolism. You should also be aware of the side effects of the first phase of the ketogenic diet. This condition is called ketoflu and is usually accompanied by fatigue, headache, nausea, dizziness, and vomiting. Ketoflu can last from several days to several weeks. Among the more serious “side effects”, it is worth noting fatty liver hepatosis, kidney stones, hypoproteinemia (an abnormal decrease in the level of protein in the blood plasma) and beriberi.

And this is only a small part of what the passion for such diets can turn out to be. Really useful from a scientific point of view is the so-called Mediterranean diet with a predominance of vegetables, fruits, cereals, olive oil and seafood. There are almost no contraindications here.

Impact of a low-fat, plant-based diet versus an animal-derived ketogenic diet on energy intake

The carbohydrate-insulin model of obesity states that a high-carbohydrate diet results in excess insulin secretion, thereby promoting fat storage and increased energy intake. To test this hypothesis, a stationary cross-sectional study was conducted with the participation of 20 volunteers (11 men and 9women) with a stable weight without diabetes at the age of 29.9 ± 1.4 years with a body mass index of 27.8 ± 1.3 kg/m2. The study took place at the Clinical Center of the National Institutes of Health. Volunteers were under stationary observation for 28 days. At baseline, participants were randomized into 2 groups: group 1 consumed minimally processed, low-fat (10.3% fat, 75.2% carbohydrate) plant foods with a high glycemic load (85 g 1000 kcal ^-1 ), group 2 – minimally processed ketogenic low-carb animal food (75.8% fat, 10.0% carbohydrates) with a low glycemic load (6 g 1000 kcal ^{− 1} ). Subjects followed the prescribed diet for 2 weeks, followed by an alternative diet for 2 weeks. One participant dropped out due to hypoglycemia while on a low carbohydrate diet. Throughout the study, volunteers wore loose clothing and were unaware of daily weight, ketone, and continuous glucose measurements. During each phase of the diet, participants were offered three meals a day at standard times and a constant supply of snacks and bottled water. Menus were rotated on a 7-day schedule, and meals were designed to match diets for total calories, protein, and non-starchy vegetables. However, diets varied widely in energy density and percentage of energy derived from carbohydrates versus fat, such that the ketogenic diet was 82% animal products, 10.0% total energy from carbohydrates, 75.8% fat, 14 .2% protein and had an energy density without drinks of 2.2 kcal/g, while the low-fat diet consisted only of plant-based foods and contained 10.3% total energy from fat, 75.2% carbohydrates, 14 .5% protein and had an energy density without drinks of 1.1 kcal/g.

Average daily energy intake was compared between each 2-week diet period, as well as between the last week of each diet. Participants’ daily respiratory chamber energy expenditure was 153 ± 24 kcal/day lower on the low-fat diet compared to the ketogenic diet (2141 ± 17 kcal/day for versus 2294 ± 17 kcal/day; P < 0. 0001), which partially offset the reduction in energy intake with a low-fat diet in terms of overall energy balance.

The low-fat diet resulted in lower sedentary expenditure (1731 ± 21 kcal/day vs. 1891 ± 21 kcal/day; P < 0.0001) and sleep energy expenditure (1392 ± 14 kcal/day vs. c 1568 ± 14 kcal/day; P < 0.0001), while expenditure on physical activity did not differ significantly (393 ± 21 kcal/day vs. 397 ± 21 kcal/day; P = 0.88) in the respiratory camera.

Accelerometry showed no significant difference in physical activity between 2-week diet periods (mean daily metabolic equivalent of 1.502 ± 0.0017 for a low-fat diet versus 1.503 ± 0.0017 for a ketogenic diet; P = 0.82).

The daily respiratory coefficient was significantly higher on the low-fat diet (0.885 ± 0.005 vs. 0.753 ± 0.005; P < 0.0001), indicating significantly greater carbohydrate oxidation (306 ± 15 g/day vs. 24 ± 15 g/day ; P < 0.0001) and lower fat oxidation (49 ± 6 g/day vs. 142 ± 6 g/day; P < 0. 0001).

The ketogenic diet resulted in rapid weight loss during the first week, and overall weight loss after 2 weeks was 1.77 ± 0.32 kg (P < 0.0001). The low-fat diet resulted in slower initial weight loss, but after 2 weeks, the weight loss was 1.09± 0.32 kg (P = 0.003), which was not significantly different from the ketogenic diet (P = 0.15).

Notably, the ketogenic diet resulted in greater net body protein loss despite consuming more protein than did the low-fat diet.

The low-fat diet resulted in significantly lower systolic blood pressure (112.2 ± 0.4 mmHg vs. 115.8 ± 0.4 mmHg; P = 0.0012) and decreased heart rate (72.6 ±0.5 beats per minute compared to 76.9± 0.5 beats per minute; P<0.0001).

Both fasting and postprandial triglycerides are believed to increase the risk of cardiovascular disease. The ketogenic diet resulted in lower fasting triglycerides from baseline, while the low-fat diet increased fasting triglycerides. Notably, despite lower fasting triglycerides during the ketogenic diet, postprandial triglycerides were higher after meals compared with isocaloric meals on the low fat diet, likely due to the very high fat content of the former.