Journal of Clinical and Scientific Research

: 2019  |  Volume : 8  |  Issue : 4  |  Page : 211--212

Ketogenic diet for weight loss

Kanchi Mitra Bhargav, S Lavanya, N Sai Ram 
 Department of Medicine, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

Correspondence Address:
Kanchi Mitra Bhargav
Assistant Professor, Department of Medicine, Sri Venkateswara Institute of Medical Sciences, Tirupati - 517 507, Andhra Pradesh

How to cite this article:
Bhargav KM, Lavanya S, Ram N S. Ketogenic diet for weight loss.J Clin Sci Res 2019;8:211-212

How to cite this URL:
Bhargav KM, Lavanya S, Ram N S. Ketogenic diet for weight loss. J Clin Sci Res [serial online] 2019 [cited 2020 Dec 4 ];8:211-212
Available from:

Full Text

Chronic non-communicable diseases are increasing in recent years.[1] Obesity is a rapidly growing endemic disease and poses a major health problem.[2] A recent study has reported that globally, more than 1.9 billion adults are overweight, and 650 million people are obese.[2] Approximately 2.8 million deaths occur as a result of being overweight or obese.[2] Diet is the cornerstone of any lifestyle intervention programme. Optimisation of nutrition is one of the foremost strategies and a desirable target to be achieved in combating obesity. Studies have shown that a diet with carbohydrate restriction has resulted in marked weight loss.[3] Among diets promoted for various health problems, the ketogenic diet (KD) has a long history. The term KD was coined by Wilder in 1921 who proposed its first use in epilepsy.[4] KD, which is a low-carbohydrate diet, has been tried for weight loss in obesity and has shown greater weight loss when compared to another dietary regimen.[5] KD limits carbohydrate intake, with high-fat levels replacing the lost calories while maintaining a normal protein intake.[1] It comprises around 80% fat, 15% protein and 5% carbohydrates.[1] There are various types of KD. The standard KD (SKD) is a very low carbohydrate with moderate-protein and high-fat diet, consisting of 70% fat, 20% protein and 10% carbohydrates.[6] The cyclical KD includes periods of higher carbohydrates in between the KD cycles, for example, 5 ketogenic days followed by two high-carbohydrate days as a cycle.[6] The targeted KD allows additional carbohydrates around the periods of the intensive physical workout, mostly used by athletes and bodybuilders.[6] The high-protein KD comprises more protein when compared to SKD, and the ratio is 60% fat, 35% protein and 5% carbohydrates.[6] Fat in most of the KDs is provided in the form of long-chain triglycerides (LCTs), e.g., meat, fish, dairy products and eggs.[7] Some KDs incorporate medium-chain triglycerides (MCTs) instead of LCT. MCTs are more ketogenic and accessible to the liver than LCTs and can be used to generate more ketone bodies (KBs).[8] Furthermore, an MCT-based KD is more palatable than LCT-based KD and just as effective as the traditional KD.[8] The main goal of a KD is to create a state of ketosis.[1] Ketosis is the process of KB generation and accumulation as a result of an excessive breakdown of fat due to inadequate carbohydrate availability.[9] Thus, the body shifts from using glucose as the main source of fuel to using KBs.[1] Glucose and fatty acids are broken down to acetyl-coenzyme A (CoA) (a product of the incomplete breakdown of free fatty acids in the liver) to enter the citric acid cycle by combining with oxaloacetate (pyruvate being precursor).[5] Due to low carbohydrates in KD, glycolysis fails and oxaloacetate is not available to combine with acetyl-CoA produced by fatty acid metabolism.[5] This results in shunting of acetyl-CoA to ketogenesis and results in the production of ketones.[10] KBs synthesised in the body are β-hydroxybutyrate, acetoacetate and acetone.[1] They can pass through the blood–brain barrier and can be used as an alternative source of fuel for the brain and other tissues.[1] Erythrocytes do not have mitochondria and cannot utilise KB.[11] Liver lacks in the enzyme thiophorase and hence does not utilise KB.[11] The possible mechanisms for greater weight loss may be decreased appetite due to higher satiety effect of proteins, due to direct appetite suppressant action of KB and also due to changes in circulating the level of various hormones, such as ghrelin and leptin which control appetite.[12],[13] Hence, KD decreases overall energy intake and results in weight loss.[5] Other mechanisms put forwarded are reduced lipogenesis, increased lipolysis, decreased insulin secretion and the thermic effect of proteins.[3],14] Ketosis is the most reliable marker of fat loss.[6] The process of ketosis is a completely physiological mechanism.[6] It was differentiated from pathological ketoacidosis seen in type 1 diabetes by Sir Hans Krebs.[15] In physiological ketosis as seen with intake of KD, serum KB levels rarely exceed 7–8 mmol/L as the brain efficiently uses these ketones and also there is no lowering of blood pH.[16] However, in diabetic ketoacidosis, it can exceed 20 mmol/L and results in lowering of the pH.[16] Besides weight loss, studies have also shown that low-carbohydrate KDs also reduce serum triglycerides and blood glucose levels and thereby reducing risk factors for various chronic diseases.[17] However, there are also various short-term and long-term adverse effects of KDs. These include headache, muscle cramps, backache, bad breath, changes in bowel habits and keto-flu.[5],[6] Other side effects observed are dyslipidaemia, hypoproteinaemia, mineral deficiencies, metabolic acidosis and increased risk of renal stones.[5] People on a KD initially experience rapid weight loss up to 4.5 KG in 2 weeks or less due to diuretic effects.[18] The early weight loss is due to water weight loss.[18] Long-term compliance is poor and can be a major concern.[18] Long-term KD causes glucose intolerance due to insufficient insulin secretion, insulin resistance and reduced beta and alpha cell mass.[19] People with diabetes mellitus taking insulin or oral hypoglycaemic agents can suffer severe hypoglycaemia if the diet is not properly timed.[18] KD is contraindicated in patients with pancreatitis, liver failure, disorders of fat metabolism, primary carnitine deficiency, carnitine palmitoyltransferase deficiency, carnitine translocase deficiency, porphyria or pyruvate kinase deficiency.[18] Diet tolerance can be improved by increasing the frequency of meal.[20] Supplements of calcium, selenium, zinc, Vitamin D and oral alkalis may be used to overcome nutritional deficiencies and kidney stones.[21] Gastrointestinal dysmotility and gastro-oesophageal reflux can be overcome using proton pump inhibitors.[20] KD may be considered for effective weight loss, but the effect is usually limited in time and may also be associated with adverse effects.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Walczyk T, Wick JY. The ketogenic diet: Making a comeback. Consult Pharm 2017;32:388-96.
2Ahirwar R, Mondal PR. Prevalence of obesity in India: A systematic review. Diabetes Metab Syndr 2019;13:318-21.
3Bueno NB, de Melo IS, de Oliveira SL, da Rocha Ataide T. Very-low-carbohydrate ketogenic diet v. Low-fat diet for long-term weight loss: A meta-analysis of randomised controlled trials. Br J Nutr 2013;110:1178-87.
4Wheless JW. History of the ketogenic diet. Epilepsia 2008;49 Suppl 8:3-5.
5Gupta L, Khandelwal D, Kalra S, Gupta P, Dutta D, Aggarwal S. Ketogenic diet in endocrine disorders: Current perspectives. J Postgrad Med 2017;63:242-51.
6Shilpa J, Mohan V. Ketogenic diets: Boon or bane? Indian J Med Res 2018;148:251-3.
7Rogovik AL, Goldman RD. Ketogenic diet for treatment of epilepsy. Can Fam Physician 2010;56:540-2.
8Liu YM, Wang HS. Medium-chain triglyceride ketogenic diet, an effective treatment for drug-resistant epilepsy and a comparison with other ketogenic diets. Biomed J 2013;36:9-15.
9Ketosis. Mosby's Medical Dictionary 8th ed. 2009. Available from: [Last accessed on 2019 Oct 12].
10Laffel L. Ketone bodies: A review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev 1999;15:412-26.
11Mikkelsen KH, Seifert T, Secher NH, Grøndal T, van Hall G. Systemic, cerebral and skeletal muscle ketone body and energy metabolism during acute hyper-D-β-hydroxybutyratemia in post-absorptive healthy males. J Clin Endocrinol Metab 2015;100:636-43.
12Gibson AA, Seimon RV, Lee CM, Ayre J, Franklin J, Markovic TP, et al. Do ketogenic diets really suppress appetite? A systematic review and meta-analysis. Obes Rev 2015;16:64-76.
13Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, et al. Ketosis and appetite-mediating nutrients and hormones after weight loss. Eur J Clin Nutr 2013;67:759-64.
14Paoli A. Ketogenic diet for obesity: Friend or foe? Int J Environ Res Public Health 2014;11:2092-107.
15Krebs HA. The regulation of the release of ketone bodies by the liver. Adv Enzyme Regul 1966;4:339-54.
16Anjana RM, Deepa M, Pradeepa R, Mahanta J, Narain K, Das HK, et al. Prevalence of diabetes and prediabetes in 15 states of India: Results from the ICMR-INDIAB population-based cross-sectional study. Lancet Diabetes Endocrinol 2017;5:585-96.
17Dashti HM, Mathew TC, Hussein T, Asfar SK, Behbahani A, Khoursheed MA, et al. Long-term effects of a ketogenic diet in obese patients. Exp Clin Cardiol 2004;9:200-5.
18Oh R, Uppaluri KR. Low Carbohydrate Diet; 2019. Available from: [Last accessed on 2019 Oct 12].
19Ellenbroek JH, van Dijck L, Töns HA, Rabelink TJ, Carlotti F, Ballieux BE, et al. Long-term ketogenic diet causes glucose intolerance and reduced β-and α-cell mass but no weight loss in mice. Am J Physiol Endocrinol Metab 2014;306:E552-8.
20Kossoff EH, Zupec-Kania BA, Amark PE, Ballaban-Gil KR, Christina Bergqvist AG, Blackford R, et al. Optimal clinical management of children receiving the ketogenic diet: Recommendations of the International Ketogenic Diet Study Group. Epilepsia 2009;50:304-17.
21Jasper's Basic Mechanisms of the Epilepsies. 4th ed. Available from: [Last accessed on 2019 Oct 12].