Keto Diet – Debunking the Myth

Introduction

Obesity continues to be a major worldwide health problem, despite the efforts of the medical community. Intensive lifestyle interventions can achieve weight loss that is sustained over the long-term. Diet is an important component of any lifestyle intervention programme. The dietary plan that restricts energy and fat is the most common strategy and based on it, several other dietary strategies have been proposed. However, the very-low-carbohydrate, high-fat keto diet differs from these approaches. 

In my post Diet Plan for Weight Loss – It’s going to be a journey, I had described various options for the treatment of obesity. As highlighted there, the core principle of any obesity treatment is that it must shift the balance between energy intake and energy expenditure – treating obesity requires creating a state of negative energy balance, therefore a reduction in energy intake is the primary factor that needs to be addressed in a dietary intervention designed to promote weight loss. In the above post, under dietary interventions for the management of obesity, I had briefly discussed the various calorie reduction strategies including reduced-calorie diets, low-calorie diets (LCD), very-low-calorie diets (VLCD) and #keto diets. In the above referred to post, I had discussed reduced-calorie diets in details; in my post, Very-Low-Calorie Diet – All you Need to Know, I had discussed the LCDs and VLCDs. Here, in this post, I shall be discussing the keto diets.

What is a keto diet?

There are three macronutrients (macro~large; nutrients that your body requires in large amounts for normal growth and development) in the diet viz. carbohydrates, proteins and fats; they all contribute to dietary energy. For a given energy intake, increases in the proportion of one macronutrient necessarily involve a decrease in the proportion of one, or more of the other macronutrients. Various research studies have examined the role of manipulating dietary macronutrient composition for a wide range of conditions, as diverse as enhancing athletic performance to the management of various medical conditions. Of these, carbohydrate manipulation is the most commonly studied.

There are several types of carbohydrate-restricted diets and are often defined based on the proportion of total daily energy (TDE) from carbohydrates and/or absolute carbohydrate intake. Generally, a carbohydrate-restricted diet is defined as carbohydrate intake below the lower range of the acceptable macronutrient distribution range (AMDR; defined as a range of intakes for a particular energy source that is associated with the reduced risk of chronic disease while providing adequate intakes of essential nutrients. An AMDR is expressed as a percentage of total energy intake); AMDR for carbohydrates for healthy adults is 45-65% of TDE intake. Based on this various carbohydrate-reduced diets can be broadly defined as under:

  • Moderate-carbohydrate diet – 26-44% of TDE from carbohydrates (130-225 grams of carbohydrates for a reference 2000 kcal diet, per day).
  • Low-carbohydrate diet – 10-25% of TDE from carbohydrates (50-130 grams of carbohydrates for a reference 2000 kcal diet, per day).
  • Very-low-carbohydrate diet – <10% of TDE from carbohydrates (<50 grams of carbohydrates for a reference 2000 kcal diet, per day).

The term keto diet is the short form of the ketogenic diet. The keto diet is a very-low-carbohydrate, fat-rich eating plan, that was developed to provide an alternative to non-mainstream fasting, which had demonstrated success as an epilepsy therapy. Keto diets emphasise carbohydrate restriction while generally allowing ad libitum (at one’s pleasure) intake of calories; besides, there is little emphasis on the type of fat that replaces carbohydrate in the keto diets, which may result in a high intake of saturated fats and cholesterol.

What is the macronutrient composition of a keto diet?

There is not one “standard” keto diet with a specific ratio of macronutrients. In 1924, Dr MG Peterman first reported the calculation of a keto diet. Peterman’s keto diet, composed of one gram of protein per kilogram of body weight in children, 10-15 grams of carbohydrates per day, and the remainder of the calories in fat, is identical to the keto diet that is used today. The classic keto diet, long used to treat epilepsy in children calls for 90 per cent of daily calories to come from fat. However, contemporary very-low-carbohydrate keto diets have become popular among the lay public and some nutritionists and dietitians for weight loss. A typical popular version of the keto diet is very low in carbohydrates (5-10% of TDE or ~ 20-50 g/d), moderate in proteins (10-20% of TDE) and high in fats (70-80% of TDE), and lays emphasis on replacement of carbohydrates with fat; thus it is a very-low-carbohydrate, high-fat (VLCHF) diet, which results in ketosis. For a 2000-calorie diet, this translates to about 165 grams of fat, 40 grams of carbohydrates and 75 grams protein. As highlighted above, typically there is little emphasis on the type of fat that replaces carbohydrate in a keto diet, which may result in a high intake of saturated fats and cholesterol.

This figure depicts the Keto diet pyramid, representing the  distribution of various macronutrients.
Fig. Keto diet pyramid

Besides, the VLCHF/keto diets are typically moderate in protein intake because eating too much protein can prevent ketosis. Some of the amino acids in protein can be converted to glucose in the body thereby stimulating insulin secretion which may reduce ketone body production by the liver. Therefore, a keto diet specifies enough protein to preserve lean body mass (1.2-1.5 g/kg/d), but that will still cause ketosis.

History of the keto diet

The role of fasting in the treatment of various ailments has been known to mankind for over two and a half thousand years and was studied in detail by ancient Greek and Indian physicians; fasting and other dietary regimens have been used to treat epilepsy since at least 500 BC. An early treatise in the Hippocratic Corpus (a collection of around 60 early ancient Greek medical works strongly associated with the Greek physician Hippocrates, often referred to as the ‘Father of Medicine’, and his teachings), “On the Sacred Disease”, describes how alterations in diet played a role in epilepsy management. The same author also describes in “Epidemics” from the same collection, how a man was cured of epilepsy when he abstained completely from consuming food or drink. Five centuries later, in King James Version of the Bible, fasting is also reported to treat seizures when Jesus cured a boy with epilepsy by asking him to pray and fast.

The first modern use of fasting as a treatment for epilepsy was proposed by a pair of physicians Guelpo and Marie in 1911 in France. In 1921, endocrinologist Dr Rollin Turner Woodyatt first discovered that three water-soluble compounds, acetone, β-hydroxybutyrate and acetoacetate (together called ketone bodies; ketone bodies are energy sources produced by the liver in the absence of glucose) were produced by the liver, in a normal subject, as a result of starvation or following a diet low in carbohydrates and rich in fats. Concurrently, Dr Russel M Wilder proposed, probably based on the work summarized by Woodyatt, “that the benefits of fasting could be obtained if ketonemia was produced by other means.” Wilder suggested that a ketogenic diet should be as effective as fasting and could be maintained for a much longer period, compensating for the obvious disadvantages of a prolonged fast. Wilder used a keto diet for the treatment of epilepsy and coined the term ‘ketogenic diet’.

For almost a decade, in the 1920s and 1930s, the ketogenic diet became popular in the medical world as a therapeutic diet for epilepsy in children and was widely used until it’s popularity ceased with the introduction of new anticonvulsant therapies. However, interest in the keto diet was again revived after the airing on the TV in 1994 of the true story of a 2-year-old boy with intractable generalised seizures, who quickly became seizure-free after being initiated on the keto diet. The keto diet as an adjunct therapy for the management of epilepsy has experienced a re-emergence in recent years and modern clinical studies have established the treatment as significantly effective.

The keto diet as a medical treatment

Besides children with epilepsy who continue to have seizures while on antiepileptic drugs, there is a growing interest in the use of a keto diet in cancer, particularly in brain cancer. However, more studies are needed on humans before this can be recommended. For people who have type 2 diabetes, a keto diet may improve blood sugar control in the short term. However, the use of these diets in patients with type 1 diabetes is still controversial and their long-term safety is still unproven. Of late, the keto diet is gaining considerable attention as a potential weight-loss strategy due to low-carbohydrate diet craze, which started in the 1970s with the Atkins diet. Here in this post, the discussion will primarily be limited to the role of the keto diet for weight loss purposes.  

What is ketosis?

The premise of the keto diet for weight loss is that if you deprive the body of carbohydrates, which are the primary source of energy for all the cells in the body, then body burns fats to produce ketones, which act as an alternative source of fuel in the body. At it’s simplest, there are two possible sources of fuel for most cellular functions – glucose (a simple carbohydrate) and fatty acids derived from the fats. Under normal healthy conditions, when an individual is on a balanced diet and well-fed, most of the body’s cells prefer to use blood glucose as their main source of energy; for the human brain, glucose is typically the sole source of energy because fatty acids cannot cross the blood-brain barrier (a barrier between the brain’s blood vessels and the cells and other components that make up brain tissue, that provides a defence against disease-causing pathogens and toxins that may be present in our blood). The brain demands the most glucose in a steady supply, about 120 grams daily because it cannot store glucose.

During fasting or when an individual is on a low-carbohydrate diet, the body first pulls stored glycogen (the storage form of glucose) from the liver and muscles. However, the glycogen store in the body is limited – in a well-fed person, muscles store about 500 grams of glycogen and liver stores about 100 grams of glycogen.

Depletion of glycogen stores forces the body to go through certain metabolic changes. Two metabolic processes come into action when there is low carbohydrate availability in the body tissues: gluconeogenesis and ketogenesis. Gluconeogenesis is the endogenous (produced inside an organism or cell) production of glucose in the body from various substrates, including amino acids derived from the breakdown of body proteins, mainly muscle proteins. When glucose availability drops further, the endogenous production of glucose is not able to keep up with the needs of the body and ketogenesis begins to provide an alternate source of energy in the form of ketone bodies. Ketone bodies replace glucose as a primary source of energy. As the ketogenic diet is sustained, the ketone bodies accumulate in the body. The metabolic state characterised by elevated levels of ketone bodies in the blood is known as ketosis. When ketosis is induced by dietary modification, it is known as nutritional ketosis. As long as the body is deprived of carbohydrates, the metabolism remains in the ketotic state. However, it is pertinent to emphasise here that achieving ketosis is a highly individualised process and some people may require a more carbohydrate-restricted diet (<20 g/d of carbohydrates) to start producing ketone bodies.

The nutritional ketosis state is considered quite safe, as ketone bodies are produced in small amounts, insufficient to cause any alterations in the blood pH (the pH of any fluid is the measure of hydrogen ion concentration. A pH of 7 is neutral. Blood has a normal pH range of 7.35 to 7.45, i.e. slightly alkaline. The lower the pH, the more acidic the blood). In contrast, ketoacidosis is a life-threatening condition in which ketone bodies are produced in extremely high amount, altering the blood pH to a dangerously low acidotic state. Ketoacidosis most often occurs in individuals with type 1 diabetes because they do not produce insulin, a hormone that prevents overproduction of ketone bodies.

Ketone bodies synthesised in the body can be easily utilised for energy production by heart, muscle tissue, and kidneys. Ketone bodies can also cross the blood-brain barrier to provide an alternative source of energy to the brain. The body uses stored and/or dietary fat for the production of ketone bodies.

How do keto diets work?

Although a keto diet allows ad libitum consumption of calories, individuals following a keto diet have been shown to have reduced appetite and hunger, due to various mechanisms, resulting in the spontaneous reduction in calorie intake, contributing to weight loss. Participants report less hunger when they are in ketosis, although the mechanisms of action of ketosis on hunger and appetite suppression are not completely understood. Also, protein and fats in the diet produce greater satiety. Furthermore, various studies have shown that low-carbohydrate diets may reduce hunger by influencing circulating levels of hormones that impact hunger and appetite control.

The initial weight loss that occurs with low-carbohydrate diets and very-low-carbohydrate ketogenic diets is largely attributable to the loss of body water, not fat. Primarily two mechanisms are responsible for this body water loss, glycogen depletion and ketonuria induced natriuresis. As highlighted above, during fasting or when an individual is initiated on a low-carbohydrate, high-fat diet, the body first uses glycogen stored in the liver and muscles. However, when glycogen is stored in the body, 3 grams of water is stored along with every gram of glycogen. When glycogen is used by the body as fuel, the water stored with it is also released. Thus, if the body uses 500 grams of glycogen, it will lose about 1500 grams of water stored with it; together this will show up as a loss of 2 kg on the weighing scale. When the individual returns to a normal diet and glycogen stores are replenished, the water weight returns.

Natriuresis is the excretion of excessively large amounts of salt (sodium) in the urine. Ketone bodies beyond what can be utilised in the body are excreted by the kidneys in the urine, in what is termed as ketonuria. Ketonuria promotes loss of sodium and water by the kidneys in the first few days of fasting or keto diet.

Foods you can/cannot eat on a keto diet

There are many versions of the keto diet, but all ban the carbohydrate-rich foods. On the other hand, the keto diet has such a high requirement of fat that a keto diet follower must eat fat at each meal. In a daily 200 calorie diet, it might involve eating about 155-175 grams of fat. This would entail chowing down on a lot of cheese, butter, lard, eggs, fatty cuts of meat and bacon. However, some healthy unsaturated fats like nuts (almond, walnut), seeds, avocados, tofu and olive oil and oily fish can also be part of the diet. Though protein is part of the keto diet, it does not typically discriminate between lean protein foods and protein sources high in saturated fat such as beef, pork and bacon.

As regards the carbohydrates, the choices are very limited. Vegetables are restricted to leafy greens (such as kale, Swiss chard, spinach), cauliflower, broccoli, Brussels sprouts, asparagus, bell peppers, onions, garlic, mushrooms, cucumber, celery and summer squashes. Among the fruits, choices are still more limited; you can have certain fruits, usually berries, in small portions. The foods rich in carbohydrates, which are excluded from the keto diet menu include starches from both refined and whole grains like bread, cereals, pasta and rice; potatoes, corn and other starchy vegetables and high-sugar fruits such as litchis (lychees), pomegranate, mangoes, bananas, oranges, grapes, kiwi fruit, guavas, pears, apples, peaches, papaya, passion-fruit etc.

Effect of a keto diet on weight loss

The National Lipid Association (NLA; a non-profit multidisciplinary medical society in the United States, focused on enhancing the practice of lipid management in clinical practice) issued a Scientific Statement, titled ‘Review of current evidence and clinical recommendations on the effects of low-carbohydrate and very-low-carbohydrate (including ketogenic) diets for the management of body weight and other cardiometabolic risk factors: A scientific statement from the National Lipid Association and Lifestyle Task Force’, which was published in the ‘Journal of Clinical Lipidology’ in Sep 2019. This statement provides a comprehensive review of the current evidence base available from recent systematic reviews and meta-analysis on the effects of low-carbohydrate and very-low-carbohydrate diets on body weight, lipoprotein lipids, glycemic control, and other cardiometabolic risk factors.

In the context of the effect of low-carbohydrate and very-low-carbohydrate diets on weight loss in adults with overweight and obesity, the statement states – “Despite the favorable effects of low-carbohydrate and very-low-carbohydrate diets on energy expenditure and intake, long-term effects on weight loss may not be superior to more conventional strategies.” The key findings of this statement are:

  • Short-term (< 6 months) hypocaloric (calorically restricted) low-carbohydrate and very-low-carbohydrate diets may result in greater weight loss than hypocaloric high-carbohydrate, low-fat (HCLF) diets.
  • Longer-term (> 6 months) results suggest that low-carbohydrate and very-low-carbohydrate diets may result in weight loss that is equivalent to that of HCLF diets.
  • Very-low-carbohydrate diets are difficult to maintain (due to their restrictive nature) and are not clearly superior for weight loss compared with diets that allow a higher amount of carbohydrate in adults with overweight and obesity with or without diabetes.
  • Long-term participation in any weight loss intervention is difficult, but adherence to the assigned macronutrient distribution (i.e. carbohydrate, protein and fat) is lower with low-carbohydrate and especially, very-low-carbohydrate diets.

According to the 2013 American Heart Association/American Cardiology/The Obesity Society (AHA/ACC/TOS) Guideline for the Management of Overweight and Obesity in Adults, published in the journal ‘Circulation’ in Jun 2014, research has not demonstrated any advantage of a very-low-carbohydrate diet on weight loss at 6 months compared with a calorie-restricted, low-fat diet.

Drawbacks/health hazards of a keto diet

Keto diet is promoted online and in the media as a weight-loss wonder and seemingly all-round magical healer, but this eating plan is actually a diet that is associated with serious risks. Keto diet, being high in saturated fats and low in nutrient-dense carbohydrate foods is inconsistent with evidence-based dietary strategies recommended by professional organisations. No matter what, the keto diet is vastly different than the United States Department of Agriculture (USDA)  dietary recommendation of 45 to 65 per cent of one’s total calories to be carbohydrates, 20 to 35 per cent from fats and 10 to 35 per cent from proteins. Recommendations of most other professional organisations, around the globe, are on similar lines. A glance at the figure below, which compares the dietary guidelines of various professional organisations with a keto diet, makes it amply evident that such a diet plan turns the whole science of nutrition on its head.

This figure compares the keto diet with nutritional guidelines of various professional organisations.
Fig. Comparison of Keto diet with nutritional guidelines of various professional organisations

There are two major drawbacks in a keto diet which may pose a serious risk to the health of the individuals. Firstly, not only the quantity of fats in the diet is disproportionately high, but also typically there is little emphasis on the type of fat that replaces carbohydrates in a keto diet, which may result in a high intake of saturated fats and cholesterol, which can have a deleterious effect on the cardiovascular health. Secondly, diet imposes the severe restriction of carbohydrates intake to mostly non-starchy vegetables and eliminates carbohydrate-containing foods that are components of cardioprotective dietary patterns, including fibre-rich starchy vegetables as well as most fruits, whole grains, nuts, seeds, and legumes. These foods are important sources of fibre, micronutrients such as magnesium, B-vitamins, and bioactive compounds such as polyphenols (naturally occurring compounds found largely in the fruits, vegetables, cereals and beverages. They are generally involved in defence against ultraviolet radiation or aggression by pathogens. These molecules are good antioxidants) all of which have been associated with a lower risk for dyslipidemia, atherosclerotic cardiovascular disease (ASCVD) events and incident type 2 diabetes. Some important health risks associated with the keto diet include:

1. Increased risk of mortality

A study titled ‘Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis’ published in the reputed journal ‘The Lancet Public Health’ in Aug 2018, investigated the association between the percentage of energy from carbohydrate intake and all-cause mortality.

The authors studied a large cohort (15428 participants) in four US communities from the diverse socio-economic background, enrolled in the Atherosclerosis Risk in Communities (ARIC) study. During the median follow up of 25 years, they examined the association between the percentage of energy from carbohydrate intake and all-cause mortality. They further examined this association combining ARIC data with data for carbohydrate intake reported from seven multinational prospective studies (432179 participants) in a meta-analysis. Finally, the authors assessed whether the substitution of animal or plant sources of fat and protein for carbohydrate affected mortality.

There was a ‘U’ shaped association between the carbohydrate intake and mortality in the Atherosclerosis Risk in Communities cohort, a finding that was consistent in the meta-analysis combining these data with those from the other cohorts. When assessing total carbohydrate without regard to the specific food source, diets with a high (> 70%) or low (< 40%) percentage of energy from carbohydrates were associated with increased mortality, with minimal risk observed between 50-55%. However, results varied by the source of macronutrients: mortality increased when carbohydrates were exchanged for animal-derived fat or protein and mortality decreased when the substitutions were plant-based.

Interpretation – Both high and low percentages of carbohydrate diets were associated with increased mortality, with minimal risk observed at 50-55% of TDE derived from carbohydrate intake. Low carbohydrate dietary patterns favouring animal-derived protein and fat sources, from sources such as lamb, beef, pork and chicken, were associated with higher mortality, whereas those that favoured plant-derived protein and fat intake, from sources such as vegetables, nuts, peanut butter, and whole-grain bread, were associated with lower mortality, suggesting that the source of food notably modifies the association between carbohydrate intake and mortality.

One more recent study also investigated the association between low-carbohydrate diets and mortality. The study titled ‘Lower carbohydrate diets and all-cause and cause-specific mortality: a population-based cohort study and pooling of prospective studies’ was published in the ‘European Heart Journal’ in Apr 2019. This study prospectively examined the relationship between low carbohydrate diets, all-cause death, and deaths from coronary heart disease, cerebrovascular disease (including stroke), and cancer in a nationally representative sample of 24825 participants of the US National Health and Nutrition Examination Survey (NHANES) from 1999-2010. Compared to participants with the highest carbohydrate consumption, those with the lowest intake had a 32% higher risk of all-cause death over an average 6.4-year follow-up. Besides, the risk of death from coronary heart disease, cerebrovascular disease, and cancer increased by 51%, 50% and 35% respectively.  The highest adherence to a diet jointly lower in carbohydrate and higher in protein increases the risk of death from any cause by 21%, cancer death by 22%, coronary heart disease death by 44%, and cerebrovascular death by 41%. The risks of all-cause and cause-specific death over an average 6.4-year follow-up rose with each fall in carbohydrate intake and remained significant after adjusting for all available factors that might have influenced the association.

The findings were supported by an accompanying meta-analysis of nine prospective cohort studies conducted in the USA, Sweden, Greece and Japan, with a total of 462934 participants and a mean follow-up of 16.1 years. The findings were similar to the NHANES study, with increased risk of mortalities with low carbohydrate diet – 22% for all-cause mortality, 13% for cardiovascular mortality and 8% for cancer mortality.

The biology that underlies the positive association between LCDs and all-cause death is not fully elucidated yet. Some potential mechanisms may mediate the unfavourable impact of LCD on health. Firstly, as highlighted above, carbohydrate-rich foods such as starchy vegetables, most fruits, whole grains, nuts, seeds and legumes are also rich sources of fibre, various micronutrients and bioactive compounds, all of which have been found to have a favourable effect on blood lipids (fats), cardiovascular diseases (CVD) and type 2 diabetes. Elimination of these foods from the diet increases the risk of various cardiometabolic diseases. Secondly, increased intake of animal proteins, saturated fat and cholesterol have an adverse effect on health. The consumption of animal proteins, particularly red and processed meat has been associated with the increased risk of various cancers and the increased intake of saturated fat and cholesterol significantly increases the risk of various cardiovascular diseases.

The increased risk of cardiovascular diseases due to increased intake of saturated fats and cholesterol in the diet is mediated through their effect on blood fats (Triglycerides) and lipoproteins (such as low-density lipoprotein cholesterol [LDL-C], colloquially known as bad cholesterol; very-low-density lipoprotein cholesterol [VLDL-C]; and high-density lipoprotein cholesterol [HDL-C], colloquially known as good cholesterol). Triglycerides are an important barometer of metabolic health; high triglyceride levels may be associated with coronary heart disease, diabetes and fatty liver.

Postprandial lipemia                                                                                                             
     Following ingestion of a meal, expectedly there is a rise in the triglyceride-rich lipoproteins (TRL). This is a physiological and transitory event; in healthy people, blood plasma triglyceride levels peak 3-4 hours after the ingestion of a meal, especially fatty meal, and tend to return to baseline within 6-8 hours. Triglycerides are vital for health – providing key substrates in metabolic pathways and being a source of energy. However, excess fat consumption can induce a lipotoxic state, wherein peak in plasma triglyceride levels is 2-3 fold higher and prolonged: plasma triglyceride levels remain elevated up to 10-12 hours. The prolonged and increased levels of triglycerides and triglyceride-rich lipoprotein levels after a meal is known as postprandial lipemia.                                                                                                                                                                                    

Health effects of postprandial lipemia                                                         
     Postprandial lipemia is a significant risk factor for cardiovascular diseases (heart diseases, stroke and peripheral artery disease) because of its role in atherosclerosis and endothelial dysfunction. This has serious implications because nowadays the common dietary habit is characterised by high-fat content and high frequency of meals; hence most individuals spend the majority of the day, approximately 18 h, in postprandial (fed) state, resulting in frequent and prolonged exposure to high lipid levels.                    

The mechanism underlying the impact of postprandial lipemia on CVD risk                                                                                                                            
     Even though the mechanisms by which postprandial lipemia increases the risk for cardiovascular diseases are poorly understood, the possible mechanisms include increased atherogenesis (the process of forming atheromas [an abnormal fatty deposit in the inner of the wall of an artery], plaques in the inner lining of arteries, leading ultimately to atherosclerosis) and endothelial inflammation and dysfunction (endothelial dysfunction can be defined as a disturbance to the vasodilatory [relating to the dilatation of blood vessels] response of the endothelium and impairment of its anti-thrombotic [preventing the formation of blood clots] and anti-inflammatory functions).                                                                                                                  


     The impairment of the endothelial function eventually translates to the development and progression of atherosclerosis and it’s complications viz. cardiovascular diseases. In addition to the traditional cardiovascular risk factors such as diabetes, hypertension, and tobacco toxins, several studies have shown that postprandial lipemia promotes endothelial dysfunction and thus increases the risk of developing cardiovascular diseases. After a high-fat meal, endothelial function is impaired within 3-4 hours, a time period often associated with peak postprandial lipemia.                                         

Factors affecting postprandial lipemia                                                           
     The postprandial lipemic response is modulated by several factors, including background dietary pattern (i.e. habitual diet) and meal composition, lifestyle conditions (physical activity, smoking, alcohol consumption), physiological factors (age, gender, menopausal status), and pathological conditions (central obesity, diabetes mellitus, insulin resistance and hypertriglyceridemia [a high level of triglyceride levels in the blood]). Besides, genetic factors may also affect the postprandial lipemic response. Though these above-mentioned factors do influence postprandial lipid response and metabolism, their effect on the lipemic response is variable. Amount of fat in the meal and pre-existing hypertriglyceridemia have the most potent effect. Even though all the other factors mentioned above also have a significant impact, however, here only meal size and composition will be discussed briefly.                                                                                      

Meal size and composition                                                                           
     Among the various factors that modulate postprandial lipemia, diet plays a significant role. Postprandial lipemia is influenced by meal size as well as meal composition, in particular by fats, carbohydrates, fibres and proteins. However, a high-fat meal, in comparison with a high-carbohydrate meal or a standard meal, is most deleterious in terms of postprandial lipemia and endothelial dysfunction. Both the amount and type of fat in the diet influences postprandial lipemia.

The National Lipid Association, in its scientific statement referred to above, had also reviewed the evidence for the effect of low-carbohydrate and very-low-carbohydrate diets on traditional cardiometabolic risk factors. According to this statement, recent systematic reviews and meta-analysis of randomized controlled trials (RCTs; a study design that randomly assigns participants into an experimental group or a control group to reduce certain sources of bias) of adults with overweight or obesity without diabetes have reported conflicting results on the effects of low-carbohydrate and very-low-carbohydrate diets on total-cholesterol (total-C) and LDL-C. Similar to total-C and LDL-C, recent systematic reviews and meta-analysis of RCTs have again found varying results on the effects of low-carbohydrate and very-low-carbohydrate diets on blood triglyceride and HDL-C levels.

The conflicting results of the studies examining the effect of low-carbohydrate and very-low-carbohydrate diets on blood fats (triglycerides) and lipoprotein levels in adults with overweight or obesity with and without type 2 diabetes may be due to variations in carbohydrate and fat quantity and quality of the diet interventions in the RCTs, and/or differences in adherence to the prescribed diets over the course of the study periods.

Besides the quantity, quality of fat (saturated, unsaturated and trans fats) in a dietary intervention has a profound effect on blood triglycerides and lipoproteins. Greater amounts of cholesterol, saturated and trans fats in low-carbohydrate and very-low-carbohydrate diets are a key factor for an increase in LDL-C, compared to a high-carbohydrate, low-fat diet. In contrast, a higher intake of unsaturated fats tends to lower LDL-C. Similarly, higher protein intake from plant sources such as soy proteins tends to lower LDL-C relative to protein from animal sources.

Regarding blood triglyceride levels, reducing dietary carbohydrate will generally lower blood triglyceride levels, particularly in individuals with elevated triglycerides. However, improvements in triglyceride and HDL-C levels were achieved at a carbohydrate intake considered low- or moderate but not ketogenic. While discussing the issue of carbohydrates on outcomes, it is also important to differentiate between the refined and non-refined carbohydrate intake. It is primarily the foods that contain high amounts of refined carbohydrates that raise blood triglyceride levels.

In addition to the aforementioned, negative energy balance (i.e. hypocaloric diet) and weight loss regardless of the dietary strategy, tend to improve triglyceride, LDL-C and HDL-C. Finally, as discussed above under postprandial lipemia, a range of factors, including genetic, play a role in the individual variability of blood fats and lipoproteins with low-carbohydrate and very-low-carbohydrate diets.

2. Keto flu

As highlighted above, in a normal healthy person eating a balanced diet, carbohydrates are the primary fuel source of the body. However, on the initiation of a keto diet, the body needs to switch to using ketones for fuel. This adaptation process is known as keto-adaptation. The first few weeks of transition to a ketogenic diet can be challenging for some people, whereas others adapt to it more easily. Keto-adaptation may result in some initial ‘brain fog’ (a usually temporary state of diminished mental capacity marked by the inability to concentrate or to think or reason clearly), but this will disappear once the body has fully adapted and some people feel sharper at this point. It is estimated that keto-adaptation takes around four weeks on average but the side effects, which can kick-in after two to seven days, themselves often disappear earlier, lasting days to weeks. The common symptoms of keto flu include:

  • Brain fog/slow thinking
  • Dizziness
  • Headache
  • Insomnia
  • Hunger cravings

3. Changes in bowel habits

Changing to a keto diet may bring about changes in bowel habits such as constipation.

4. Loss of salts

As discussed above, as the body uses up it’s stored glycogen, water stored with it is also released and excreted in the urine. As the fluid is passed out of the body, salts in the body are also lost and can get depleted too.

5. Bad breath

Bad breath, sometimes referred to as keto breath, can sometimes occur as you enter the fat-burning state of ketosis. Ketones can also be released in the breath and sweat in addition to urine. One of the ketone bodies, acetone when released in the breath may lead to less-than-pleasant smelling breath.

Why is the keto diet so popular?

A recent survey of registered dietitians in America named the low-carbohydrate keto diet yet again as the most popular diet in the United States. Despite some major drawbacks associated with the keto diet, one just wonders as to what is fuelling its popularity?

The most important factor for this popularity seems to be related to hunger and satiety. As highlighted above, any hypocaloric diet if followed diligently will produce weight loss. However, following weight loss, the individual experiences increased weight-loss induced drive to eat; this increased hunger has a physiological basis. Following weight loss, levels of various appetite-related hormones are perturbed; there is a significant and persistent reduction in the level of hormones which suppress appetite (anorexigenic hormones) and increase in the level of hormones which stimulate hunger (orexigenic hormones). Findings from various studies have revealed that these hormonal alterations in response to weight loss tend to persist long-term i.e. one year or longer. This persistent hunger is one of the major reasons for poor long-term compliance to the most dietary interventions resulting in loss of body weight, in the short term.

However, in contrast, the keto diets elicit weight loss (albeit in short-term only) with ad libitum intake and without feelings of deprivation and hunger, as due to various mechanisms discussed above, keto diets suppress hunger and appetite. For some, it’s the promised land of diets. There are few rules on which high-fat foods to eat. Instead of cringing through carrot sticks, they can fill up guilt-free on bacon sausages fried in butter, as this technically meets the criteria of a keto diet. As a result, in the short term compliance to the diet is easy, although due to the restrictive nature of the diet, long-term compliance is poor.

However, as discussed above, keto diets are associated with severe health hazards. To address the issue of increased appetite following a dietary intervention, some healthy measures are available. Consuming low-energy-dense foods has been discussed in my post Diet plan for weight loss referred to above. If required, your treating physician can prescribe appetite suppressant drugs. A healthy eating plan, in brief, for weight loss is discussed below.

Best diet plan for weight loss

As highlighted in my post ‘Diet plan for weight loss’, referred to above, the core principle of any obesity treatment is that it must shift the balance between energy intake and energy expenditure; therefore, treating obesity requires creating a state of negative energy balance. Various research studies have convincingly demonstrated that the macronutrient composition (proportion of the three macronutrients in the diet, viz. carbohydrate, fat and proteins) of a diet does not impact the weight outcome; any reduced-calorie diet will result in clinically meaningful weight loss, regardless of which macronutrient they emphasise. After all, a calorie reflects food energy, regardless of the food source. In contrast, a keto diet has an ad libitum approach to calorie intake; while limiting carbohydrates, it has few rules on which high-fat foods to eat. It defies all nutritional logic; after all a keto diet is not going to magically alter your metabolism to where calories don’t matter anymore.

Another important factor which predicts the success of the dietary intervention is adherence to a diet. Various studies have revealed that the success of a diet is most predicted by adherence, with little effect of the brand or type of diet. Ultimately, the best diet plan for weight loss is the one patient will follow and incorporate into his or her daily life for lifelong maintenance of healthy weight. An in-depth review suggests the most effective strategy for long-term weight loss and heart health is a healthy diet pattern that’s compatible with your food preferences and lifestyle. A balanced, unprocessed diet, rich in very colourful fruits and vegetables, lean meats, fish, whole grains, nuts, seeds, olive oil, and lots of water seems to have the best evidence for a long, healthier, vibrant life.  For control of hunger, a healthier strategy is to eat low-energy-dense foods, as discussed in my post on Diet plan for weight loss referred to above. It is feasible to consume less energy while at the same time achieving a greater degree of hunger control, by eating a lower energy density diet. In brief, by choosing the low-energy-dense food, you get to eat a lot more food for the same number of calories.

Taking various studies into account, the message of moderation is perhaps the most convincing one of all – dietary extremism, wherein the diets focus too heavily on a single macronutrient, whether carbohydrates, fats or proteins, is likely to adversely impact health in the long-term. This principle of moderation has been extended to a healthy eating plan, the portion-controlled diet, discussed in my post referred to above.

Synthetic ketone bodies

Research on a novel approach to weight management, wherein ketosis can be mimicked through exogenous administration of synthetic ketones, is underway. A study titled ‘Kinetics, safety and tolerability of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate in healthy adult subjects’ published in the journal Regulatory Toxicology and Pharmacology in Aug 2012, determined the kinetic parameters, safety and tolerability of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate, a ketone monoester and administered in the form of a meal replacement drink to healthy human volunteers. The study results suggested that ingestion of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate is a safe and simple method to elevate blood ketone levels, compared with the inconvenience of preparing and consuming a ketogenic diet.

Originally synthetic ketones were developed as an alternative means of mimicking ketosis to treat neurological conditions such as refractory epilepsy, Parkinson’s Disease and Alzheimer’s disease; however, artificially mimicking ketones opens up the possibility of allowing individuals to reap the benefits of suppression of the drive to eat, while at the same time adhering to a diet with a more flexible distribution of macronutrients, which would promote long-term adherence to energy-restricted diets via increased control of the drive to eat.

Conclusion

Nutritional advice, particularly online, is highly unregulated. Low-carbohydrate diets might be useful in the short-term to lose weight and improve blood glucose control. However, due to their restrictive nature, these diets are not sustainable in the long-term. Besides, the results of various studies suggest that in the long-term they are linked with an increased risk of death from all-causes and due to specific causes such as cardiovascular disease, cerebrovascular disease and cancer. These findings suggest that low-carbohydrate diets are unsafe and should not be recommended.

The key to maintaining a healthy weight in the long-term is an eating pattern that you can sustain over time. Instead of engaging in the next popular diet that would last only a few weeks to months (for most people that includes a ketogenic diet), try to embrace change that is sustainable over the long-term. One thing is certain: any meaningful change starts with behaviour.

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