About the Author(s)


Sarah M. Rice Email symbol
Independent, Cape Town, South Africa

Douglas B. Reynolds symbol
Independent, Corpus Christi, Texas, United States of America

Citation


Rice SM, Reynolds DB. Practical guidelines for addressing common questions and misconceptions about the ketogenic diet. J. metab. health. 2025;8(1), a113. https://doi.org/10.4102/jmh.v8i1.113

Guideline

Practical guidelines for addressing common questions and misconceptions about the ketogenic diet

Sarah M. Rice, Douglas B. Reynolds

Received: 24 Oct. 2024; Accepted: 04 Apr. 2025; Published: 21 July 2025

Copyright: © 2025. The Author(s). Licensee: AOSIS.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Research publications on the ketogenic diet have experienced an exponential increase in recent years, driving clinical interest, which has expanded along with media interest. The ketogenic diet, originally developed as an epilepsy treatment, has a broad range of applications that include metabolic disorders such as obesity, insulin resistance, and type 2 diabetes, and extends to a range of neurometabolic conditions such as neurodegenerative disorders and mental health conditions. The ketogenic diet promotes a state of nutritional ketosis that has unique benefits via multiple mechanisms. Heightened awareness of the potential benefits of a ketogenic diet has led to an increase in clinicians using this approach, and patients who are keen to explore this option may present having self-administered ketogenic diet therapy. Common misconceptions about the ketogenic diet abound on social media, causing confusion and distracting from its potential benefits, where nuance around diet quality and personalisation are key features of a successful implementation. By selecting common questions and misconceptions about the ketogenic diet from a social media platform, this article seeks to provide a concise, evidence-based guide to address these questions and support clinicians seeking to implement ketogenic diets in their practice.

Keywords: ketogenic diet; ketosis; insulin resistance; ketones; type 2 diabetes; obesity; therapeutic carbohydrate reduction.

Introduction

Over 100 years ago, researchers first used the ketogenic diet (KD) as a treatment for epilepsy after observing that fasting improved the condition. It was developed to mimic the biochemistry of fasting while meeting nutritional requirements, thereby offering a sustainable approach. A very low-carbohydrate diet is described by Sir William Osler for the treatment of obesity in his textbook from 1892,1 and at a similar time, Joslin and Allen were separately developing a low-carbohydrate high-fat diet for the treatment of type 1 diabetes.2,3 The modern-day KD has its roots in the work of these early pioneers, and there remains a difference in the formulation of the diet for metabolic versus neurological disorders. Variations of the KD have been studied and developed to evaluate clinical effect and tolerance for a range of conditions (see Table 1). The strongest evidence for the utility of a ketogenic approach can be found for obesity, diabetes, metabolic syndrome or insulin resistance, and epilepsy.4,5 Hyperinsulinaemia is a core feature of many chronic diseases, which the KD may address.6,7

TABLE 1: Possible therapeutic applications for a ketogenic diet.

Increasingly, clinicians are recognising the utility of a KD as one approach that can address a range of conditions through various mechanisms. A document was compiled in response to common questions raised by the lay public, and this practical guide seeks to address these questions and misconceptions, and provide concise evidence-based answers to support practitioners wishing to implement ketogenic therapies.19

Methods

Data concerning common questions raised about the KD were selected from the YouTube channel of a clinician using a ketogenic dietary approach in their practice. A search engine optimisation (SEO) specialist compiled a list of common questions appearing over 10 years (approximately February 2014 to February 2024) from 28 000 000 YouTube subscribers, and the type and frequency of questions were assessed on a prima facie basis. The queries addressed were selected according to their clinical relevance, strength of evidence and estimated frequency of occurrence. Feedback was received from clinicians on an informal basis, which guided the selection of questions and answers for inclusion in this paper.

To answer the frequently asked questions (FAQs), a non-systematic literature search of human studies was conducted using PubMed, Google Scholar and a private database of articles, from inception to October 2024. Keywords such as ‘ketogenic’, ‘ketones’, ‘ketosis’, ‘low carbohydrate’, ‘low-carbohydrate’ and the key topics of interest, were combined using Boolean operators. Where relevant, studies were selected in the ketogenic range (< 50 g carbohydrates, < 10% total energy intake (TEI), or measured ketones). On occasion, this was relaxed to include a broader range which may be ketogenic for some (20 g – 70 g carbohydrates),20,21 or where ketones were not specifically measured, to allow for inclusion of studies representative of real-world situations. Where possible, systematic reviews and meta-analyses and randomised controlled trials were used to compile responses, although all types of studies were included. Quality analysis and risk of bias assessment were not carried out, which is a limitation of these findings. Reference to clinical guidelines and a textbook authored by experts in the field of therapeutic carbohydrate reduction helped guide the answers to these FAQs.6,22 An FAQ document was compiled addressing the questions raised and reviewing the benefits of a KD.19 The material has been condensed and revised for the purposes of this article.

Results and discussion

This section is presented as a series of FAQs.

What is a ketogenic diet?

A well-formulated KD meets nutritional and energy requirements, and is commonly defined by the amount of carbohydrates (grams) consumed per day (see Table 2). A therapeutic KD, where higher levels of ketones may be required for therapeutic effect, is more likely to be required in conditions such as epilepsy, other neurological conditions and for the treatment of mental health conditions, and may be referred to as ketogenic dietary therapy or ketogenic metabolic therapy.16,18

TABLE 2: Different types of ketogenic diets.

The goal of a KD is to promote a state of nutritional ketosis where low insulin levels initiate lipolysis, the release of fatty acids from triacylglycerols in adipose tissue. These fatty acids are metabolised by the liver hepatocytes into acetyl-coenzyme A. Low blood glucose concentrations drive the accumulation of acetyl-coenzyme A, which is converted to acetoacetate, beta-hydroxybutyrate and acetone. This is distributed to extrahepatic tissues, where it is converted back to acetyl-coenzyme A and enters the tricarboxylic acid cycle to be used as an alternative energy source.25 This state of nutritional ketosis generates measurable ketone levels generally of the order of 0.5 mmol/L – 3 mmol/L. A therapeutic KD may require more consistent and higher levels of ketones to reach a sufficient signalling effect on target pathways (target may be ≥ 3 mmol/L), but it is unusual for ketone levels to go above 5 mmol/L.18,25

A discussion of the neurological applications of the KD, which includes ketogenic metabolic therapy for mental health conditions, is outside the scope of this paper. These applications require more targeted macronutrient and diet composition management. For metabolic conditions, a well-formulated KD contains the following elements adapted from Volek et al:20

  • Supports nutritional ketosis. Ketone levels may be measured to guide this. Ketosis may occur over a range of carbohydrate intakes, depending on the individual (~20 g/day to > 70 g/day), although it typically occurs at < 50 g/day.20,21
  • Carbohydrate reduction (avoid high carbohydrate foods, high glycaemic fruits and starchy vegetables).
  • Carbohydrate intake from non-starchy vegetables and low-sugar fruits (berries, tomatoes, olives, avocados). Small amounts of carbohydrate are contained in dairy and other protein sources.
  • Adequate protein to maintain or improve lean body mass and performance demands. Estimates may be based on 1.2 g/kg to 2.0 g/kg reference weight (~80 g/day – 150 g/day),20 or, as a starting point, 1.5 g/kg of a medium-frame ideal weight.23 Requirements for essential amino acids may be more readily achieved using animal-sourced foods.
  • Fat to be added to satiety. Sources of fat include meats, full-fat dairy (cream, cheese, butter, etc.), nuts, seeds, olives, avocados, olive and avocado oils, cooking fats (e.g. tallow, butter, coconut oil).
  • Emphasis on nutrient-dense and minimally processed whole foods and the avoidance of highly processed foods and added sugars.
  • Monitor for adequate essential vitamin and mineral intake.
  • Tracking energy intake is not necessary for success, depending on therapeutic goals.20,23
Are there any contraindications?

While the list of absolute contraindications is straightforward, the conditions requiring caution may be broad and nuanced.6 A recent review looking at the scientific evidence underlying contraindications to the KD found that many concerns are focused on fragile populations, where there is a lack of clinical studies, rather than being based on evidence supporting the risk of serious events.26 Careful management and individual tailoring by physicians experienced in the use of ketogenic approaches is recommended for complex cases. The KD and associated metabolic changes may affect the pharmacokinetics of medications, notably drugs used in the treatment of diabetes, epilepsy, cardiovascular disease (CVD) and psychiatry.27 Clinical supervision is recommended when making significant dietary changes, especially if there are existing medical conditions or medications that may need to be adjusted.6,16,28,29 Contraindications and cautions are listed in Table 3.

TABLE 3: Contraindications and cautions when using a ketogenic diet.
Does transitioning to a ketogenic diet have any side effects?

Entering nutritional ketosis may provoke symptoms that vary on an individual basis.31 This acute response to carbohydrate withdrawal occurs across different levels of carbohydrate reduction as individuals enter nutritional ketosis over a range of low-carbohydrate intakes.20,21 Typically, these effects are short-lived, with reports ranging from 1 to 4 days,21 and up to 10 days.6 Many of the symptoms are because of physiological changes as insulin lowers and regulatory systems drive natriuresis and diuresis, promoting loss of sodium, potassium and magnesium. Failure to replace fluids and electrolytes promotes many of the common side effects, such as fatigue, light-headedness (especially on standing), muscle cramps, headache and constipation.20,21 In this phase, it is essential to maintain fluid intake and replace sodium (in the range of 2 g – 3 g of sodium or 5 g – 7 g of salt) and potentially, potassium (3 g/day – 4 g/day).6,11,22 Persisting muscle cramps and constipation may be alleviated by magnesium supplementation of 200 mg/day – 400 mg/day elemental magnesium or milk of magnesia and individualised dietary adjustments.

Ongoing symptoms may indicate nutritional insufficiency, vitamin deficiencies or changes in medical condition. Potassium supplementation and further evaluation of nutritional and medical status may be required in these cases. Some individuals benefit from ongoing salt supplementation. Patients with more complex medical histories may need an adapted approach and baseline measurements of sodium, potassium and magnesium. Dietary restrictions for other conditions may need to be maintained.6,11,20

Patients taking medications for diabetes, hypertension, gastrointestinal conditions and those taking psychiatric medications, need to be monitored carefully, as some medications require adjusting within days of carbohydrate reduction, with others reducing over time, as covered in the previous section. In general, adaptation symptoms pass quickly, indicating it is changes in metabolism, rather than the diet itself, that cause these symptoms. Ensuring adequate calorie consumption may improve symptoms during adaptation.21 Following adaptation, improvements in wellbeing, mood, sleep and sugar craving are readily appreciated and may explain decisions to continue nutritional ketosis, even in healthy individuals.31

Is there an increased risk of gout when transitioning to a ketogenic diet?

In individuals with a history of gout flares, caution may be required when transitioning to ketogenic levels of carbohydrate restriction, as ketone bodies and uric acid compete for the same organic anion transporters involved in renal excretion pathways. This may result in a short-term increase in uric acid concentration over 2–8 weeks as physiological adaptations to nutritional ketosis occur.11 Overall, carbohydrate reduction reduces uric acid production and addresses the features of insulin resistance, strongly associated with gout.6 Clinical assessment of individual risk for a gout flare (and appropriate treatment) during transition should be considered. A slower transition and consistent adherence to carbohydrate restriction may be beneficial in this setting.32

Does the ketogenic diet cause ketoacidosis?

Nutritional ketosis is a normal physiological state where feedback loops regulate the generation of ketone bodies via the action of succinyl-CoA:3-oxoacid-CoA transferase (SCOT) to reduce ketone conversion from acetoacetate to maintain ketone and plasma pH concentrations in the normal range.25

Ketoacidosis is an unregulated state driven by impaired insulin signalling and is commonly associated with type 1 diabetes. This is a unique setting, where there is insufficient insulin production and a lack of adequate exogenous insulin supplied, and the usual pathways that manage ketone use and production are impaired, leading to ketoacidosis.20 This pathological ketoacidosis is distinct from nutritional ketosis, and individuals with type 1 diabetes have successfully adopted ketogenic approaches;33,34 although more liberal low-carbohydrate ranges may be applied (e.g. 25 g/day – 75 g/day).35 Typically, a KD on its own does not induce acidosis, but only in combination with other drivers which may include a state of starvation, illness, drug interactions (e.g. sodium-glucose co-transporter [SGLT2] inhibitors), genetic disorders of metabolism, lactation and alcohol withdrawal.25,36,37,38 Under these conditions, rising levels of ketone bodies can exceed the physiological pathways for maintaining normal plasma pH. Overall, ketoacidosis occurring in the context of a KD is rare and normally involves a combination of factors.36 A recent study examining illnesses associated with ketosis, including diabetic ketoacidosis, found events to be rare and comparable to those not following a carbohydrate-reduced approach, even where SGLT2 inhibitors were in use (with ketone body monitoring in place).36 Their data support the overall safety of individuals following a very low-carbohydrate KD for metabolic diseases such as obesity, prediabetes and type 2 diabetes.36 If clinically necessary, the surveillance of ketone levels is possible with readily available measuring devices.

Does a ketogenic diet result in nutrient deficiencies?

A well-formulated KD has been studied across a wide demographic, from children to the elderly, and can be nutritionally complete.20,39,40 Younger populations may require vigilance if strict macronutrient ratios are required for therapeutic levels of ketosis often required for epilepsy and other neurodevelopmental conditions; however, the KD has been successfully applied in this context with no adverse effects.41 Where a KD is being utilised for metabolic improvements in a paediatric population, the approach can be more liberal and still successful.42,43 In older populations, KDs have been successfully implemented.40,44 Nutritional needs should be evaluated on an individual basis, especially where underlying conditions exist, and adjustments to the diet or supplementation may be considered as required.20

Concerns around bone health and the KD generally occur in the context of children with epilepsy, but a ketogenic approach can be successful long-term, without ill effects.41 Type 2 diabetes and insulin resistance are risk factors for the development of osteoporosis, and the use of a KD in this population can benefit.9 In a recent study, long-term adherence to a well-formulated KD in healthy women did not adversely affect bone health.45

Is it safe to consume saturated fats on a ketogenic diet?

The diet-heart hypothesis with saturated fat as a central theme emerged in the 1950s and has persisted despite recent evidence demonstrating that the relationship between saturated fat and CVD is complex, where the saturated fatty acid (SFA) profile of foods can confer physiological and metabolic benefits.46,47,48 Historically, concern around SFA consumption relates to low-density lipoprotein cholesterol (LDL-c) effects; yet, changes in LDL-c concentrations do not predictably occur with changes in SFA intake (though the beneficial pattern A subtype has been shown to increase)49 nor do they reliably predict changes in CVD risk.46,50 Increased SFA intake tends to favourably increase high-density lipoprotein cholesterol (HDL-c).46 Reducing dietary carbohydrates typically improves LDL subtypes and increases HDL-c, irrespective of any changes in dietary fat intake.46,51

Saturated fats are composed of SFAs that have distinct biological functions that include cell membrane stability, cell signalling and immune function; therefore, they are required to maintain a healthy physiology. These SFAs are derived both endogenously and exogenously, and certain types of fatty acids are deemed essential; we cannot manufacture them.48 Saturated fatty acids may be classified according to their carbon chain length as short-chain fatty acids, medium-chain fatty acids and long-chain SFAs, and different foods contain different combinations of these fatty acids. Recently researchers have begun to identify SFAs that appear cardioprotective in their physiological effects. In particular, C15 (pentadecanoic acid) has been associated with health benefits, and it has been proposed as an essential fatty acid. Sources of C15 are predominantly dairy, ruminant meat and some types of plants and fish, which may be key components of a KD.46,48

The biological effects of SFAs vary with their subtype, the food matrix, and the carbohydrate content of foods. Whole foods such as full-fat dairy, unprocessed red meat and dark chocolate have a SFA profile that does not demonstrate an increased risk for CVD or type 2 diabetes.46,47 Critical examination of the data has failed to show an association between saturated fat intake and CVD or cardiovascular mortality.47

Dietary cholesterol may be increased on a KD as animal-based foods are often a key feature. The main sources of dietary cholesterol are meats and poultry, eggs (yolks), shellfish and full-fat dairy.52 Cholesterol is a major sterol required as a precursor of steroid hormones (including vitamin D) and bile acids; it is a structural component of cell membranes, and it is important for cellular signalling and repair. Cholesterol homeostasis is maintained via feedback mechanisms that balance exogenous dietary cholesterol and endogenous de novo synthesis, predominately in the liver, and transported to peripheral tissues via lipoproteins.52,53 Overall, dietary cholesterol is not correlated with plasma cholesterol concentrations and the liver produces cholesterol in accordance with physiological requirements.52,53,54 The limit on dietary cholesterol consumption has been removed from the United States (US) dietary guidelines because of a lack of evidence where they state dietary cholesterol is ‘not a nutrient of concern for overconsumption’.54

Metabolic associated fatty liver disease (MAFLD) is a disorder of metabolism where hormonal dysregulation drives de novo lipogenesis and fat accumulation in hepatocytes. Hyperinsulinaemia, a driving component of this condition, responds rapidly to carbohydrate reduction, where a diet higher in fat has been found to be an effective strategy.6,10,55

What if I have gallbladder disease?

Gallbladder or gallstone disease is strongly associated with obesity and metabolic syndrome, where it is proposed that low HDL-c and high triglycerides increase the cholesterol saturation index, promoting the development of cholesterol crystals, a precursor of gallstone formation.56,57 While there may be an increased risk of gallstone development during periods of acute weight loss, diets higher in fat have been found to be protective for the development of gallstones during this phase.57 Studies demonstrate that a reduced-carbohydrate approach rapidly improves triglyceride and HDL-c, key risk factors for gallstone disease, without significant adverse effects.12,58 Individual assessment of risk factors may determine if a slower transition or a modified ketogenic approach is appropriate. Clinical experience supports a slower transition into a ketogenic approach where a cholecystectomy has been performed.32

How does the ketogenic diet affect cardiovascular health?

According to recent studies, the majority of the US population has suboptimal cardiometabolic health (approximately 90%) assessed using standard metrics of insulin resistance.59,60 These metrics associate strongly with CVD risk,61,62 and these same metrics consistently demonstrate improvements with the application of a reduced carbohydrate diet or a KD.8,12,58

The KD promotes weight loss without tracking energy intake,9,20,25 although caloric targets may be specified; depending on the intervention and therapeutic goals.18,20,25 It is effective in patients both with and without type 2 diabetes.25,58 Visceral adiposity and waist circumference, are significant predictors of CVD risk and the waist-to-height ratio has been recognised as improving the ability to detect risk where it acts as a proxy for visceral adiposity.63 A KD consistently demonstrates significant improvements in these metrics,64,65 with the results of one meta-analysis finding an average reduction in waist circumference of 9.17 cm.64

Improvements in dysglycaemia, fasting blood glucose and insulin typically occur in patients with or without type 2 diabetes using a ketogenic approach,58 and may occur without weight loss.66 Type 2 diabetes, a leading cause of CVD,61 consistently improves with a KD, demonstrating improved glycaemic control, reduction of medications and a possibility of remission for a subset of this population.9,67 Glycaemic improvement in response to a KD requires medication adjustments and a comprehensive guide of considerations and approaches by Cucuzzella et al., is recommended reading.28

Improvements in HDL-c and triglycerides consistently occur with a reduced carbohydrate or ketogenic approach, and are associated with improvements in LDL-c subtypes58,68,69 and may also occur without weight loss.70 Overall, studies show little change in LDL-c; but it should be noted that LDL-c, as an isolated metric, is not a good predictor of CVD risk,6,51 as significant variation of plasma LDL-c concentration occurs in those with and without coronary artery disease.71,72,73 Measuring LDL subtypes improves risk prediction in that large (pattern A) LDL particles have no predictive value for CVD risk and associate with lower triglyceride and insulin levels, and a higher HDL-c.74 Conversely, small LDL subfractions are independently associated with CVD risk and predominate in the insulin resistant phenotype,74 which consistently improves using low-carbohydrate and ketogenic approaches.68,69,74 Assessing markers of dysglycaemia and hyperinsulinaemia, are more reliable predictors of CVD risk.46,51 The triglyceride to HDL-c ratio reflects insulin sensitivity (target < 1.5 in mmol/L, or < 3.0 in mg/dL)75 and is a stronger predictor of risk than isolated cholesterol metrics, and would also give an indication of LDL subtypes.74,76

While data show the metric of LDL-c, in isolation, to be a poor predictor of increased risk of CVD,71 a significant elevation in LDL-c in a small subset of individuals who adopt a reduced carbohydrate diet, has raised concerns and is driving more research on this topic.73,77 These individuals, referred to in the literature as lean mass hyper-responders tend to be metabolically healthy (generally with a body mass index [BMI] < 25 kg/m2) with cholesterol cut points defined as LDL-c ≥ 200 mg/dL (5.2 mmol/L), HDL-c ≥ 80 mg/dL (2.1 mmol/L) and triglyceride ≤ 70 mg/dL (0.8 mmol/L).77 These individuals benefit from monitoring and evaluation according to personalised risk-benefit metrics. In individuals with a LDL-c ≥190 mg/dL (4.9 mmol/L), a coronary artery calcium (CAC) may be used to stratify risk, with a zero CAC score reflecting low risk for future CVD events.72 Recent data comparing metabolically healthy individuals on a KD (mean duration 4.7 years) with LDL-c ≥190 mg/dL (4.9 mmol/L) and matched controls found no association between LDL-c and plaque burden using CAC imaging and coronary computed tomography angiography (CCTA).73 These results are promising and emphasise the importance of considering a range of biomarkers for determining CVD risk.71 An option to reduce LDL-c by increasing the amount of carbohydrates to 50 g/day – 100 g/day (from fruit or starchy vegetables) has been demonstrated and may have a role as determined on an individual basis.77 A KD is primarily a whole foods approach that may be adjusted according to individual responses and therapeutic targets and can accommodate a wide range of dietary patterns, such as vegetarian or Mediterranean approaches.

Hypertension strongly associates with CVD risk and improves with a KD.9,61,78 Complex regulatory systems are involved in blood pressure homeostasis that include the hypothalamic-pituitary-adrenal (HPA) axis and the renin-angiotensin-aldosterone system (RAAS).78,79 The KD acts via these systems to normalise blood pressure by reducing visceral adiposity and driving positive adaptations to the HPA axis and RAAS. These mechanisms of action may result in a rapid reduction in blood pressure, requiring appropriate surveillance and reduction of medication as necessary.28,80

Is the ketogenic diet contraindicated in kidney disease?

Traditionally, the KD has been regarded with caution in the context of kidney disease because of concerns about protein intake. Higher protein diets have been thought to compromise kidney function because of increased filtration and elimination of the by-products of protein metabolism with potentially damaging effects. However, a Cochrane review from Jiang et al. (2023) found uncertainty regarding the effect of a low-protein diet on estimated glomerular filtration rate (eGFR) or progression to kidney failure, and another recent study concluded a higher-level intake of protein to be protective.81,82 The standard KD is moderate in protein, similar to general diets, and typically falls in the range 0.6 g/kg to 1.4 g/kg, well below the threshold of concern.11

A significant body of evidence has shown that the KD can address key features of the pathophysiology of cardio-metabolic-renal (CMR) disease, namely hyperinsulinaemia and hyperglycaemia, with no reduction in kidney function.12,83 Approximately 40% of patients with type 2 diabetes have chronic kidney disease (CKD) and there are a number of studies showing the application of a reduced carbohydrate or KD in this setting.11 These studies have demonstrated safety and improved eGFR,84,85,86 as well as the possibility of regression from CKD stage 3 to 2.87 A very low-carbohydrate diet in the ketogenic range (≤ 30 g/day) has demonstrated safety and efficacy of this approach in patients with metabolic syndrome and CKD stages 3–4.24

Autosomal-dominant polycystic kidney disease (ADPKD) is a genetic kidney disease involving the progressive development of cysts and declining kidney function, eventually leading to kidney failure. Ketogenic interventions are showing promise in the management of ADPKD, with improvements in kidney function observed and one study showing higher levels of ketones associated with a lower rate of decline of kidney function.11,88

A risk of kidney stones is generally low for individuals on a KD, although certain populations are more at risk, for example, children with epilepsy who are also on antiseizure medication.6,11 Obesity and CKD are risk factors for the development of kidney stones irrespective of diet, and this risk may also be genetically driven.11 Taking account of medical and family history allows for appropriate mitigation of risk through increasing fluid intake and the use of sodium or potassium citrates.6,11 The benefits of reducing obesity and the components of CMR disease need to be weighed against the risk of kidney stones, where CKD generally improves on implementing a KD.

Can the ketogenic diet be safely sustained long-term?

A number of studies have reported on appetite and cravings as experienced by participants, with positive feedback showing reduced symptoms compared to control groups.89 Mechanisms for these reports include reduced insulin, increased lipolysis, ketogenesis and the attenuation and normalisation of hunger hormones such as ghrelin and leptin. Early data has shown a ketogenic approach can be successful for the treatment of food addiction symptoms and binge eating disorders6,90 These data could explain reported improvements in cravings and satiety experienced by individuals when consuming a low-carbohydrate diet or a KD, even in healthy individuals.31

Critics have suggested the KD may promote disordered eating. The evidence suggests a KD may normalise eating behaviours via modulating neurobiological responses involved in mental health conditions, a key driver of eating disorders.17 A KD is able to facilitate weight loss, weight gain or maintenance through appropriate adjustment of nutritional intake meeting nutritional requirements. It is a whole foods approach that encompasses a wide range of dietary options that can be tailored to individual preferences and therapeutic goals.

Studies show that a whole foods, well-formulated KD may be nutrient dense and cost-effective.91 Even in under-resourced communities, a KD may be successfully adopted with cost savings incurred because of reduced reliance on ultra-processed foods (UPFs), improved satiety (less frequent snacking) and reductions in clinic visits and medications required.6,92

Questions around long-term data on the KD are commonly cited as a concern and short-term use is often suggested. In type 2 diabetic populations, there are up to 5 years of published data on a cohort measured as being in nutritional ketosis.93 Studies on healthy individuals in nutritional ketosis over 4–5 years have shown no adverse effects.45,73,94 Historically, metabolic flexibility was a feature of ancestral populations where certain populations existed in ketosis and were able to meet nutritional needs and experience good health.6,95 Taken together, these data suggest a state of metabolic flexibility, which may include nutritional ketosis, aligns with ancestral patterns. Ongoing monitoring of metabolic markers as clinically indicated is suggested.

Limitations

A range of studies were used, spanning a broad evidence base with a risk of bias. In some areas the evidence is emergent, and the studies cited reflect this.

Conclusion

This review speaks to the benefits of a KD across a range of therapeutic applications and addresses common questions raised by patients and clinicians who may be unfamiliar with this approach. The totality of evidence supports a well-formulated, whole-food KD as being safe and effective for key features of metabolic dysfunction, a condition affecting approximately 90% of the US population. Many healthcare providers are successfully using carbohydrate reduction as an adjunct to pharmaceutical therapy, and an experienced healthcare provider can personalise this approach according to therapeutic targets. This may include increasing, decreasing or maintaining energy density; changing macronutrient ratios; excluding problematic foods; or adjusting for personal or cultural preferences. Nutrient sufficiency can generally be achieved using a well-formulated, whole foods approach, and appropriate supplementation can be applied if required. As with any intervention, regular monitoring of biomarkers guides a personalised approach with necessary adjustments as required.

Acknowledgements

The authors would like to thank Dr. Eric Berg for providing an overview of queries received through his social media platforms. They acknowledge pioneers in the field of therapeutic carbohydrate reduction and ketogenic diet research who are working to advance the field and whose work underpins this article.

Competing interests

The authors declare that they have no financial or personal relationship(s) that may have inappropriately influenced them in writing this article.

Authors’ contributions

The authors S.M.R. and D.B.R. developed, read and agreed to the submitted version of the article.

Funding information

This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

Data availability

No datasets were generated or analysed during the current study.

Disclaimer

The views and opinions expressed in this article are those of the authors and are the product of professional research. The article does not necessarily reflect the official policy or position of any affiliated institution, funder or agency, or that of the publisher. The authors are responsible for this article’s results, findings, and content.

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