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  • Unveiling the Ketogenic Diet: Its Potential in combatting Obesity and Improving Health Markers

  • AISSMS College Of Pharmacy, Pune, Maharashtra, India 411001.

Abstract

Obesity is a major global health issue, with more than 650 million obese adults worldwide, and?is associated with serious diseases such as heart disease, type 2 diabetes, and certain cancers. It is?generally evaluated using Body Mass Index (BMI). The increasing prevalence?of obesity is linked to the modern lifestyle, with unhealthy eating habits and a sedentary way of life, combined with environmental factors. Furthermore, the mental effects of obesity are profound due to social prejudices, which result in anxiety, depression, and poor self-worth, rendering the management even?more difficult. The?classical ketogenic diet (KD), a high-fat, low-carbohydrate diet, is an effective treatment for obesity and metabolic syndrome that has been utilized in clinical and experimental settings for decades. Studies have shown that a KD can contribute to weight loss by increasing?fat burning and decreasing appetite, as well as by improving metabolic health factors, including insulin sensitivity. However, the diet is?very restrictive, so nutritional deficiencies may occur, and critical organs can be overworked without proper medical monitoring. Long-term studies are also essential in order to understand the effect of the ketogenic diet on health, insulin resistance, cardiovascular health, and even cancer?. In addition, new insights into the role of the gut microbiome?in the context of metabolism are beginning to allow for personalized dietary recommendations to enhance metabolic responses. In conclusion, a multi-dimensional strategy, integrating?diet, activity, and psychological aspects, is required for the successful combating of the obesity epidemic

Keywords

Obesity, Ketogenic Diet, Metabolic Health, Insulin Sensitivity, Gut Microbiome, Weight Loss, Dietary Interventions

Introduction

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Obesity is one of the biggest health problems in the world today, affecting millions of people across the globe. It’s not just an issue of how people look, coolly invoked about themselves or others; it’s a major medical problem that increases your risk of deadly diseases like heart disease, type 2 diabetes, high blood pressure, and even some cancers. According to the World Health Organization (WHO) in 2021, the number of adults who are obese has exceeded 650 million, whereas almost 2 billion people were found to be overweight[1]. Being overweight and obese are commonly defined as Body Mass Index (BMI), where overweight means a BMI of 25 or more, and obesity means a BMI of 30 or more. Class I, Class II, and Class III, also called morbid obesity, are the three classes classified as obesity[2]. The drop in the thin and the rise in the fat is a product of changes in modern life. A significant factor is poor eating habits, particularly overconsumption of processed foods, sugary drinks, and high-fat diets. Moreover, most of us have increasingly sedentary lifestyles, spending hours in front of computers or sitting at desks with little to no physical activity. Genetics does come into play, but  environmental and lifestyle choices that have the greatest effect. But obesity isn’t just damaging your body and brain’s blood vessels[3]. Obesity comes with a deep social stigma for many people, which can result in things like anxiety, depression, and low self-esteem. This societal stigma can lead to a sense of isolation and judgment that only serves to exacerbate the challenge of dealing with obesity. Economic costs associated with obesity are enormous, including greater spending for health care to treat conditions associated with obesity, lost productivity, and reduced life span. It’s not easy fighting obesity[4]. It must be addressed on multiple fronts, involving lifestyle modifications, medication, and awareness. One promising choice in this field is the ketogenic diet (KD), which is high in fat and low in carbs and makes the body enter a state of ketosis, fat burning, instead of carb burning. Some early research indicates that a very low-carb ketogenic diet may be an effective way to treat and prevent obesity and other metabolic conditions, including type 2 diabetes and even some types of cancer[5]. However, such a limited eating regimen isn’t easy to stick with, and if it’s not done right, it can cause nutritional deficiencies or put too much stress on organs such as the kidneys and liver. The ketogenic diet holds great promise, but more research is needed to fully understand its long-term consequences and devise a means to make it more sustainable for people.The obesity epidemic won’t be overcome based on diets alone. It involves encouraging better eating, more physical activity, and a more nuanced understanding of the social and psychological factors at play. The good news is that by small steps on the individual and societal levels, we can, make a difference in battling obesity[6].

Advanced Understanding of the Ketogenic Diet: How Ketosis Works

Ketosis is a metabolic state in which the body drastically switches from using glucose as energy to using fat-derived energy-rich compounds called ketone bodies. Ketones share a distinct chemical structure, which is distinguished by the presence of a carbonyl group (C=O) surrounded by carbon-containing side chains. In the human body, ketone generation (Ketogenesis) occurs mainly in the mitochondria of liver cells. Although ketones are produced in the liver, most cells in the body can utilize ketones as an energy source, particularly during low glucose levels[7].

During an overnight fast, ketones supply 2–6% of this energy in non-diabetic persons. But, after a few days of fasting or strict ketogenic dieting, Maximum can begin to increase quite substantially (30–40% in some cases) as the body gets upregulated in terms of both producing and dumping ketones[8].

The body produces three ketone bodies: acetone, acetoacetic acid, and 3-β-hydroxybutyric acid. Strictly speaking, 3-β-hydroxybutyrate is not a ketone but a ketone body, a molecule related to the ketone, acetone, having the relation to acetone that acetoacetic acid has to benzoic acid, though not chemically similar of these, 3-β-hydroxybutyrate is the most prevalent in the bloodstream, followed by acetoacetate[9]. As it's a volatile product, even your breath, not energy, is a good way to get rid of acetone. The concentrations of ketones in the blood are regulated by ketogenesis (assembly) and ketolysis (dismantling and utilization). Hormones influence these processes: glucagon tends to make the body produce it, while insulin suppresses its production[10]. The average blood ketone level after fasting for a healthy person would be 0.1–0.2 mmol/L, but it can be much higher for someone with obesity or for someone who is on a ketogenic diet. Ketone concentrations in blood can vary from 0.5 mmol/L to 8 mmol/L, depending on whether one is fasting or following a very-low-carbohydrate ketogenic diet (VLCK)[11]. Severity of diabetes is typically based on the value of HbA1C, but in the case of ketoacidosis, ketones can reach 25 mmol/L. Under some conditions, such as a ketogenic diet, exogenous ketones can make metabolic improvements that result in neuroprotection and increased energy due to combustion efficiency. In situations such as neurological conditions, a good ketone level is 7-8 mmol/L. Ketone production is initiated by breaking stored fat into free fatty acids by lipolysis. These fatty acids are transported to the liver, transforming them into acetyl-CoA, a key molecule in energy metabolism. In a low-carb state, Acetyl-CoA accumulates and is shuttled into ketone synthesis instead of being used in the normal carbohydrate pathways.

The ketogenesis pathway involves several key enzymatic steps[12]:

  1. Two acetyl-CoA molecules are joined to form acetoacetyl-CoA.
  2. This is then converted into HMG-CoA (β-hydroxy-β-methylglutaryl-CoA) by the enzyme HMG-CoA synthase.
  3. HMG-CoA is broken down into acetoacetate, which can either be converted into 3-β-hydroxybutyrate (a reversible reaction depending on NAD+/NADH ratio) or spontaneously break down into acetone, which the body cannot use and expels.

 

 

 

Fig 1. Mechanism of Ketogenesis: Enzymatic Conversion of Acetyl-CoA to Acetoacetate and β-Hydroxybutyrate

 

When produced, 3-β-hydroxybutyrate and acetoacetate become part of the bloodstream and are able to travel to other organs (like the brain, heart, and muscles), where they can be used as fuel. This use of ketones by non-liver tissues is referred to as ketolysis and effectively reverses the process of ketogenesis using these compounds as substrates. This acetyl-CoA goes into the Krebs cycle to produce around 22 ATP per 1 ketone (as ATP is made in 3 different places during this metabolic cycle, so I'm giving a rough estimate), feeding cells a ton of energy. It's curious that the liver prefers to secrete ketones but does not consume them for its own energy. The reason is that liver cells do not have an enzyme called SCOT (succinyl-CoA:3-ketoacid CoA transferase), which is required to metabolize ketones. This makes sure that ketones are sent to other tissues that are in need of them in times of carbohydrate deprivation[13].

Types of Ketogenic Diets

The ketogenic diet (KD) was first introduced as a treatment in the early 20th century to control epileptic seizures. It has gradually developed as a treatment option, especially for patients with epilepsy that is refractory to routine drugs. In addition to seizure control, the KD has been increasingly considered as a potential neuroprotective therapy owing to the production of ketone bodies and the decreased dependence of the body on glucose for energy[14]. The phrase “ketogenic diet” often gets thrown around fast enough to make you want to sprint to the nearest store for a guilt-free turkey jerky. Follow-up, but as it turns out, it refers to more than one type of high-fat, low-carb diet. All of these diet regimens have one goal: putting the body into a state of ketosis, which is when the body burns fat, instead of carbohydrates, for fuel. The ketogenic diet replicates the same effect of starvation by tricking the body into burning fat to produce energy without actually abstaining from food[15]. It's important to understand that not all low-carbohydrate diets are truly ketogenic. Some diets may significantly reduce carbohydrate intake but still include high amounts of protein. In such cases, ketosis may not occur.

 

 

 

Fig. 2. Understanding the Ketogenic Diet: Fat Distribution and Nutrient Breakdown

 

This is because specific amino acids found in protein can be converted into glucose by the body, which may prevent the shift into full ketosis. The ketogenic diet has several recognized forms, each tailored to different needs and preferences[16]. These include:

  1. Classical Ketogenic Diet (CKD)

This is the most traditional form and is typically used in clinical settings, especially for managing epilepsy in children. It involves a strict ratio of fats to combined protein and carbohydrates, often as high as 4:1. This means that for every 4 grams of fat, there's only 1 gram of protein and carbohydrate combined. The CKD requires careful planning and monitoring[17].

  1. Modified Atkins Diet (MAD)

A more flexible version of the classical diet, the Modified Atkins Diet allows for a higher intake of protein and does not require precise weighing of foods. Carbohydrate intake is still limited, but the structure is easier to maintain, making it a popular option for adults or older children[18].

  1. Atkins Diet (AD)

Originally developed for weight loss, the Atkins Diet is high in fat and protein with a very low carbohydrate intake, especially in its initial phases. While not always intended to induce ketosis for medical purposes, it can produce similar metabolic effects if carbohydrate intake remains low[19].

  1. Medium-Chain Triglyceride Ketogenic Diet (MCTKD)

This version uses medium-chain triglycerides (a type of fat that is more easily converted into ketones) to allow for more carbohydrates and protein compared to the classical diet. Since MCTs are efficiently turned into ketones by the liver, this approach provides more dietary flexibility while still maintaining ketosis[20].

  1. Low Glycemic Index Treatment (LGIT)

This form emphasizes carbohydrates that have a low glycemic index, meaning they have a minimal impact on blood sugar levels. It includes slightly more carbohydrates than other ketogenic diets but focuses on foods that cause only slow and steady rises in blood glucose. This is another less restrictive option that may still support ketone production to some degree[21].Each type of ketogenic diet has its own balance of fats, proteins, and carbohydrates, offering different levels of flexibility and effectiveness depending on individual needs, health goals, and medical conditions. Whether for therapeutic use or general wellness, choosing the right version often involves considering factors like lifestyle, age, tolerance, and metabolic response.

Classic Ketogenic Diet (CKD)

The Classic Ketogenic Diet (CKD) The classic ketogenic diet is the most rigorous and tightly controlled version. It's made to provide a specific ratio of macronutrients: usually about four parts fat to one part protein and carbs[22]. This comes to 80-90% total daily calories from fat, with (ideally) no more than 10-20% of those calories coming from protein, and a minimal amount of carbohydrates. This is a high-fat, low-carb way of eating and can prompt the body to go into a state known as ketosis. To support this metabolic switch, protein consumption is purposefully kept low as excess protein can be converted into glucose that could negatively affect getting and staying in ketosis. CKD is mainly used for medical reasons, such as intractability to medication, epilepsy treatment, among others, which are recommended in case of pre-pubertal children and a lack of medication control. In the case of growing children, the fat-to-protein-plus-carbohydrate ratio is sometimes slightly relaxed to 3:1 to provide sufficient protein for healthy growth[23]. Traditionally, the CKD began with a short fasting period, which was done perhaps within the confines of a hospital to get the body into ketosis as soon as possible and also to observe if there were any side effects. This diet must be initiated and followed up under strict medical and nutritional supervision. Because it may take dozens of hours of dietitian counseling to incorporate CKD for one patient properly, the use of CKD is resource-intensive in terms of both time and cost[24]. Liquid formulas for infants and children who cannot take solid food are also available and can be formulated to provide the stringent macronutrient ratios of the CKD. Adult Formula: These formulas can also be used for adults as needed. Although CKD has therapeutic advantages, it isn't easy to follow. This diet's very restrictive and unbalanced nature makes it hard to adhere to, and many others don't like the taste and mouth feel of high-fat foods over time. For that reason, modified versions of the keto diet have been introduced, offering increased flexibility while still having many of the same health advantages.

 

 

 

Fig. 2. A Visual Comparison: Macronutrient Breakdown in the Typical American Diet vs. Ketogenic Diet

 

Atkins Diet (AD)

The Atkins Diet has four distinct phases designed to help a person balance a gradual approach to weight loss with the goal of achieving and maintaining one's desired weight. Phase 1, or Induction, is the most restrictive and limits carbohydrate intake to around 20 grams of net carbs per day, mainly from leafy and low-carb vegetables[25]. This phase is supposed to push the body into ketosis, a metabolic state where fat becomes fuel for the body. Once the diet reaches phase 2, Balancing, tiny amounts of carbs are introduced back into the diet at a rate of 5 grams per week. This is the phase in which nuts, seeds, berries, and, in some people, even dairy, can be introduced into a person's diet without gaining weight. Pre-Maintenance, Phase 3, introduces more carbs, increasing them to where their weight loss slows, and allowing the dieter to establish the maximum personal carb threshold they can consume and maintain the current, lower weight. 4) Phase 4 is called Lifetime Maintenance, and it explains how to maintain the ideal weight for you according to balanced consumption of carbohydrates and the ability of your life. This phase focuses on long-term eating habits and lifestyle, not temporary dieting[26].

What Is the Atkins Diet and the Ketogenic Approach to: Positives , Background, Phases, Cautions?

The Atkins Diet, one step at a time. Less restrictive than far more noticeably strict kilojoule churners, blueprints of the Atkins Diet put the diet under much less strain because once one passes through every phase, the diet plan gives one a broader variety of food options to come back into the fold. Nevertheless, ketosis—what it is in the body when burning fat for energy instead of carbs—is generally only reached in the first phase with minimal carb consumption. The Atkins Diet has undergone changes over the years based on new evidence and user complaints[27]. The diet has continued to evolve and is marketed via the official Atkins website even after the death of Dr. Robert Atkins in 2003. Most people do quite well on the Atkins Diet in the early days, especially if they are only focused on losing the first bit of weight fast. However, some health professionals have condemned the diet. Many have questioned the long-term health effects of a high-fat, high-protein, and extremely low-carbohydrate diet. That may include possible hazards to cardiovascular health, renal wellness, and overall dietary balance. However, until more long-term studies are completed, many health care practitioners are hesitant to recommend Atkins as a viable, long-term solution for everyone. That said, for metabolisms that benefit from low-carbohydrate plans, Atkins can be a useful tool for weight loss designations, when done responsibly (with a doctor and monitoring, if necessary)[28]. Recently, low-carb, high-fat dietary models, particularly the ketogenic diet (LCKD), have received great recognition due to their promising health effects and possible effects on weight loss. Though Atkins and keto revolve around restricting carbs, how they impact metabolism is not very similar. Most low-carb diets reduce carbs to 50–150 grams per day, below that of a typical Western diet, but too high to put your body in ketosis. Generally, this means cutting carbs to less than 50 grams per day to reach ketosis. It forces the body to enter the state of burning fat for energy instead of burning glucose, which is the core metabolic transition of ketogenic. Unlike conventional dietary advice, which has long espoused foods composed mainly of carbohydrates, the ketogenic diet focuses on fat as the primary energy source. With fewer carbs, Blood glucose and insulin levels fall, and the body shifts into a fat-burning state. The liver subsequently creates ketone bodies — acetone, acetoacetate, and beta-hydroxybutyrate — in a process referred to as ketogenesis. They fuel most of the body, such as the brain, muscles, and many organ cells. Interestingly, beta-hydroxybutyrate is a signaling molecule that may contribute to appetite suppression, which will be especially beneficial for those seeking to control body weight[29]. Like the Atkins diet, the ketogenic diet defies traditional practices and provides new routes to health and shedding pounds. However, this success is highly contingent on individual response, compliance, and continued nutritional counseling.

The Modified Atkins Diet (MAD) 

The Modified Atkins Diet (MAD) has been established as a looser variant of the classical ketogenic diet (CKD) primarily for seizure control. MAD, started at Johns Hopkins Hospital, is a less aggressive approach that also focuses on maintaining a state of ketosis. MAD differs from the traditional Atkins Diet in that the latter gradually reintroduces carbohydrates in stages, while MAD keeps the first phase of the Atkins Diet perpetually active. This is important for maintaining ketosis in the long term. One of the main differences with MAD over any other form of a ketogenic diet is that it was originally a more therapeutic approach (for seizures, as opposed to losing weight). This means the diet is based mostly on reducing carbs, usually lower than 20g per day. There are no hard restrictions on total calories, protein, or fluid consumption, as in the case of classic ketogenic or Atkins diets. This results in a more favorable and practical fat-to-protein-and-carbohydrate ratio for MAD at an estimated 1:1, increasing long-term adherence to MAD. The extra benefit of the Modified Atkins Diet is that it gives freedom in meals. Some vegetables are higher in total carbohydrates than the fibrous part of the carbohydrate, so high-fiber vegetables may be more acceptable since the carbohydrate is not counted as a total in the diet[30]. However, sugar alcohols(which come in many processed low-carb foods) are included in the carbohydrate count. When starting, MAD usually does not need to be done in a hospital or under medical supervision. This is largely because it is simple to perform. Individuals can initiate the diet at home, making it a more user-friendly and accessible long-term dietary management approach.

Focuses on how to use a ketogenic diet to manage body weight.

The ketogenic diet (KD) has gained popularity in recent years as a means to achieve weight loss and improve metabolic health. According to the findings of a survey conducted by the International Food Information Council (IFIC) Foundation in which 2,000 American adults were interviewed and placed on a diet (including KD), The only dietary trend that experienced a substantial increase in followers  was keto, which the majority of participants said they followed for weight loss .This trend highlights the need for more research into how safe and effective the diet is for long-term use in the management of obesity[32].

During the last five years, the clinical studies have mainly been short- to medium-term interventions that last from a few weeks to a year. Most of these studies utilized very-low-calorie ketogenic diets (VLCKD) and limited calories to 500–800 kcal/day[33]. Participants saw significant decreases in their body weight, body mass index (BMI), and fat mass throughout the program. That said, it is unclear if these results were mediated by the presence of ketosis or just the massive caloric deficit. Many of the studies lack control groups, so it is impossible to tell whether macro composition or calorie restriction was responsible for the weight loss. In addition, VLCKD may have a higher dropout rate due to the more restrictive pattern of VKD compared to other diets in the long term, which will also require more rigorous medical supervision during the intervention. Recent studies shed new light. A three-month KD trial resulting in substantial weight loss and improvements in parameters suggesting better metabolic health (i.e., insulin sensitivity) and loss of body weight that spared lean body mass was reported in a 2024 paper in the journal iScience[33]. However, a study by UT Health San Antonio cautioned that such long-term effects, including loss of cellular aging in the heart and kidneys, could also occur on the diet, but only when they are spaced with planning for time off the diet. Another review pointed out that compared with other dietary approaches, VLCKDs appear to facilitate a more significant weight loss over the short term compared with other diets that are designed to promote weight loss[34]. At the same time, the overall state of cardiovascular health is worrisome; a 2024 meta-analysis published in The American Journal of Clinical Nutrition reported some beneficial lipid profile changes but some possible adverse effects related to high saturated fat intake. Meanwhile, Stanford Medicine also found that people with severe mental illnesses who were on a KD improved metabolically and psychologically, hinting that the diet could have broader potential. KD has beneficial short-term consequences on weight and metabolism (particularly in its very-low-calorie form), but long-term security and maintenance remain to be established[35]. It needs medical supervision, individual assessment, and most probably dietary changes to be used successfully for the treatment of obesity.

 

Table 1. A Decade of Evidence: Clinical Trials Assessing Ketogenic Diets for Obesity Control

Type of Ketogenic Diet

Study Group

Inclusion Criteria

Duration

Assessment Method

Main Outcomes

Reference

Synthetic protein

n=20, BMI=29.85 ± 3.98

BMI >30; weight stability; desire to lose weight

4 months

Level of β-hydroxybutyrate

Significant reduction in weight, fat mass

36

VLCKD (PNK Method)

n=20, BMI=35.5 ± 4.4, Age=47.2 ± 10.2

Age 18–65; BMI >30

4 months

Level of β-hydroxybutyrate

Reduced weight, fat mass, improved sleep and activity

37

VLCKD (<700 kcal/day)

n=54, BMI=31.31 ± 3.32, Age=44.60 ± 15.06

Age 18–65; BMI ≥25; high body fat %

3 weeks

Non-specified

Reduced BMI, waist circumference

38

VLCKD (550/660 kcal/day)

n=31, BMI=37 ± 4.5, Age=43 ± 10

BMI 30–45; sedentary; stable weight

8 weeks

Food records

Reduced weight, fat mass, insulin; increased ghrelin

39

Exclusive ketogenic drink

n=13+13, BMI ~30, Age ~27

BMI >25; stable weight

2 weeks

Ketone sticks

Fat mass & weight loss, lipid profile improved

40

Ketogenic (~5% carbs)

n=25, BMI=30.7 ± 8.0, Age=61.5 ± 8.5

Ovarian/endometrial cancer; BMI ≥18.5

12 weeks

β-hydroxybutyrate, food records

Reduced visceral fat, insulin, IGF-I

41

VLCKD (Ketostation)

n=119, BMI=41.5 ± 7.6, Age=43.6 ± 9.8

Age 18–62; BMI >44

30 days

Β-hydroxybutyrate

Reduced weight, liver volume; lipid profile improved

42

Micronutrient-enriched KD

n=27, BMI ~45, Age=41 ± 16.7

Obese, pre-bariatric surgery

4 weeks

Food records, 72-h recalls

Reduced liver volume, improved nutrition

43

VLCKD (<30g carbs/day)

n=72, BMI=46.3 ± 6.3, Age=43.4 ± 12.1

Morbid obesity

3 weeks

Non-specified

Weight loss, shorter hospital stay

44

KD (5–10% carbs)

n=35, BMI=36.1 ± 5.6, Age=37 ± 7

BMI >30; stable weight

12 weeks

Food dairies, β-hydroxybutyrate

Reduced fat mass, improved fitness & cognition

45

VLCKD (<800 kcal/day)

n=52, BMI=44.7 ± 8.3, Age=49 ± 12.5

BMI >40 or >35 with comorbidities

25 days

Ketone sticks

Reduced BMI, insulin; increased lysosomal activity

46

Recent: VLCKD Study (2024)

n=60, BMI=34.5 ± 6.0, Age=45.2 ± 11.1

Obese adults, stable metabolic health

3 months

Blood ketones, DEXA

Improved body comp., reduced insulin

47

 

The ketogenic diet, a high-fat, low-carb eating plan, has gained attention for its wide-ranging benefits. It's more than just a diet for weight loss—it has potential health benefits that extend to various conditions and systems in the body.

  1. Cancer: The ketogenic diet works by lowering insulin levels and reducing signals that promote the growth of cancer cells. It helps decrease blood glucose levels, which cancer cells rely on for fuel. This shift in metabolism makes cancer cells more vulnerable to treatments like chemotherapy and radiation while protecting normal cells[48].
  2. Microbiome: The ketogenic diet positively impacts gut health by increasing the ratio of Bacteroidetes to Firmicutes bacteria in the microbiome. This alteration enhances genetic diversity, improving insulin resistance, inflammation, and conditions like dyslipidemia and obesity[49].
  3. Diabetes: For individuals with diabetes, the ketogenic diet helps regulate blood sugar by reducing HbA1c levels and lowering insulin requirements. It has even shown potential in reversing insulin resistance, providing a significant tool for managing the disease[50].
  4. Weight Loss: One of the most popular reasons people try the ketogenic diet is for weight loss. The diet helps reduce appetite, lowers visceral fat, and promotes fat burning while maintaining lean muscle mass. This results in effective weight loss without compromising metabolic health[51].
  5. Cardiovascular Health: The ketogenic diet contributes to heart health by lowering triglycerides, increasing HDL (the "good" cholesterol), and decreasing sdLDL (the harmful form of LDL cholesterol). It also improves the ApoB/ApoA1 ratio, a key marker for cardiovascular risk[52].
  6. Epigenome: The diet affects gene expression by altering the epigenome. Beta-hydroxybutyrate (BHB), a key compound produced during ketosis, is a signaling molecule that can influence gene activity. It inhibits enzymes known as HDACs, which play a role in regulating histone acetylation and gene expression[53].

 

 

 

Fig.3. Potential health benefits of the Keto Diet that extend to various conditions and systems in the body.

 

Table 2. Impact of Ketogenic Diet on Cancer Progression: A Comprehensive Review of Preclinical and Clinical Studies

Study

Year

Cancer Type/Model

Diet Protocol

Main Outcomes

Reference

Nature Communications

2025

Colorectal cancer (humanized mouse model)

KD vs. standard diet

KD reduced tumor burden; the microbiome played a causal role in tumor suppression

54

Cedars-Sinai Medical Center

2025

Glioblastoma multiforme (Phase 2 trial)

KD vs. standard anti-cancer diet

Ongoing trial assessing KD's impact on survival

55

Penn Medicine

2024

Diffuse large B-cell lymphoma (mice)

KD vs. other diets

KD enhanced CAR T-cell efficacy; BHB improved tumor control and survival

56

Columbia University

2024

Breast cancer (mouse model)

KD vs. control diet

↓ Primary tumor growth, ↑ lung metastases via the BACH1 pathway

57

University of California

2024

Pancreatic cancer (mouse model)

KD + eFT508 drug

Combination slowed tumor growth more than the drug alone

58

Osaka University Hospital

2023

Advanced-stage cancers (humans)

Long-term KD (≥12 months)

Longer adherence is associated with improved overall survival

59

Choi et al.

2018

Brain cancer (mice)

KetoCal

↓ Tumor growth, ↑ survival

60

Cohen et al.

2018

Ovarian, endometrial cancer (women)

12-week KD

↑ Physical function, ↑ energy, ↓ cravings for starchy/fatty foods

61

Klement et al.

2016

Meta-analysis (29 animal studies)

Various KDs

72% of studies showed ↓ tumor growth

62

Perez et al.

2024

DIPG (Diffuse Intrinsic Pontine Glioma)

Ketogenic Diet (KD)

5 out of 6 patients adhered to KD for ≥3 months. Mild side effects observed (GI complaints, hypoglycemia, hyperketosis). Median OS = 18.7 months.

63

Morsher et al.

2015

Neuroblastoma (mice)

KD with/without calorie restriction

Best outcomes in calorie-restricted KD group

64

Weber et al.

2020

Gastric, lung cancer (mice)

KD, Calorie-restricted KD

↓ Tumor growth, ↑ survival; ↓ angiogenesis

65

 

The Influence of Diet and Lifestyle on the Gut Microbiome and Metabolic Health

Trillions of microscopic organisms — chief among them bacteria, viruses and fungi — live inside the gastrointestinal tract, and that ecosystem is termed the human microbiome. Over 8,000 different microbial species comprise this complex ecosystem, each one performing different physiological tasks. Emerging data have shown that the microbiome composition and genetic potential are shaped by a multitude of lifestyle factors, including sleep, exercise, antibiotic exposure, and most prominently, dietary factors[66]. Perhaps the most interesting discovery is that the microbiome actually can alter our bodies' responses to different foods. Microbial community composition can modulate energy extraction from food and may directly affect PPGR. This is particularly relevant as stable blood glucose levels are associated with a lower risk of metabolic diseases, including diabetes and obesity[67]. One remarkable study from the Weizmann Institute showed that personalized responses to different foods with respect to blood glucose levels could be predicted very accurately, with an algorithm based on the gut microbiome profile of each individual. Model-favorable foods were associated with steady blood glucose levels among the participants. A follow-up study at the Mayo Clinic among an independent population subsequently confirmed these findings, providing additional evidence that microbiome-informed dietary recommendations are able to exert metabolic effects[68]. The gut microbiome, which is now thought to be one of the most influential factors on human health, is determined more by the environment and lifestyle than by genes. Research by Rothschild et al. For example, their review of studies of gut microbiome taxa showed that the average heritability of gut microbiome taxa was 1.9%, whereas >20% of the OBV was associated with diet and lifestyle. Such findings have spurred an expanding interest in investigating the complex crosstalk between diet, gut microbes, and metabolic health[69]. For example, a study means that meals excessive in prebiotics like inulin and oligosaccharides increased the quantity of advantageous intestinal bacteria, together with Bifidobacteria and different species that provide butyrate. One study reported that dietary patterns—particularly Westernized diets—were more strongly associated with the diversity of the gut microbiota than body mass index (BMI). Those in the Western-style group showed an increase in Firmicutes and a fall in Bacteroidetes, regarded as an adverse change in microbial composition. And, relating to gastrointestinal bacteria, literature has also evidenced beneficial alterations of gut microbiota composition among people on energy-restricted or plant based, high fibre diet plans. A diet high in fruits and vegetables was associated with increased microbiome diversity, while a diet high in highly processed and non-nutritive substances was associated with reduced microbiome diversity. In addition, a reduction in gut microbiota diversity has been linked with higher body fat, insulin resistance, dyslipidemia, and inflammatory responses[70].

 

Table. 3. Key Findings on the Effects of Ketogenic Diet on Metabolism, Gut Microbiome, and Health

Study/Source

Year

Focus

Main Findings

Reference

Effect of restricting free sugars vs. ketogenic diet on metabolism and gut microbiome

2024

Healthy adults

Free-sugar restriction vs. ketogenic diet

 

 

71

Nature Communications

2025

KD and colorectal cancer

KD led to lasting functional

changes in the gut microbiome, reducing colonic tumors

burden through microbial

metabolite stearate-induced apoptosis

72

Karger - KETO-MOOD Study

2024

Very low-calorie KD and microbiome diversity

VLCKD increased gut microbiota diversity compared to a standard low-calorie diet in a weight-loss trial

 

73

Nutrients Journal

2024

KD in women with overweight/obesity

6-week KD decreased microbial diversity and altered short-chain fatty acid profiles

 

74

Nature Communications

2024

Dietary fiber in clinical KDs

Fiber content in KDs differentially impacted seizure outcomes and gut microbiome composition in mice

75

Frontiers in Endocrinology

2024

KD and metabolic disturbances

KD disrupted glucose and lipid metabolism in mice; gut microbiota played a key role in

glucose intolerance

76

Mental Health Daily

2023

KD for ADHD treatment via gut modulation

KD showed potential in

modulating gut

microbiota, suggesting benefits

for ADHD treatment

77

Weizmann Institute

2015

Algorithm-based food prediction

Microbiome profiling

predicted individual

glycemic response to food

78

Mayo Clinic

2017

Validation of Weizmann study

Confirmed Weizmann findings in

a different population

79

Rothschild et al.

2018

Microbiome heritability study

Only 1.9% of microbiome

variation is genetic; >20%

from diet/lifestyle

80

Prebiotic Food Study

2019

Inulin and oligosaccharides

↑ Bifidobacteria and butyrate-producing bacteria

81

Western Diet Study

2015

Diet influence vs. BMI

Western diet ↓ diversity: ↑ Firmicutes, ↓ Bacteroidetes

82

Review Article

2022

Diet types vs. microbiome

High-fiber, vegetable-rich diets ↑ promote microbiome diversity

83

 

Diabetes, Chronic Hyperglycemia, and the Therapeutic Role of the Ketogenic Diet

The ketogenic diet (KD), which is very low in carbohydrates and high in fat, has been shown to significantly impact diabetes and its complications by improving blood sugar and reducing chronic hyperglycemia— including chronic hyperglycemia caused by insulin treatment of the diabetes mentioned in the CDC’s new report. By reducing carbohydrate intake, KD decreases blood glucose and maintains insulin sensitivity, achieving a significant reduction in the level of glycated hemoglobin (HbA1c), which measures long-term glucose control effects and predicts microvascular and macrovascular complications associated with diabetes, including retinopathy, nephropathy, neuropathy, and cardiovascular disease[83]. Clinical studies and meta-analyses reliably demonstrate that individuals with T2D adhering to a ketogenic diet often experience greater reductions in HbA1c compared to those following alternative dietary approaches to managing this condition, resulting in a decreased chronic hyperglycemia-driven tissue damage. Additionally, KD-associated positive changes in the lipid profile—namely lowering triglycerides and raising HDL cholesterol—may lower the high risk of cardiovascular factors in the diabetic population[84]. The health of our gut microbiota—especially the presence of beneficial bacteria like bifidobacteria and butyrate-producing species—is crucial for both local immune defenses and systemic anti-inflammatory responses, which play a significant role in maintaining metabolic balance. While the exact effects of the ketogenic diet on fostering a gut environment that supports these bacteria are still being studied, it is clear that maintaining or boosting their levels helps preserve the integrity of the gut barrier and reduce systemic inflammation. Both of these factors are strongly linked to the progression and complications of diabetes[84]. Thus, the ketogenic diet may influence diabetes management in two key ways: first, by directly lowering or stabilizing blood glucose levels, which improves chronic hyperglycemia as reflected by better HbA1c values; and second, by reshaping the gut microbial community to indirectly promote metabolic health, potentially lowering the risk of metabolic diseases and diabetes-related complications. This comprehensive perspective highlights the ketogenic diet not only as a method to control blood sugar but also as a strategy that involves metabolic and microbiome-related mechanisms working together to reduce the burden of diabetes.

 

Table 4. Summary of Key Findings on Ketogenic Diets for Metabolic and Cardiovascular Health in Type 2 Diabetes"

Study (Author, Year)

Population

Type of Diet

Duration

Key Outcomes

Results

Reference

Sidharthan, 2025

T2D patients

KD

Not specified

Metabolic health

Improved glycemic control, lipid profiles, and insulin sensitivity

85

Pellegrini & Rastrelli, 2024

Obese T2D patients

VLCKD

Review

Weight, HbA1c, lipids

Positive effects on blood glucose, body weight, HbA1c, and lipid profiles

86

Ghasemi et al., 2024

T2D patients

VLCKD

Meta-analysis

Cardiovascular risk factors

Improved HDL cholesterol and reduced triglycerides; no significant changes in glycemic control or weight

87

Luong et al., 2024

Obese individuals

KD

3 weeks

Insulin sensitivity

Increased skeletal muscle insulin sensitivity

88

Gower et al., 2023

T2D patients

Low-carb diet

12 weeks

Beta-cell function

Improved insulin secretion and beta-cell responses; potential for medication reduction

89

Li et al., 2023

Newly diagnosed obese T2D patients

2-meals-a-day KD

2 months

Weight, glucose, lipids

Significant improvements in weight, blood glucose, and lipid control compared to conventional diet

90

Zaman et al., 2023

T2D patients

KD & LCD

Review

Glycemic control, weight

Both diets effective; KD showed greater improvements in glycemic control and weight loss

91

Muecke, 2023

T2D patients with macular edema

KD

9 months

Vision, insulin use

Reversal of diabetes-related blindness; discontinued insulin use

92

Feinman et al., 2023

T2D patients

KD

Meta-analysis

Glycemic control, weight

No significant difference in glycemic control or weight loss compared to control diets; improved lipid profiles

93

Westman et al., 2008

T2D patients (n=49)

LCKD vs. LGID

Randomized trial

HbA1c, medications, weight

Greater improvements in HbA1c and medication reduction in LCKD group

94

 

Ketogenic Diet: Effective Fat Burning and Metabolic Health Enhancement

Widespread interest in the ketogenic diet (KD), which is high fat, very low carbohydrate, has arisen since it is known to be a powerful intervention for the treatment of obesity. In essence, the keto diet changes your metabolic state, so instead of relying on the glucose from carbohydrates as your primary fuel, you burn fat. The change encourages fat breakdown and lowers insulin, the hormone involved in fat storage[96]. In various settings, including adults with obesity, metabolic abnormalities (e.g., type 2 diabetes), and women with polycystic ovary syndrome (PCOS), numerous clinical studies have shown that it induces significant reductions in body weight, body mass index (BMI), and fat mass. Preliminary data from short (weeks) to much longer (months) trial periods show losses of 5% to >20% of initial body weight[97]. It also has been proven to preserve muscle mass compared to other low-fat diets which is quite essential to keep up the metabolic rate when losing weight, A decrease in calorie consumption and better compliance may be related to the appetite-suppressing effects of the ketogenic diet, probably related to increased protein consumption coupled with the preferential provision of ketone bodies. Long-term studies showing sustained weight loss and benefits on metabolic factors with minimal adverse effects of a ketogenic diet are available, but longer-term studies are needed. In conclusion, the ketogenic diet is a highly effective weight-loss approach with an exceptional capacity to induce fat burning and suppress appetite whilst enhancing metabolic health, particularly where low-carbohydrate approaches are not practical alone[98].

 

Table 5. Summary of Recent and Key Studies on the Effects of Ketogenic and Related Diets on Weight Loss and Metabolic Health

Sr No.

Author(s) (Year)

Diet Type

Duration

Subjects/

Participants

Study Focus

Key Findings

Reference

1

Luong et al. (2024)

Ketogenic Diet (KD)

3 weeks

Not specified

Skeletal muscle insulin sensitivity in obesity

KD increased insulin-stimulated glucose disposal in skeletal muscle without affecting liver glucose production.

99

2

Xing et al. (2024)

Ketogenic Diet (KD)

12 weeks

Obese/overweight women with PCOS

Effects on PCOS metabolic parameters

Significant reductions in weight (−9.13 kg), BMI (−2.93), waist circumference (−7.62 cm), fat mass (−5.32 kg).

100

3

Pellegrini & Rastrelli (2024)

Very-Low-Calorie Ketogenic Diet (VLCKD)

8 weeks

Not specified

Obesity and type 2 diabetes

VLCKD improved blood glucose, weight, HbA1c, neurological disorders, plasma lipids.

101

4

Heo & Yang (2023)

Ketogenic Diet (KD)

6 weeks (mouse)

Mouse model of diet-induced obesity

Effects on weight gain, insulin sensitivity, microbiota

KD reduced body weight gain, altered insulin sensitivity, and gut microbiota.

102

4

Buren et al.(2024)

Ketogenic Low-Carbohydrate High-Fat (LCHF)

4 weeks

17 healthy, young, normal-weight women

.Impact of ketogenic LCHF diet on body composition

Significant reduction in lean mass (−1.45 kg) and fat mass (−0.66 kg); lean mass loss was greater; strength training recommended to counteract muscle loss

103

6

Zoccali et al. (2023)

Ketogenic Diet (KD)

12 weeks

Obese stage G1-3a CKD patients

Weight loss and metabolic parameters

Study ongoing comparing KD with low-energy diet on weight loss and metabolic parameters.

104

7

Najafabadi et al. (2023)

Portfolio Low-Carb Diet vs KD

24 weeks

Overweight/obese women with PCOS

PCOS management

Protocol to compare effects of portfolio low-carb and KD on PCOS management.

105

8

Patikorn et al. (2023)

Ketogenic Diet (umbrella review)

Various

Various

Meta-analyses of KD benefits

KD shows benefits in weight loss and metabolic health improvements.

106

9

Bueno et al. (2013)

Very-Low-Carb Ketogenic Diet (VLCKD) vs Low-Fat Diet

6 months

Not specified

Comparison of KD with other diets

KD showed superior effectiveness in reducing weight, BMI, waist circumference.

107

10

Kowis et al. (2021)

Ketogenic diet

6–7 months

3 obese participants

Obesity with binge eating and food addiction

Reduced binge episodes, food addiction, 10–24% BW loss maintained

108

11

Barrea l et al. (2021)

VLCKD

Various

Various obese subjects

Obesity treatment

Very effective for obesity treatment

109

12

Kong z et al.  (2020)

Ketogenic diet

4 weeks

20 obese females

Effects on weight and metabolic markers

Decreased weight, BMI, waist/hip circumference, fat %, fasting leptin

110

13

Ashtary-Larky D et al

Review/Hypothesis

N/A

N/A

Mechanism of KD in obesity

KD may prevent lipid inhibition on glycolysis, maintaining thermogenesis

111
 

KD: Impact on Cholesterol and Cardiac Risk

The ketogenic diet (KD) is a very low carbohydrate/high fat diet that can lead to complex alterations in lipid profiles and cardiovascular risk factors, with variations in the size and direction of individual responses. For example, research on the KD documents a significant reduction in triglycerides — known to be a potent risk factor for cardiovascular disease — and a rise in protective HDL cholesterol[112]. However, the impact of KD on LDL-cholesterol is more heterogeneous, with some studies reporting an increase and others reporting no effect or even a decrease. Notably, new data imply that the increase in LDL on the KD is largely from the larger, buoyant, less atherogenic LDL particles, whereas small dense LDL particles have been associated with increased cardiovascular risk. New data show that standard lipid markers, e.g., total cholesterol and LDL-C, may not adequately identify cardiovascular risk. In contrast, several more specific markers, including apolipoprotein B (ApoB), apolipoprotein A1 (ApoA1), LDL particle size, and the ApoB/ApoA1 ratio, provide superior risk prediction. The KD has also been demonstrated to decrease the small dense LDL particles and improve the ApoB/ApoA1 ratio, suggesting a reduced risk for future cardiovascular events. KD has been associated with beneficial effects on lipid profiles, reducing triglycerides and sometimes LDL while increasing HDL, and these effects have been observed in several populations, including obese and diabetic patients and in studies measuring multiple cardiovascular biomarkers. Possible mechanisms include decreased intake of carbohydrate resulting in decreased insulin secretion, increased insulin sensitivity, and changes in fat metabolism that favor fat use for energy. But this is not without its benefits: LDL goes up in some, but favoring unsaturated over saturated fat may mitigate risks[113]. The short- and medium-term studies support the cardiovascular advantages of KD, but long-term studies are needed to assess cardiovascular effects. In summary, a ketogenic diet seems to improve lipidological and cardiovascular risk profile, particularly when combined with an emphasis on higher quality fats and regular assessment of lipid subfractions and other biomarkers.

Epigenetic Impact of the Ketogenic Diet

 The ketogenic diet (KD) significantly impacts the epigenome and modulates gene expression via the generation of beta-hydroxybutyrate (BHB) during ketosis. Ketosis is when your body switches from a sugar burner to a fat burner. BHB is a ketone body that your body makes when there is insufficient glucose or sugar to produce energy. BHB not only acts as a reserve fuel but also as a signalling molecule that facilitates downstream alterations in gene expression. It is known that BHB represses histone deacetylases (HDACs), i.e. enzymes that remove acetyl groups from histones, hence reducing an open chromatin structure and the expression of genes. BHB inhibits HDACs and leads to hyperacetylation of histones and a more open chromatin structure, enabling greater access to DNA, enhancing gene expression[114].

This action has important implications in a variety of biological functions. A metabolite of BHB, for instance, was associated with anti-inflammatory effects by downregulating pro-inflammatory cytokines due to regulating gene expression. It is also critically involved in the control of metabolism, particularly through the activation of genes involved in mitochondrial function and the metabolism of fatty acids, a process vital for energy production when in ketosis. Further, BHB-mediated alterations in gene expression are believed to promote cell survival programs that allow the cell to become resistant to stress. These benefits are especially significant for the brain, as BHB has been demonstrated to increase expression of neurotrophic factors such as brain-derived neurotrophic factor (BDNF), which help to grow, maintain, and survive neurons[115,116]. Epigenetic regulation by BHB may also contribute to its therapeutic potential in neurodegenerative diseases. By generating neuroprotection via gene expression modulation, the ketogenic diet could have protective potential against disorders such as Alzheimer’s and other cognitive disorders. Moreover, mounting data show that KD-induced epigenomic effects might inhibit the growth of cancerous cells by reducing inflammation and changing cellular-building pathways. These may serve as new tactics in cancer therapies. In addition, the effect of the KD on gene expression is not restricted to the brain and metabolism but extends to cellular health and may increase longevity. The ketogenic diet upregulates genes involved in autophagy, the process of the body clearing out damaged cells and proteins, which is crucial to maintaining the body’s natural balance and preventing ageing and disease. In conclusion, the ketogenic diet, through its action at BHB, regulates the epigenome and, thereby, gene expression, suggesting a myriad of health benefits that can result from a metabolic switch, ranging from metabolic improvements to prevention of life-long chronic disease such as neoplasias and neurodegenerative diseases[117].

CONCLUSION

The ketogenic diet (KD) has been increasingly recognized as a potent, multifaceted therapeutic modality for the treatment of obesity and its related comorbidities. Studies have consistently shown that KD confers significant weight loss and improvements in insulin sensitivity and lipid profiles, all well-known factors for reducing the risk of cardiovascular disease and type 2 diabetes. Moreover, in addition to shifts in metabolism, the ketogenic diet might have a host of other favourable effects on gut microbiota composition, inflammation, and mental health to illustrate its more systemic role than expected. However, it is also a very stringent eating plan, and must be closely monitored for severe nutrient deficiencies and even organ stress. Long-term investigations are needed to determine a ketogenic diet's safety, sustainability, and long-term health implications. To sum up, in a combined metabolic, microbiome, and behavioral picture, the ketogenic diet emerges as a promising, personalized tool for not only fighting against the worldwide obesity pandemic but also improving our metabolic health

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Dr. Swati Kolhe
Corresponding author

AISSMS College Of Pharmacy, Pune, Maharashtra, India 411001

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Mayuri Sakharkar
Co-author

AISSMS College Of Pharmacy, Pune, Maharashtra, India 411001

Swati Kolhe , Mayuri Sakharkar, Unveiling the Ketogenic Diet: Its Potential in combatting Obesity and Improving Health Markers, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 5, 826-854, https://doi.org/10.5281/zenodo.20033932

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