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Comparing Ketogenic, Carnivore, and Carbohydrate-Based Approaches for Personalized Nutrition and Disease Prevention

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dr. Karunia Valeriani Japar

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Introduction

Dietary patterns shape the foundation of human metabolic health, orchestrating the efficiency with which our bodies utilize energy, regulate glucose, and maintain cardiometabolic balance. Across populations, the way individuals combine proteins, fats, and carbohydrates on their plates exerts a direct and lasting influence on risk for obesity, type 2 diabetes, and cardiovascular disease. While traditional dietary recommendations have long emphasized the benefits of balance, whole-food patterns, a growing body of research now highlights how certain macronutrients arrangements, particularly the proportion of carbohydrate can recalibrate fundamental pathways of metabolism and disease resilience.

The scientific interest in dietary composition is not recent phenomenon. Low-carbohydrate approaches have roots stretching back more than a century, originating as clinical tools for diabetes before insulin therapy and as a therapeutic cornerstone for drug-resistant epilepsy. Over the past several decades, rigorous studies have explored the metabolic advantages of ketogenic and carnivore diets, revealing improvements in glycemic control, lipid profiles and weight management especially for individuals navigating metabolic syndrome and related disorders. Today, the resurgence of low-carbohydrate patterns marks a critical shift in nutritional research, focusing attention on how various dietary structures can selectively activate glycolysis, fatty acid oxidation, and ketogenesis. These evolving insights continue to challenge and refine clinical practices in metabolic disease prevention and inspire ongoing debate about the long-term health impact and practical application of these dietary strategies.

Dietary Patterns and Their Compositional Differences

Dietary patterns are formalized approaches to food selection and macronutrient distribution, and they serve as the blueprint for how energy and nutrients are delivered to the body. In recent years, much scientific focus has been directed at understanding the metabolic consequences of distinct dietary paradigms, namely the ketogenic diet, carnivore diet, and carbohydrate-based or high-carbohydrate diets, each differing markedly in both philosophy and physiological effects [1,2,3].

The ketogenic diet is defined by its high-fat, moderate-protein, and very low carbohydrate macronutrient composition, typically allocating about 70-80% of daily calories from fat, 10-20% from protein, and only 5-10% from carbohydrates, often restricted to less than 50 grams per day. This composition aims to induce nutritional ketosis, a metabolic state in which the liver converts fatty acids into ketone bodies as primary substrates for cellular energy, replacing glucose as the dominant fuel source. Variants of the ketogenic diet, such as the classic long-chain triglyceride (LCT) and medium-chain triglyceride (MCT) ketogenic diets, modified Atkins diet (MAD), and targeted/cyclical ketogenic diets, customize macronutrient ratios and food selections for clinical applicability and individual tolerance [1,3,4,5].

The carnivore diet represents a more restrictive, animal-derived approach, often considered an extreme form of low-carbohydrate eating where all plant foods are excluded. By design, the diet consists almost exclusively of meats, fish, eggs, and some dairy, resulting in a macronutrient profile that is inherently zero-carbohydrate, with fat and protein amounts unconstrained except by the composition of consumed animal products. Unlike the ketogenic diet, which still allows small amounts of plant-based foods and carbohydrate, the carnivore diet is truly “zero-carb,” essentially guaranteeing continuous ketosis in susceptible individuals [2,6].

Carbohydrate-based diets, often described as “high-carb” or “standard western” diets, emphasize grains, fruits, vegetables, and other starch-rich foods. Macronutrient distributions in these patterns typically range from 50-60% of daily calories from carbohydrates, 15-20% from protein, and 20-30% from fat. This composition provides an abundance of glucose for energy metabolism and supports glycogen storage, insulin activity, and a variety of anabolic processes. Subtypes of carbohydrate-centric diets, such as whole food plant based, Mediterranean, and DASH diets, may further stipulate sources and quality of carbohydrates and fats for clinical preventive goals. The quantitative differences in macronutrient composition and food sources among ketogenic, carnivore, and carbohydrate-based diets underlie their divergent metabolic effects, spanning blood glucose regulation, ketone production, lipid metabolism, satiety and energy balance. Understanding these compositional architectures is fundamental for the rational evaluation of both the mechanistic and therapeutic impacts of dietary patterns on metabolic health [7,8].

The quantitative differences in macronutrient composition and food sources among ketogenic, carnivore, and carbohydrate-based diets underlie their divergent metabolic effects, spanning blood glucose regulation, ketone production, lipid metabolism, satiety, and energy balance. Understanding these compositional architectures is fundamental for rational evaluation of both the mechanistic and therapeutic impacts of dietary patterns on metabolic health [1,2,3,7,8]

Mechanisms of Metabolic Influence

Glucose Metabolism vs Ketone Metabolism: Biochemical Pathways

Glucose and ketone bodies represent two fundamentally different fuel sources whose utilization is governed by distinct biochemical pathways and regulatory mechanism begins with cellular uptake via facilitated diffusion through glucose transporter proteins, followed by phosphorylation to glucose-6-phosphate by hexokinase or glucokinase, effectively trapping glucose within the cell. This phosphorylated intermediate serves as the entry point of glycolysis, cytosolic pathway comprising ten enzymatic reactions that convert one molecule of glucose into two molecules of pyruvate, yielding a net gain of two ATP molecules and two NADH molecules. Under aerobic conditions, pyruvate enters the mitochondrial matrix, where it is oxidatively decarboxylated by the pyruvate dehydrogenase complex to form acetyl-CoA, which subsequently enter the tricarboxylic acid cycle, generating additional reducing equivalents and ultimately producing approximately 30-32 ATP molecules per glucose molecule through oxidative phosphorylation [9,10].

In contrast, ketone metabolism is activated when glucose availability is limited and insulin levels are low, typically during prolonged fasting, carbohydrate restriction, or metabolic disease states. Ketogenesis occurs primarily in hepatic mitochondria and begins with the mobilization of fatty acids from adipose tissue via hormone-sensitive lipase, a process stimulated by glucagon and inhibited by insulin. Fatty acids are transported into hepatocyte mitochondria via the carnitine palmitoyltransferase system and undergo beta-oxidation to generate acetyl-CoA. When acetyl-CoA production exceeds the oxidative capacity of tricarboxylic acid cycle, often due to limited oxaloacetate availability, acetyl-CoA molecules condense to form acetoacetyl-CoA via thiolase, which is subsequently converted to beta-hydroxy-beta-methylglytaryl-CoA by HMG-CoA synthase, the rate-limiting enzyme of ketogenesis. HMG-CoA lyase then cleaves this intermediate to yield acetoacetate, the primary ketone body, which can be reduced to beta-hydroxybutyrate or spontaneously decarboxylated to acetone. In peripheral tissues, beta-hydroxybutyrate is reconverted to acetoacetate, which is activated to acetoacetyl-CoA by succinyl-CoA transferase, ultimately generating acetyl-CoA for oxidation in the tricarboxylic acid cycle and ATP production [11,12,13].

Figure 1. Regulation of Hepatic Gluconeogensis [13]

Lipid Oxidation, Glycolysis and Ketogenesis: Core Mechanisms

The interplay among lipid oxidation, glycolysis, and ketogenesis defines the metabolic flexibility of and organism and its capacity to switch fuel sources in response to nutrient availability and energy demands. Glycolysis serves as the primary pathway for glucose catabolism, with key regulatory enzymes including glucokinase, phosphofructokinase-1, and liver-type pyruvate kinase, which are subject to allosteric regulation and transcriptional control by insulin, glucagon, and various metabolites. During fed states, insulin promotes glycolysis by activating phosphofructokinase-1 and pyruvate kinase while simultaneously inhibiting gluconeogenesis, thereby directing glucose toward energy production and anabolic processes [10,14].

Lipid oxidation, particularly beta-oxidation of fatty acids, becomes the predominant energy source during fasting or carbohydrate restriction. Fatty acids undergo sequential removal of two-carbon units as acetyl-CoA, generating NADH and FADH2, which feed into the electron transport chain to produce ATP. The transcription factor peroxisome proliferator-activated receptor alpha plays a central role in upregulating genes involved in fatty acid uptake, mitochondrial and peroxisomal beta-oxidation, as the abundance of acetyl-CoA derived from beta-oxidation drives the condensation reactions that form ketone bodies [12,15].

The reciprocal regulation of glycolysis and lipid oxidation is mediated by the glucose-fatty acid cycle, whereby elevated fatty acid oxidation increases acetyl-CoA and citrate levels, which inhibit phosphofructokinase-1 and pyruvate dehydrogenase, thereby suppressing glycolysis and glucose oxidation. Conversely, high glucose and insulin levels stimulate acetyl-CoA carboxylase, producing malonyl-CoA, which inhibits carnitine palmitoyltransferase-1 and prevents fatty acid entry into mitochondria, favouring glucose utilization over fat oxidation. This dynamic interplay ensures efficient energy production while preventing futile cycling of metabolic intermediates [13,14].

The Role of Protein and Amino Acid Metabolism

Protein and amino acid metabolism occupy a critical position in whole-body energy homeostasis, nitrogen balance, and the provision of gluconeogenic and ketogenic substrates during metabolic stress. Amino acids derived from dietary protein or endogenous protein turnover undergo deamination or transamination reactions to liberate their alpha-amino groups, which are subsequently converted to urea via the hepatic urea cycle for excretion. The remaining carbon skeletons are classified as either glucogenic or ketogenic based on their metabolic fates. Glucogenic amino acids, including alanine, glutamine, serine, and glycine, are converted to pyruvate or tricarboxylic acid cycle intermediates such oxaloacetate and alpha-ketoglutarate, serving as substrates for hepatic and renal gluconeogenesis during fasting or carbohydrate restriction. The alanine cycle exemplifies this process, wherein skeletal muscle exports alanine to the liver, where it is transaminated back to pyruvate for glucose synthesis, effectively transferring amino groups and carbon skeletons between tissues [15,16,17,18,19,20,21].

Figure 2. Amino Acid Catabolism in The Liver [16]

Ketogenic amino acids, such as leucine and lysine, are catabolized to acetyl-CoA or acetyl-CoA, which cannot yield net glucose production but instead contribute to ketone body synthesis or direct oxidation for ATP generation. Certain amino acids, including isoleucine, phenylalanine, and tyrosine, are both glucogenic and ketogenic, reflecting the complexity of amino acid catabolism and its integration with broader metabolic network. The regulation of amino acid, degrading enzymes is highly responsive to dietary protein intake, with high protein diets including hepatic expression of catabolic enzymes to accommodate excess amino acid flux.

Protein turnover in skeletal muscle is governed by the balance between synthesis and degradation pathways, with the mechanistic target of rapamycin complex 1 serving as a central regulator of protein synthesis in response to amino acid availability, particularly branched-chain amino acids such as leucine. During fasting , starvation , or metabolic stress, muscle protein breakdown accelerates via the ubiquitin, proteasome system and autophagy-lysosomal pathways, releasing amino acids for hepatic gluconeogenesis and peripheral tissue oxidation. This catabolic response is mediated by hormonal signals, including elevated glucagon and cortisol along with reduced insulin and insulin like metabolism, with the intestine and liver serving as primary sites for amino acid catabolism and the gut microbiota contributing to amino acid fermentation and metabolite generation. Overall, protein and amino acid metabolism provide essential substrates for gluconeogenesis and ketogenesis while maintaining nitrogen homeostasis and supporting tissue-specific metabolic demands across diverse nutritional and physiological states.

Comparative Effects on Metabolic Health

Energy Utilization, Fuel Selection, and Metabolic Flexibility

The capacity to efficiently switch between glucose and fatty acid oxidation termed metabolic flexibility is a hall mark of metabolic health and is differentially influenced by ketogenic, carnivore, and carbohydrate based dietary patterns. Low-carbohydrate ketogenic diets fundamentally alter substrate metabolism by reducing carbohydrate availability and lowering insulin secretion, thereby promoting lipolysis and hepatic ketogenesis. During ketogenic diet intervention, the respiratory quotient decreases significantly, reflecting a shift from predominantly carbohydrate oxidation to fatty acid and ketone body oxidation as the primary fuel sources. This metabolic reprogramming is accompanied diets can increase daily energy expenditure by approximately 200-280 kilocalories compared to isocaloric high-carbohydrate diets, particularly in individuals with high-pre-weight-loss insulin secretion [22,23,24,25,26,27].

The carnivore diet, being inherently zero-carbohydrate, maintains continuous ketosis and maximal fatty acid oxidation, effectively eliminating metabolic reliance on exogenous glucose. However, this extreme restriction may paradoxically reduce true metabolic flexibility by limiting the body’s capacity to efficiently utilize glucose when reintroduced, a phenomenon distinct from the adaptive metabolic inflexibility observed in insulin resistance. In contrast, carbohydrate-based diets maintain reliance on glycolytic pathways and insulin dependent glucose uptake, which can support metabolic flexibility in insulin-sensitive individuals but may contribute to metabolic inflexibility in those with insulin resistance, obesity, or type 2 diabetes, where impaired substrate switching between fed and fasted states is characteristic [23,27].

Recent evidence suggests that cyclical or targeted ketogenic approaches, which strategically incorporate carbohydrate intake around periods of high energy demand, may optimize metabolic flexibility by preserving both glucose oxidation capacity and fat oxidation efficiency. Studies employing hyperinsulinemic-euglycemic clamp methodologies have demonstrated that short-term ketogenic diets can increase skeletal muscle insulin sensitivity and insulin-stimulated glucose disposal even in individuals with obesity, through this occurs without improving overall metabolic flexibility as assessed by respiratory exchange ratio dynamics during insulin infusion [25,26].

Body Weight Regulation and Adiposity

Ketogenic and low-carbohydrate diets have consistently demonstrated superior short- to moderate-term efficacy for body weight reduction compared to low-fat or higher-carbohydrate dietary interventions. Meta-analyses reveal that low-carbohydrate diets achieve approximately 2.0-2.8 kilograms greater weight loss than low-fat diets at 6-month follow up, with dose-response analyses indicating that each 10% decrease in carbohydrate intake produces approximately 0.64 kilograms of additional weight loss. This weight-reducing effect is sustained at 12 months, where low-carbohydrate interventions yield approximately 1.15 kilograms greater reduction, though differences attenuate beyond 12-18 months as dietary adherence wanes [28,29,30,31,32,33,34,35].

The mechanisms underlying enhanced weight loss on ketogenic diets are multifactorial and include appetite suppression. Mediated by ketone bodies, particularly beta-hydroxybutyrate, which prevents compensatory increases in ghrelin during caloric restriction. Very low calorie ketogenic diets produce substantial reductions in fat mass, visceral adipose tissue, and waist circumference while preserving lean body mass, particularly when protein intake is adequate. In one controlled study, participants following a very low calorie ketogenic diet lost approximately 17 kilogram of fat mass over 4 months with minimal reduction in fat-free mass, which was transiently decreased during maximum ketosis due to water loss and subsequently recovered [7,28,31].

Carnivore diet adherents report significant body weight reductions in observational surveys, with one study documenting a mean weight loss of 4 kilograms over 3 weeks, alongside reduction in body fat percentage and visceral fat. However, the long-term sustainability and safety of carnivore diets remain poorly characterized, and concerns regarding nutrient adequacy and cardiovascular risk necessitate further rigorous investigation. Carbohydrate-based diets, particularly plant based-approaches, can also achieve meaningful fat mass reduction, with studies showing that vegan diets produce approximately 4.3 kilograms of fat mass loss over 16 weeks, associated with increased plant protein and decreased animal protein intake, as well as reduced consumption of branched-chain amino acids such as leucine [36,37].

Glycemic Control and Insulin Sensitivity

Low carbohydrate and ketogenic diets exert profound effects on glycemic regulation and insulin sensitivity, particularly in individuals with prediabetes, metabolic syndrome, and type 2 diabetes. Meta-analyses demonstrate that ketogenic diets reduce fasting blood glucose by approximately 1.29 milimoles per liter and glycated hemoglobin by 1.07%, alongside reductions in body weight averaging 8.66 kilograms. Similarly, low carbohydrate diet interventions in individuals with elevated hemoglobin A1c produce net reductions of 0.23-0.36% compared to usual or high-carbohydrate diets at 6-month follow-up, accompanied by decreased fasting insulin, HOMA-IR, and 24-hour mean glucose as assessed by continuous glucose monitoring [23,26,38,39,40,41].

The improvement in glycemic control is mediated by reduced intestinal glucose absorption, lower postprandial glycemic excursions, decreased insulin secretion and enhanced insulin sensitivity, particularly in skeletal muscle. A randomized crossover trial employing hyperinsulinemic euglycemic clamp methodology demonstrated that a 3-week ketogenic diet increased insulin stimulated glucose disposal by approximately 30% in individuals with obesity,  reflecting improved skeletal muscle insulin sensitivity. However, this improvement occurred in the absece of enhanced metabolic flexibility during insulin stimulation, and the relative suppression of hepatic glucose production and lipolysis remined unchanged or slightly impaired [23,26,38,42].

Importantly, the beneficial effects of ketogenic diets on glycemic control appear to be largely dependent on concomitant weight loss, as weight-maintaining ketogenic interventions have shown no improvement in glucose tolerance, insulin sensitivity, or metabolic parameters when body weight is held constant. In contrast, carbohydrate based dietary patterns, particularly those emphasizing whole grains, legumes and low-glycemic index foods, can also support glycemic control and insulin sensitivity when coupled with caloric restriction, weight loss and adequate fiber intake [25,37,43].

The carnivore diet’s impact on glycemic control remains inadequately studied, though its zero-carbohydrate composition theoretically minimizes glycemic fluctuations and insulin demand. However, the evolutionary’ “carnivore connection” hypothesis posits that prolonged consumption of very low-carbohydrate, high protein diets induces physiological insulin resistance as a metabolic adaptation to maintain glucose homeostasis for glucose-dependent tissues, particularly during reproduction and fasting. This intrinsic insulin resistance may paradoxically increase diabetes risk when population transition to high-glycemic load diets, highlighting the complex interplay between dietary macronutrient composition, insulin sensitivity, and long-term metabolic health [43,44,45].

Lipids, Cardiovascular Markers, and Inflammation

The effects of ketogenic, carnivore, and carbohydrate- based diets on lipid profiles and cardiovascular risk markers are complex, heterogeneous, and dependent on baseline metabolic status, dietary composition, and individual genetic factors. In normal-weight individuals, ketogenic diets significantly increase total cholesterol, low density lipoprotein cholesterol, and apolipoprotein B, alongside increases in high-density lipoprotein cholesterol and apolipoprotein A, while triglyceride levels show inconsistent changes. Meta-analyses report mean increases in total cholesterol of approximately 1.47 millimoles per liter and LDL cholesterol of 1.08 milimoles per liter in normal-weight adults following ketogenic diets, raising concerns about potential atherogenic risk despite compensatory HDL elevations [46,47,48].

In individuals with obesity or metabolic syndrome, ketogenic and low-carbohydrate diets tend to improve the lipid profile by significantly reducing triglycerides and increasing HDL cholesterol, with variable effects on LDL cholesterol depending on dietary fat composition, weight loss, and individual lipid metabolism phenotypes. Some individuals experience marked hypercholesterolemia on ketogenic diets, necessitating advanced lipid testing beyond standard panels to assess particle size, oxidation status and apolipoprotein ratios for accurate cardiovascular risk stratification [28,48,49].

The carnivore diet, characterize by high intake of saturated fat from red and processed meats, has been associated with elevated LL cholesterol in observational surveys thorugh participants also report favourable HDL cholesterol, reduced body mass index, and improved subjective health markers. Cardiovascular health organizations, including the Americal College of Cardiology and American Heart Association, express concern over the long-term cardiovascular implication of animal based, low carbohydrate diets due to associations between red meat consumption and increased risk of cardiovascular disease, cardiovascular mortality, and type 2 diabetes, particularly in Western populations [50,51].

Regarding inflammation, low-carbohydrate diets demonstrate beneficial effects on systemic inflammatory markers, with meta-analyses showing significant reductions in C-reactive protein and interleukin-6 compared to low-fat diets, effects that are partially mediated by weight loss. Low-carbohydrate interventions reduce C-reactive protein levels with a standardized mean difference of approximately -0,1 to -0,33, while tumor necrosis factor alpha remains unchanged. Conversely, low-fat diets also reduce C-reactive protein, particularly when coupled with weight loss, suggesting that both macronutrient restriction strategies can attenuate chronic low-grade inflammation characteristic of metabolic syndrome. Plant-based carbohydrate rich diets,w hen emphasizing anti-inflammatory nutrients such as polyphenols, omega-3-fatty acids, and dietary fiber, may confer additional cardiovascular and anti-inflammatory benefits independent of macronutrient distribution [51,52,53,54].

Therapeutic Potential and Clinical Applications

Low-Carbohydrate Diets in Metabolic Disease Prevention and Management

Low-carbohydrate diets have emerged as a viable and evidence-based therapeutic strategy for the prevention and management of metabolic disorders, particularly type 2 diabetes, obesity, and metabolic syndrome. The American Diabetes Association formally recognizes low-and very-low-carbohydrate diets as safe and effective options for adults with type 2 diabetes, emphasizing that reducing overall carbohydrate intake has the strongest evidence for improving glycemic control. Systemic reviews and meta-analyses demonstrate that low-carbohydrate dietary interventions produce short-term improvements in glycemic control, weight loss, and cardiovascular risk markers, with moderate to low certainty evidence indicating higher rates of diabetes remission at six months compared to control diets [55,56,57,58,59].

In a pooled analysis of eight randomized controlled trials, patients adhering to low-carbohydrate diets achieved diabetes remission defined as hemoglobin A1c below 6.5%, at a rate of 57% compared to 31% in control groups, yielding a risk difference of 0.32. This effect was particularly pronounced in patients not using insulin, while remission rates markedly decreased in insulin dependent individuals. At 12 months, the benefits on remission became less certain, with data ranging from small effects to trivial increased risk, highlighting challenges in long-term adherence and sustainability. Secondary outcomes reveal that low-carbohydrate diets lead to clinically important reductions in triglycerides and insulin resistance as measured by HOMA-IR, alongside greater reductions in diabetes medication requirements [55,57,58].

The physiological rationale supporting carbohydrate restriction centers on its capacity to reduce postprandial glycemic excursions, decrease insulin demand, and allow pancreatic beta-cell recovery during periods of reduced workload. By lowering carbohydrate intake, the nutrient with the greatest impact on glycemic control, patients can achieve rapid improvements in blood glucose regulation independent of weight loss, though weight reduction further amplifies metabolic benefits. However, it is important to note that low-carbohydrate diets are not inherently superior to other evidence-based dietary patterns, and long-term side effects remain incompletely characterized. Epidemiological evidence supports dietary patterns rich in vegetables, fruits, whole grains, seafood, legumes, and nuts as associated with better overall health outcomes, suggesting that low-carbohydrate approaches should be presented as one useful tool among multiple sustainable alternatives for metabolic disease management [25,56,58].

Ketogenic and Carnivore Diets in Obesity, Diabetes, and Other Disorders

Ketogenic diets demonstrate robust efficacy. In the treatment of obesity and type 2 diabetes, with evidence supporting substantial reductions in body weight, hemoglobin A1c, fasting glucose, and triglycerides. A 12-week randomized clinical trial comparing ketogenic diet to a standard diabetic diet revealed significantly greater reductions in body weight, blood glucose, blood lipids, and uric acid in the ketogenic intervention group. Meta-analyses confirm that very-low-calorie ketogenic diets effectively reduce hemoglobin A1c, total cholesterol, LDL cholesterol, and triglycerides while increasing HDL cholesterol, with several studies documenting disease remission and medication discontinuation or reduction. The therapeutic value of ketogenic diets extends beyond weight loss to include restoration of first-phase insulin secretion, decreased insulin requirements, and improved beta-cell function in individuals with type 2 diabetes [5,59,60,61].

Beyond metabolic disorders, ketogenic and carnivore diets are being explored for novel therapeutic application in inflammatory bowel disease, mental health disorders, autoimmune conditions, and neurological diseases. A case series of 10 patients with histologically confirmed ulcerative colitis or Crohn’s disease treated with ketogenic or carnivore diets reported universal clinical improvements, with IBDQ score increases ranging from 72 to 165 points. Fecal calcprotectin levels decreased dramatically, with one patient’s levels dropping from 4,291 micrograms per gram to 9 micrograms per gram, and multiple patients successfully discontinued immunosuppressive medications while remaining in remission. Patients described their carnivore diets as pleasurable, sustainable , and life-enhancing, attributing symptom resolution to the elimination of plant-based foods and adoption of animal-derived nutrition [49,62,63,64].

similarly, case reports document remission of schizophrenia and other serious mental illnesses with carnivore ketogenic dietary therapy, suggesting potential benefits for brain function and mental health symptom resolution even in difficult socioeconomic circumstances. Survey data from carnivore diet adherents indicate that over 50% initiated the diet to address allergic, skin, autoimmune, or digestive health conditions, with many reporting subjective improvements in the domains. However, the carnivore diet remains poorly studied in controlled clinical trials, and concerns regarding long-term cardiovascular risk, nutrient adequacy, and absence of dietary fiber necessitate cautious interpretation and ongoing research. The British Heart Foundation and other cardiovascular health organization express reservations about carnivore diets due to high saturated fat content and potential adverse effects on lipid profiles and cardiovascular outcomes [62,63,66].

Carbohydrate-Based Diets: Benefits, Risks, and Misconceptions

Carbohydrate-based dietary patterns, particularly those emphasizing whole grains, legumes, fruits, vegetables, and other minimally processed plant foods, confer substantial cardiometabolic benefits and are associated with reduced risks of obesity, type 2 diabetes, cardiovascular disease, and all-cause mortality. Higher consumption of whole grains is associated with lower incidence of and mortality from cardiovascular disease, type 2 diabetes, and certain cancers, effects mediated in part by beneficial impacts on the gut microbiota, insulin sensitivity, glucose metabolism, and lipid profiles. The fiber, nutrients, and phytochemicals in whole grains slow the breakdown of starch into glucose, maintain steady blood sugar levels, lower cholesterol, promote healthy digestion, and may protect against cancer through antioxidant and anti-inflammatory mechanisms [37,68,69,70].

Plant-based diets, including vegetarian and vegan patterns, demonstrate impressive cardiometabolic advantages, with meta-analyses showing that these diets reduce the risk of coronary heart disease events by an estimated 40% and cerebral vascular disease events by 29% compared to omnivorous diets. Vegetarian dietary interventions achieve significant reductions in body mass index, total cholesterol, LDL cholesterol, glucose, hemoglobin A1c, blood pressure, and inflammatory markers, with effect sizes comparable to or exceeding those of conventional therapeutic diets and, in some cases, pharmacological interventions such as statins. A randomized controlled trial comparing omnivorous and vegan diets in identical twins demonstrated that the vegan diet conferred significant protective cardiometabolic advantages, including greater reductions in LDL cholesterol, fasting insulin, and body weight [69].

Despite robust evidence supporting carbohydrate-rich, plant-based dietary patterns, several misconceptions persist, including beliefs that people with diabetes should universally adopt low-carbohydrate diets, that high-carbohydrate diets cause insulin resistance, and that carbohydrates are inherently fattening. Scientific evidence refutes these notions, demonstrating that people who consume high-carbohydrate diets tend to be slimmer and often healthier than those consuming low-carbohydrate diets, particularly when carbohydrate sources are whole, fiber-rich, and minimally processed. Even high-glycemic-index foods, when consumed within the context of an overall healthful diet, are not consistently associated with higher body weights or increased disease risk in large-scale population studies. The majority of patients with diabetes in the United States consume moderate carbohydrate intakes approximately 44-46% of total calories suggesting that neither extreme restriction nor extreme consumption is necessary or practical for most individuals [71].

The recommended dietary allowance for carbohydrate is 130 grams per day, representing the average minimum requirement based on the brain and central nervous system’s need for glucose as an energy source. Monitoring carbohydrate intake remains a key strategy in achieving glycemic control, but the quality of carbohydrate emphasizing whole grains, legumes, fruits, vegetables, and low-glycemic foods is at least as important as quantity. Current dietary guidelines appropriately emphasize that approximately 50-55% of daily calories should derive from carbohydrates, with at least half of grains consumed as whole grains to maximize nutrient density, fiber intake, and disease-protective phytochemical exposure. Properly planned carbohydrate-based diets are healthful, effective for weight and glycemic control, and provide metabolic and cardiovascular benefits that should be promoted alongside other evidence-based dietary approaches for comprehensive metabolic disease prevention and management [37,67,69,71,72].

Potential Risks, Limitations, and Safety Considerations

Dietary interventions with extreme macronutrient modifications such as ketogenic, carnivore, and strict low-carbohydrate diets require careful consideration of potential risks, limitations, and long-term safety profiles. The ketogenic diet, while producing notable short-term improvements in metabolic outcomes, can trigger metabolic derangements such as fatty liver, impaired blood sugar regulation, and cellular stress in key organs over the long term, as observed in both rodent models and growing human studies. Adverse effects include increased risk for kidney stones, dehydration, electrolyte disturbances, and hypoglycemia, as well as gastrointestinal symptoms, low blood pressure, and risk for osteoporosis. Rapid weight loss on ketogenic diets may also contribute to muscle loss, and some users experience “keto flu” symptoms during adaptation [1,7,73,74].

Micronutrient inadequacies present a significant concern with both ketogenic and carnivore patterns, particularly when dietary diversity is limited. The carnivore diet’s exclusion of plant foods can lead to deficiencies in vitamin C, fiber, magnesium, calcium, potassium, and certain B vitamins, nutrients abundant in fruits, vegetables, and whole grains but scarce in animal-derived products. Chronic lack of fiber from exclusive animal diets may impair digestive health, alter gut microbiota, and increase long-term risk for heart disease and colon cancer. Additionally, high intake of saturated fats and cholesterol, characterizing both ketogenic and carnivore diets, raises concern for cardiovascular health, although recent debates question the absolute impact and highlight genetic variability in lipid responses [7,36].

Carbohydrate-based diets, particularly those centered on refined carbohydrates and limited food diversity, also pose risks for micronutrient inadequacy, especially in resource-constrained settings. Diets dominated by cereals and lacking vegetables, dairy, and animal protein often result in insufficient intake of calcium, iron, zinc, vitamin A, thiamin, riboflavin, folate, and vitamin B12, nutrients crucial for physiological function across life stages. Effective measures to safeguard long-term health across different dietary patterns include improving dietary diversity, targeted supplementation, and careful monitoring of both macro- and micronutrient status, especially for vulnerable populations or those undertaking restrictive regimens [36,75,76,77].

Personalization and Practical Considerations

Personalized nutrition is increasingly recognized as essential in clinical practice, as genetics, gut microbiome, lifestyle, and cultural factors all influence how individuals respond to different diets. Variation in genes and microbiome composition can affect nutrient absorption, metabolic flexibility, and the success of dietary interventions, highlighting the need for individualized approaches. Patient preferences, food culture, and quality of life also strongly determine adherence, with personalized dietary guidance associated with better compliance and improved health outcomes compared to a “one-size-fits-all” approach. Addressing individual needs including metabolic, lifestyle, and psychosocial factors that is critical for optimizing the effectiveness and sustainability of any dietary strategy.

Future Directions in Research

The future of metabolic health research is increasingly shaped by advances in biomarker discovery, mechanistic studies, and digital health technologies. Multi-omics platforms including genomics, metabolomics and proteomics are revealing novel biomarkers and molecular signatures that enable early disease detection, risk stratification, and personalized dietary interventions for metabolic disorders. These tools are helping to clarify how nutritional patterns and specific nutrients modulate metabolic pathways, immune responses and disease progression, opening pathways to targeted therapies and individualized prevention strategies [78.79.80,81].

Simultaneously, the integration of AI, machine learning, and data analytics with dietary research is accelerating the era of precision nutrition. AI-driven systems now support real time dietary monitoring, prediction of individual metabolic responses, and personalized meal planning based on clinical genetic and microbiome data. This convergence of digital technologies and system biology is poised to transform clinical nutrition by enabling scalable, adaptive, and evidence based dietary guidance tailored to each person’s unique biology and lifestyle, moving beyond one size fits all recommendations [82,83,84,85].

Conclusion

In conclusion, the comparative analysis of ketogenic, carnivore, and carbohydrate-based dietary patterns underscores the profound influence of macronutrient composition on metabolic health outcomes. Evidence demonstrates that low-carbohydrate and ketogenic diets offer distinct advantages for glycemic control, weight management, and adiposity reduction, especially in populations with insulin resistance or metabolic syndrome. Nonetheless, concerns regarding long-term safety, micronutrient adequacy, and cardiovascular risk highlight the need for ongoing monitoring and individualized patient care. While carbohydrate-rich, plant-based diets remain foundationl for population cardiometabolic health, the emerging role of personalized nutrition, guided by genetic, microbiome, and lifestyle factors marks. Paradigm shift in diet prescription. Integration of biomarkers, mechanistic insights, and artificial intelligence is paving the way toward precision metabolic health, enabling more targeted evidence-based therapeutic strategies for both prevention and management of metabolic disease.

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