Why keto appears to lower blood pressure for some people but not others

By Vijay Kumar MalesuReviewed by Susha Cheriyedath, M.Sc.Aug 17 2026

From weight loss and insulin sensitivity to fluid balance and inflammation, the review maps several ways ketogenic diets could reduce blood pressure while highlighting why the benefits may differ substantially between individuals.

Review: The Ketogenic Diet in the Prevention and Treatment of Hypertension (HTN). Image Credit: Natali Ximich / Shutterstock

In a recent review published in the journal Biomedicines, a group of authors critically analyzed the available evidence on the effects of the ketogenic diet (KD) on blood pressure and the mechanisms that may contribute to these effects.

Background

Hypertension (HTN) remains difficult to control despite decades of prevention efforts, partly because existing strategies may have limited acceptability and adherence and may not always fit well with clinical practice or everyday life. Between 1990 and 2019, cases nearly doubled among adults aged 30 to 79. About 1.28 billion adults are affected, and nearly 46% are unaware of their condition.

Dietary strategies remain an important component of prevention and treatment. The KD, used for more than a century for drug-resistant epilepsy, has been studied in metabolic and cardiovascular conditions. Its relationship with blood pressure is of interest because HTN is linked with obesity, insulin resistance (IR), visceral adiposity, fluid balance, and inflammation.

Further research is needed to clarify its long-term effects and the contribution of diet quality.

Blood pressure evidence

HTN is defined in the review as blood pressure at or above 130/80 mmHg. A meta-analysis of 29 clinical trials involving 2,359 patients with type 2 diabetes found that very-low-calorie ketogenic diets (VLCKDs) reduced systolic blood pressure (SBP) by 2.85 mmHg and diastolic blood pressure (DBP) by 1.40 mmHg compared with control diets. Among participants with a body mass index (BMI) above 35 kg/m², the reduction in SBP was 3.15 mmHg.

Another meta-analysis of 27 randomized controlled trials (RCTs) involving 1,278 participants found a significant reduction in DBP of 1.41 mmHg but no significant difference in SBP. It also reported reductions in body weight, glucose, insulin, and triglycerides, alongside increases in total cholesterol, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C). The review cautions that these lipid changes should be weighed against potential blood pressure benefits, particularly in people with elevated cardiovascular risk.

Evidence comparing KD with established dietary approaches is also reported. The Dietary Approaches to Stop Hypertension (DASH) diet remains a standard dietary strategy for HTN. In one RCT involving people with HTN, prediabetes, or type 2 diabetes, and overweight or obesity, a very-low-carbohydrate ketogenic diet produced a greater reduction in mean SBP than DASH (−9.77 versus −5.18 mmHg).

Glycated hemoglobin (HbA1c) and body weight also decreased more with the ketogenic intervention. However, the review emphasizes that not all analyses demonstrate significant reductions in blood pressure and that ketosis cannot always be separated from calorie restriction, weight loss, and metabolic improvements.

The review notes that DASH emphasizes vegetables, fruits, whole grains, legumes, and dairy products, and limits sodium, while KD limits carbohydrates. With DASH, 55% of energy intake comes from carbohydrates, 27% from fats, and 18% from protein, whereas in the review's illustrative comparison, KD provides 10% from carbohydrates, 70% from fats, and 20% from protein. These differences highlight the importance of diet composition when interpreting blood pressure outcomes.

The authors also note that evidence specifically examining high-quality, normocaloric ketogenic diets in people with hypertension remains limited, as much of the available research involves very-low-calorie or broadly low-carbohydrate interventions.

Potential mechanisms

Several interconnected pathways may explain the observed blood pressure effects. First, KD may promote weight loss by increasing satiety, reducing appetite, and facilitating an energy deficit. Weight control is important because excess weight and HTN are strongly associated.

The review also highlights visceral adipose tissue (VAT), which surrounds internal organs and is strongly associated with metabolic disorders and HTN. Studies cited in the review found reductions in VAT with ketogenic interventions.

Second, KD may improve IR, as lower carbohydrate intake reduces postprandial glucose and insulin responses. IR is an important factor in HTN pathophysiology and can occur even with normal body weight. Reduced hyperinsulinemia may influence vascular function and the renin–angiotensin–aldosterone system (renin-angiotensin-aldosterone system">RAAS), thereby affecting blood pressure regulation.

Third, KD influences water and electrolyte balance. Reduced carbohydrate intake decreases glycogen stores and insulin concentrations, promoting natriuresis, diuresis, and losses of water, sodium, potassium, and magnesium, particularly during early keto-adaptation.

Low plasma volume can result in a decrease in blood pressure, making it important to focus on adequate magnesium, potassium, and hydration. Finally, inflammation may affect HTN indirectly through oxidative stress, endothelial dysfunction, and sodium handling. β-hydroxybutyrate (BHB), the principal ketone body, may inhibit the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome and reduce production of inflammatory cytokines, including interleukin-1β (IL-1β) and interleukin-18 (IL-18).

Practical considerations and limitations

The review stresses that diet quality is central. A high-quality KD should emphasize natural, minimally processed foods rather than highly processed products marketed as “keto.”

Early diuresis may cause dehydration and electrolyte losses, while inadequate fluid intake may adversely affect vascular function and blood pressure. Keto-adaptation may also produce transient symptoms such as headache, fatigue, and lethargy, and, in some individuals, a temporary increase in blood pressure.

In people receiving antihypertensive medication, especially diuretics or angiotensin-converting enzyme (ACE) inhibitors, rapid blood pressure reductions and increased diuresis may require close monitoring and timely medication adjustment. Increasing potassium intake is not appropriate for everyone, particularly people with chronic kidney disease or those taking medications that increase hyperkalemia risk, and should be individualized where necessary.

The review itself is narrative rather than systematic and therefore lacks a predefined study-selection protocol, formal quality assessment, and systematic evidence synthesis, which may increase the risk of selection bias.

Studies are heterogeneous in KD formulation, participant characteristics, and follow-up duration; many have small samples and short intervention periods, and blood pressure was often not the primary endpoint.

Long-term evidence on KD and blood pressure remains limited, while randomized evidence on cardiovascular events, cardiovascular mortality, all-cause mortality, and adherence remains limited across virtually all dietary models, including KD.

Conclusions

The review concludes that the KD may reduce blood pressure through interconnected effects on body weight, visceral adipose tissue, insulin resistance, water and electrolyte balance, and inflammation.

Meta-analyses, systematic reviews, and RCTs reviewed indicate blood pressure reductions, although these are not always statistically significant and do not consistently exceed those achieved with comparator diets.

Diet quality, adequate potassium and magnesium, hydration, and adaptation are important. Patients taking antihypertensive medications may require closer monitoring because blood pressure can decrease during dietary intervention.

The review emphasizes that evidence is heterogeneous, often short-term, and limited for long-term cardiovascular outcomes.