Studies Raise Questions About Keto’s Impact on Liver and Heart Health
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STORY AT-A-GLANCE
While short-term ketogenic diets may aid weight loss, new research links prolonged ketosis to liver stress, impaired insulin secretion, and cardiovascular problems
Long-term fat reliance increases circulating free fatty acids, burdening the liver, disrupting glucose regulation, and weakening metabolic flexibility — key factors in overall energy stability and heart health
Elevated liver enzymes and triglyceride levels on keto indicate hepatic overload. This signals that the body is struggling to manage excess fat turnover and oxidation
Treat keto as a short-term metabolic intervention, not a lifestyle diet. Gradually reintroduce whole-food carbohydrates to support steady energy, hormonal balance, and overall metabolic health
To support balanced metabolism and long-term liver and heart health, keep total fat below 30% of daily calories, eliminate seed oils from your diet, and consume sufficient dietary fiber
For several years, I recommended the ketogenic diet as a way to optimize your metabolic and mitochondrial health. Restricting carbohydrates and shifting the body to rely on fat for fuel seemed, at the time, to be a sound strategy for stabilizing blood sugar and enhancing endurance. Backed by a growing body of published research, it appeared to offer a logical and effective route toward better energy regulation and improved metabolic flexibility.
However, after studying the work of the late Ray Peat, Ph.D., my perspective shifted. His insights into the bioenergetic theory of health revealed how carbohydrate availability is tied to your body’s capacity to sustain healthy energy production. The more I examined his work, the clearer it became that long-term carbohydrate restriction could work against many of the very systems it was meant to support.
Your liver and heart appear to be especially vulnerable under the metabolic strain of a high-fat, low-carb diet. That vulnerability has come under closer scrutiny in a recent Science Advances study1 that examined how prolonged adherence to a ketogenic diet affects metabolic balance, insulin regulation, and organ function. Their findings raise important questions about whether keto side effects outweigh its benefits.
Does Keto Raise Liver Enzymes or Cause Fatty Liver?
In the featured study, researchers examined the long-term keto liver effects in mice for nearly a year. The goal was to determine whether a ketogenic diet, often promoted for weight management and metabolic improvement, might instead strain the liver’s ability to process and regulate fat over time and compromise overall metabolic health.2
Liver distress emerged despite lower body weight — The study found that even though mice on the ketogenic diet gained less weight than those fed a high-fat, high-carb diet, their liver profiles revealed signs of distress. Plasma triglycerides and non-esterified fats (free fatty acids released from stored fat) were significantly elevated, pointing to hyperlipidemia, a state of excess circulating fat in the bloodstream.
<label class="hide-text" contenteditable="false">Text within this block will maintain its original spacing when published</label>Male mice also developed hepatic steatosis (fat accumulation in the liver), along with increased alanine aminotransferase (ALT) activity. ALT is an enzyme concentrated inside liver cells and plays a role in amino acid metabolism. When liver cells are damaged or die, ALT leaks into the bloodstream, raising measurable levels. Elevated ALT directly reflects hepatocellular injury and indicates that the liver is under metabolic or inflammatory stress.
Broader metabolic stress accompanied liver injury — Mice on the ketogenic diet developed glucose intolerance, meaning their bodies were less able to keep blood sugar stable after eating, and impaired insulin secretion, showing that the pancreas was not releasing enough insulin to regulate glucose. Together, these findings indicate that liver stress was part of a whole-body imbalance.
<label class="hide-text" contenteditable="false">Text within this block will maintain its original spacing when published</label>In particular, the pancreatic β cells (the cells that make and release insulin) showed disruptions in protein trafficking within the endoplasmic reticulum and Golgi apparatus, which fold and package proteins for secretion. This dysfunction resembled what is seen in early diabetes, where the machinery for insulin release becomes compromised.
Microscopic evidence confirmed cellular damage — Electron microscopy revealed lipotoxic injury in the liver cells. The Golgi apparatus appeared dilated and fragmented, and genes linked to protein stress responses were upregulated. This pattern shows that long-term exposure to high lipid levels not only drives fat buildup but also interferes with protein processing and communication within cells, further aggravating liver dysfunction.
Animal findings suggest parallels to human liver responses — Although this work was conducted in mice, the core mechanisms involved in fat regulation, glucose control, and protein processing are highly conserved across species. The authors wrote that their findings “have relevant translational ramifications” and “caution against the systematic use of a KD as a health-promoting dietary intervention.” The table below summarizes the animal findings alongside their human relevance:
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