A new study shows that a ketogenic diet may be an effective way to prevent colorectal cancer. The diet triggers the liver to make a natural molecule called b-hydroxybutyrate (BHB), significantly slowing mouse cancer growth. It also causes cancer cells to be less resistant to chemotherapeutic drugs and radiotherapy.
Ketones Suppress Tumor Growth
When there isn’t enough glucose (sugar) for energy, your body breaks down fats into a chemical called ketones. You can check the level of these in your blood with a test kit. Ketones Pruvit may also be helpful for people who have cancer because they might help suppress tumor growth. This might be because cancer cells often grow because of oxidative stress or an imbalance between free radicals and antioxidants. Caloric restriction and a ketogenic diet limit blood glucose availability for glucose-dependent cancer cells and increase circulating ketone bodies in the blood and urine. These changes have anticancer effects in various animal models and human studies. They inhibit insulin/IGF signaling pathways and activate AMPK to suppress aerobic glycolysis, tumor proliferation, and migration. They also reduce lipid levels in the plasma and tumor microenvironment. These dietary manipulations have been shown to limit tumor progression in various cancer types, including glioblastoma, pancreatic cancer, and breast cancer.
It Suppresses Tumor Replication
Ketones, produced by the liver when there is not enough sugar to burn, have been shown to inhibit tumor replication. This is because ketone bodies act as a signaling compound that jump-starts a pathway in epithelial cells, which line the colon, instructing them to stop dividing. Another crucial role of ketones is that they activate a specialized enzyme called SCOT, which transfers the CoA of succinyl-CoA to acetoacetate to form acetyl-CoA, a vital fuel for mitochondrial ATP production. Without the SCOT enzyme, cancer cells cannot use fatty acids for the citrate condensation reaction of the Krebs cycle. The metabolites that accumulate after treatment of cancer cells with ketone bodies are known growth inhibitors such as proline and lysine, as well as TCA metabolites that inhibit glycolysis and promote apoptosis. However, the exact mechanism of ketone body treatment that suppresses cancer cell proliferation is not fully understood.
It Suppresses Tumor Migration
Ketones are a byproduct of your body’s natural process of using fat for energy. When your body doesn’t have enough carbs to fuel the cells, it breaks down fat for energy. These fatty acids are then converted into molecules called ketones, which serve as an emergency fuel. These ketone bodies are important in many conditions, such as diabetic ketoacidosis (DKA), where blood sugar levels can get dangerously high, and the body can’t use insulin to regulate glucose. Glucose is the primary energy source for most cancer cells, and they rely heavily on glycolysis to synthesize glucose for cellular growth and survival. However, a higher rate of aerobic glycolysis is detrimental to cancer cell survival because it increases the conversion of pyruvate to lactate, resulting in acidosis and acidic microenvironments in tumors that encourage metastasis and cancer invasion. Treatment with ketone bodies inhibits glucose uptake and reduces lactate release from cancer cells. The resulting metabolic alterations are thought to decrease cancer cell proliferation, stimulate apoptosis, and suppress c-Myc expression.
It Suppresses Tumor Invasion
Ketones are an acid the body produces when glucose (the sugar from carbohydrates) cannot be used for energy. The amount of ketones in your blood depends on various factors, including the type of diet you’re eating, your insulin levels, and underlying health conditions. Cancer cells can’t efficiently use ketone bodies for energy, unlike healthy tissues. Instead, they convert them to acetone and acetoacetate (AcAc) before they’re oxidized to b-hydroxybutyrate (b-HB) by the enzyme b-hydroxybutyrate dehydrogenase (BDH1). The study showed that dietary ketones triggered a starvation response in colorectal cancer cells. This led to a decrease in new epithelial cells lining the colon. This slowdown, which inhibited tumor growth, was caused by BHB jump-starting a signaling pathway that instructed the cells to stop dividing.
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