Raspberry ketone, a chemical compound found in red raspberries and other fruits, has gained popularity as a weight-loss supplement. While it's commonly consumed in foods, its effectiveness and safety as a weight-loss aid are subjects of ongoing debate. This article examines the evidence surrounding raspberry ketone, its potential mechanisms of action, and associated risks.
What is Raspberry Ketone?
Raspberry ketone (RK) is a natural substance that gives red raspberries their distinctive aroma. It's also present in smaller quantities in other fruits like kiwifruit, peaches, blackberries, and cranberries. Beyond its natural occurrence, raspberry ketone is used in cosmetics, soft drinks, ice cream, and other processed foods as a flavoring agent. People use raspberry ketone for obesity, hair loss, male pattern baldness, and other conditions, but there is no good scientific evidence to support these uses.
Potential Mechanisms of Action
The appeal of raspberry ketone as a weight-loss supplement stems from its structural similarity to capsaicin (found in chili peppers) and synephrine (a stimulant). Studies suggest these molecules can boost metabolism. Researchers have speculated that raspberry ketone might exert similar effects.
- Increased Fat Breakdown: Test-tube studies involving fat cells from mice suggest that raspberry ketone may increase fat breakdown by making cells more susceptible to norepinephrine, a fat-burning hormone.
- Increased Adiponectin Release: Raspberry ketone has been shown to increase the release of adiponectin, a hormone secreted by fat cells that plays a role in regulating metabolism and blood sugar levels. Higher adiponectin levels are associated with normal weight, while lower levels are linked to obesity, type 2 diabetes, fatty liver disease, and heart disease.
It is important to note that these effects have primarily been observed in isolated cells and animal studies.
Evidence from Animal Studies
Some animal studies have shown promising results regarding raspberry ketone's effects on weight and metabolic health.
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- One study involving mice fed a high-fat diet found that those receiving raspberry ketone gained less weight (10% less) than those who did not.
- Another study in rats indicated that raspberry ketone increased adiponectin levels and protected against fatty liver disease.
However, it's crucial to consider the dosages used in these studies. The dosages were significantly higher than those typically recommended for human consumption.
Lack of Human Studies
Despite the buzz surrounding raspberry ketone, there is a significant lack of human studies to support its weight-loss claims. To date, only one small clinical trial of raspberry ketone has been conducted. Its results were published in two papers and suggest that daily supplementation with raspberry ketone improved biomarkers of oxidative stress and HDL, but not total cholesterol, LDL, triglycerides, blood glucose, liver enzymes, or body weight in 20 women with obesity. However, these findings have a high risk of bias due to several important methodological limitations. These include the lack of preregistration, double-blinding (to keep investigators from knowing which treatment group the participants were randomized to), and a power calculation (to justify the small number of included participants, 20). This limits the reliability of the findings. It should also be noted that these two papers were submitted, accepted, and published on the same dates, do not have a DOI number (a digital identifier that is necessary for a journal’s database indexing), and do not report any funding sources.
One study examined a multi-ingredient supplement containing raspberry ketone along with caffeine, garlic, capsaicin, ginger, and synephrine. Participants who combined the supplement with a calorie-restricted diet and exercise lost more fat mass than those on a placebo. However, it's impossible to attribute the weight loss solely to raspberry ketone, as the other ingredients could have contributed to the effect.
Safety and Side Effects
When taken by mouth: Raspberry ketone is commonly consumed in foods. When used as medicine, there isn't enough reliable information to know if raspberry ketone is safe. It is chemically related to a stimulant called synephrine, so it's possible that it might cause jitteriness, and increase blood pressure and heart rate.
- Potential Side Effects: Due to its structural similarity to stimulants, raspberry ketone might cause side effects such as jitteriness, increased blood pressure, and a rapid heartbeat.
- Interactions: Raspberry ketone might interact with certain medications. For example, it could reduce the effects of warfarin, a blood thinner, potentially increasing the risk of blood clots. It may also interact with stimulants, leading to serious problems like increased heart rate and high blood pressure.
- Special Precautions: There isn't enough reliable information to know if raspberry ketone is safe to use as medicine when pregnant or breast-feeding. Stay on the safe side and avoid use. Raspberry ketone might affect blood sugar levels. This might make it more difficult to control blood sugar in people taking medicines for diabetes.
Case Report of Adverse Effects
A 47-year-old woman experienced a range of adverse symptoms, including diarrhea, sweating, tachycardia, and hypertension, shortly after taking raspberry ketone tablets for the first time. She subsequently developed chest pain and ECG changes indicative of intermittent acute coronary occlusion. While the patient had other comorbidities, the timing of the symptoms in relation to raspberry ketone ingestion suggested a potential link.
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Raspberry Ketone's Role in Cardiovascular Health
Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide. They mainly include atherosclerosis, hypertension, cardiac hypertrophy, myocardial infarction, and heart failure. Myocardial infarction (MI), or a heart attack, occurs due to the fact of cardiac ischemia. Occlusion of coronary arteries decreases the oxygen supply to cardiac cells, causing necrosis of the cells, leading to MI. Intracellular oxygen levels are of significant importance to the normal functioning of cardiac cells. Cardiac cell necrosis due to the reduced oxygen levels leads to deleterious effects, leading to the loss of cell membrane integrity and an uncontrolled release of intracellular content into extracellular space. The most important effect of cardiac cell necrosis is the development of cardiac arrhythmias due to the loss of functional contractile muscle mass and electrolyte imbalance caused by cell lysis. Myocardial infarction progresses into heart failure eventually, due to the overactivation of the neurohumoral system, increased inflammatory response, oxidative stress, disordered cardiac growth, fibrosis deposition, altered gene/protein synthesis, and energy starvation. The chronic dysregulation of these systems leads to heart failure causing congestion and pulmonary edema leading to incapacitation and poor outcomes. Teasing out the mechanisms leading to heart failure due to the fact of MI is an essential step in the development of new therapies. The most commonly used treatment options for CVDs are angiotensin-converting enzyme (ACE) inhibitors, triglyceride-lowering agents, anti-platelet agents, aspirin, nitroglycerine, and beta-blockers.
One group studied the effect of RK on isoproterenol (ISO) induced MI. ISO-induced MI in rodents is a well-accepted strategy to study MI as it causes severe oxidative stress in the myocardium, which is considered the main mechanism of myocardial necrosis. In Wistar rats with ISO-induced MI, they found increased oxidative stress due to the fact of ROS and also an increase in MDA levels which led to a decrease in antioxidant levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), dysregulated lipid metabolism, and inflammation due to an increase in reactive nitrogen species. The histological sections of ISO-treated rats showed extensive myocardial damage with edema, disrupted cardiac myofibrils, inflammatory cells, and necrosis of ventricular regions. The study found that treating rats with 100 mg/ka and 200 mg/kg of RK could reverse the levels of ROS enzymes, which could be attributed to an increase in PPAR-α expression. Raspberry ketone was able to normalize lipid parameters, reduce peroxynitrite levels, and normalize myocardial tissue architecture. The study speculates that these effects were mainly brought about by the ability of RK to increase the expression of PPAR-α. It is speculated that PPAR-α functions by binding to PPAR-responsive elements (PPREs), which have been identified in the promoter regions of several antioxidant, anti-inflammatory, and lipid homeostasis genes. A follow-up study by the same group demonstrated that RK has an affinity to bind PPAR-α, by docking analysis.
Raspberry Ketone's Role in Liver Health
Globally, 844 million people are considered to be affected by chronic liver disease, with a mortality rate of 2 million per year. Most liver diseases are caused due to the fact of viruses (hepatitis A, B, and C), drug or alcohol consumption (alcoholic liver disease), and metabolic liver disease (non-alcoholic fatty liver disease), leading to cirrhosis of the liver and liver failure. The pathophysiology of chronic liver disease involves hepatocyte death, resulting in inflammation and fibrosis, and studies have shown a close relation between liver diseases and metabolic diseases such as obesity, diabetes, and hyperlipidemia. Apart from a liver transplant, very few treatment options are available to effectively treat and reverse the progression of chronic liver diseases. Dietary and lifestyle changes with a combination of drug therapy are the currently available methods of managing liver diseases like NAFLD.
Raspberry ketone was initially studied for its role as a weight-reducing agent, but recently, more interest has been generated in studying its function in treating other diseases as well. One study demonstrated that intragastric administration of RK could improve the liver condition in high-fat diet-fed rats after four weeks of treatment. Their results show that RK decreased lipids and free fatty acid (FFA) generation in serum and hepatic tissue thus protecting liver cells. The antioxidant activity of RK was demonstrated by the increase in total antioxidant capacity (TAC), an increase in superoxide dismutase (SOD), with a concomitant decrease in the thiobarbituric acid reactive substances (TBARS) level. The study also found peroxisome proliferator-activated receptor-α (PPAR-α) and low-density lipoprotein receptor (LDLR) levels to be lower in NASH rat livers compared to the control rats, which is considered the main cause of disrupted fatty acid metabolism and liver lipidosis. Raspberry ketone treatment was successful in elevating the levels of PPAR-α and LDLR thus suggesting a role for RK as a hepato-protectant and re-establishing the lipid balance. In another study, researchers demonstrated that RK could prevent hepatic damage in rats that were exposed to carbon tetrachloride (CCL4) induced hepatic damage. The CCL4 caused hepatotoxicity by increasing oxidative stress and DNA fragmentation, indicative of increased apoptosis. The CCL4 also induced the expression of inflammatory cytokines such as nuclear factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α). Raspberry ketone was found to effectively reduce oxidative stress and also maintain hepatocyte integrity and microstructure after histological assessment. Raspberry ketone demonstrated antiapoptotic activity by reducing cytoplasmic expression of cytochrome C and caspases and also by inhibiting DNA fragmentation. Another group similarly demonstrated that RK in combination with white tea could protect rats from acrylamide hepatotoxicity by functioning as an anti-inflammatory, antioxidant, and anti-apoptotic agent. The combination treatment of RK and white tea, after acrylamide-induced liver damage, showed a decrease in elevated liver enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). The mechanism of action of RK is still unclear but based on the limited animal studies that have been conducted, it can be surmised that RK, when consumed as a dietary supplement, could protect the liver in several ways based on the type of trigger leading to liver damage. High-fat diet-induced steatohepatitis in rats was reversed by RK, mainly by reducing fat deposits in the liver cells as well as decreasing apoptosis and degeneration of the liver cells. Raspberry ketone treatment helped improve leptin resistance, reduce the release of TNF-α, increase superoxide dismutase (SOD) activity, and decrease malondialdehyde (MDA) levels as well as adjust fatty acid metabolism by increasing PPAR-α receptors and LDLR expression. It is speculated that acrylamide-induced liver toxicity could be improved after RK and white tea treatment by increasing levels of SOD and catalase, which helps in clearing out free radicals and preventing oxidative stress. Raspberry ketone and white tea treatment also led to increased adiponectin levels and a decrease in caspase-3, an apoptosis marker level. Histopathological studies showed concurrent improvement in hepatic cell structure and function. The CCL4-induced liver toxicity could be similarly reversed by RK treatment, thus strengthening the evidence for RK to be considered as a possible treatment for acute and chronic liver diseases.
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