Red wine lowering cholesterol

For years, studies have shown a relationship between drinking a moderate amount of red wine and good heart health, but experts say it’s important to understand what that means before you prescribe yourself a glass or two a day.

No research has established a cause-and-effect link between drinking alcohol and better heart health. Rather, studies have found an association between wine and such benefits as a lower risk of dying from heart disease.
It’s unclear whether red wine is directly associated with this benefit or whether other factors are at play, said Dr. Robert Kloner, chief science officer and director of cardiovascular research at Huntington Medical Research Institutes and a professor of medicine at the University of Southern California.
“It might be that wine drinkers are more likely to have a healthier lifestyle and a healthier diet such as the Mediterranean diet, which is known to be cardioprotective,” he said.
But you may not even have to drink red wine to get the benefit, Kloner said. Moderate amounts of beer and spirits also have been linked to a lower risk of heart disease.
It’s a common assumption that red wine may be good for the heart because it contains antioxidants such as resveratrol, which is primarily found in the skin of grapes but also peanuts and blueberries. Some studies suggest resveratrol can reduce cholesterol and lower blood pressure.
“There’s a debate about whether resveratrol is really cardioprotective or not,” Kloner said. “In addition, there is debate about the amount of resveratrol you would need to ingest to get a protective effect. To get the equivalent of the amount of resveratrol that has been reported to be protective would probably mean ingesting an excess of wine.”
Federal guidelines and the American Heart Association recommend that if you do drink alcohol, to do so in moderation. That means no more than one to two drinks per day for men and one drink per day for women. (According to the AHA, one drink is 12 ounces of beer, 4 ounces of wine, 1.5 ounces of 80-proof spirits or 1 ounce of 100-proof spirits.)
Studies have found that moderate alcohol consumption may have some health benefits, including raising “good” HDL cholesterol levels and lowering the risk of diabetes. However, excessive drinking can lead to a host of health problems, including liver damage, obesity, some types of cancer and stroke, not to mention its negative effect on the heart.
“Alcohol in excess is really bad for the heart,” Kloner said. “It can cause high blood pressure and promote arrhythmias. It can cause cardiomyopathy where the alcohol is actually toxic to the heart muscle cells, and that can lead to heart failure.”
Proving moderate alcohol use causes better heart health would be tricky, Kloner said. Ideally, it would require a large prospective study that not only randomly assigns people to a no-drinking group versus a moderate-drinking group, but that also compares different types of alcohol – red wine, white wine, beer, spirits – to determine if one really is better.
“And then you’d have to control for various factors – age, gender, cardiovascular risk, their diet. You’d have to follow them for many years,” he said, noting the added ethical dilemma of taking people who are not drinkers and telling them to become drinkers.
For now, the message certainly isn’t to go out and start drinking, Kloner said. “But if you do drink, drinking in moderation is the way to go.”

If you have questions or comments about this story, please email [email protected]

We’ve all heard that moderation is key when it comes to alcohol levels, right? But what if you have a medical condition, such as high cholesterol or heart disease? What sort of impact can drinking alcohol have on that?

Regardless of your current health situation, it’s important to understand the link between alcohol consumption and cholesterol levels. Let’s take a closer look.

What is cholesterol?

Cholesterol is a waxy, fat-like substance that is a natural component of all the cells in your body. Contrary to popular belief, it is actually an essential part of your body as it helps produce hormones, make vitamin D, provide your cells with structure, and helps make bile, which is needed for digesting fats.

What many people find surprising is that your body makes all the cholesterol that it needs. This means that you do not need to get it from foods. Foods that come from animals such as meat, cheese, and eggs all provide extra cholesterol.

The 2 main types of cholesterol are high-density lipoproteins (HDL) and low-density lipoproteins (LDL).

  • HDL is thought of as the “good” type of cholesterol because it carries cholesterol from your blood to your liver to be removed, which is good for your heart.
  • LDL is the “bad” type of cholesterol because high levels of LDL can contribute to plaque buildup in your arteries, known as atherosclerosis. This condition restricts the flow of blood to other parts of your body, hardens your blood vessels, and can lead to serious heart conditions, including stroke and heart attack.

Triglycerides are often included on cholesterol tests since they have a similar impact on heart health. They are a type of stored fat in the blood and come from eating excess calories that aren’t needed, especially calories from sugars.

What’s considered high cholesterol?

The normal ranges for cholesterol and triglyceride levels for adults 20 years of age and older are as follows:

Lab Normal range
Total cholesterol 125-200 mg/dL
LDL cholesterol Lower than 100mg/dL
HDL cholesterol Men: 40mg/dL or higher
Women: 50mg/dL or higher
Triglycerides Lower than 150mg/dL

According to the Centers for Disease Control and Prevention (CDC), 95 million U.S. adults age 20 or older have total cholesterol levels higher than 200 mg/dL, and nearly 29 million have levels higher than 240 mg/dL. As you can see, this is an issue in our country, and it’s not an uncommon one.

The good news? There are many things you can do to control it, such as eating a healthier diet, exercising regularly, and taking medication.

Don’t miss out on savings! Get the best ways to save on your prescriptions delivered to your inbox. By signing up, I agree to GoodRx’s terms of service and privacy policy.

Does alcohol increase cholesterol levels?

While alcohol itself does not contain cholesterol, it can affect cholesterol levels in the blood in good and bad ways. To understand the link between alcohol and cholesterol, it is helpful to first understand how alcohol is broken down in the body.

The liver metabolizes alcohol and also produces cholesterol. Consuming alcohol can raise cholesterol levels because alcohol is processed through the same organ that is responsible for making cholesterol. For example, studies show that excessive drinking may increase LDL levels, which is the “bad” type of cholesterol.

In addition, alcohol is known to raise triglyceride levels. Your body will break down calories from alcohol to use as fuel before other nutrients in your body. Because alcohol is often consumed in addition to food, your body is more likely to store calories from food as fats in the form of triglycerides. Many alcoholic drinks also contain added sugars, which further increases the risk of raising triglyceride levels. High triglyceride levels can lead to liver damage, including fatty liver disease.

On the other hand, light to moderate intake has been shown to possibly raise HDL, the good type of cholesterol. Specifically, some research has shown that drinking one 4-ounce serving per day of red wine has been linked to heart health, including increasing HDL levels. However, this benefit may be coming more from the other beneficial components of wine including resveratrol, rather than the alcohol itself.

How much alcohol is too much?

While alcohol often gets a bad rap,research is showing that it may not need to be avoided altogether to have good heart health.

The interpretation of “too much” will vary from person to person. Factors such as age, body size, and liver size all determine how quickly alcohol will be metabolized. Some people can break down alcohol more quickly than others.

The general recommendation is for adults to not participate in anything more than moderate drinking, with less drinking being even better. Moderate drinking is defined as 1 to 2 drinks per day for men and 1 drink per day for women.

In the United States, 1 standard drink is considered to be:

  • 12 ounces of regular beer
  • 5 ounces of wine
  • 1.5 ounces of 80-proof distilled spirits

Keep in mind that aside from raising cholesterol and triglyceride levels, excessive drinking is also linked to a long list of other health consequences including cancer, heart disease, birth defects, injuries caused by driving under the influence, memory problems, mental health disorders, alcohol poisoning, and more.

If you drink alcohol or have liver damage, talk to your doctor before taking cholesterol medications known as statins. These medications may cause liver problems, and alcohol use may increase the risk of liver issues.

Does the type of alcohol matter?

Ultimately, it’s the quantity and frequency of drinking that has more of an impact on your cholesterol levels rather than the type of alcohol. Your body reacts to alcohol the same way whether it’s coming from beer, wine, or hard liquor.

As described above, some research has shown a positive relationship between red wine and HDL cholesterol levels, yet the exact way that wine impacts cholesterol levels needs more research. That’s probably why the American Heart Association currently does not recommend drinking wine or any other form of alcohol to gain potential benefits.

The bottom line

Studies have shown that alcohol can have either positive or negative effects on cholesterol levels and heart health depending on how much you drink. The overall recommendation, though, is that less is better.

The good news? You are in control. So, while you may still be able to enjoy some red wine on occasion, it is best to limit alcohol as much as possible for the most protective effects on your heart, cholesterol levels, and body.

Put drug prices & coupons in your pocket! We’ll text you a link to download our free Android or iPhone app Get GoodRx Mobile App Your link is on the way!

We’ve sent a link to download the GoodRx mobile app to your phone.

Something went wrong

We were unable to send a link to your phone.

  • 5 Favorite Recipes: Super Bowl Snacks

    Q: Is it true that wine lowers your bad cholesterol?

    A: First of all, what is “bad” cholesterol? The term refers to low density lipids (LDL) found in the bloodstream. High levels of LDL can contribute to atherosclerosis—the hardening and narrowing of arteries due to plaque deposit—which can lead to heart disease.

    In clinical studies, some foods and drinks, especially wine, have been shown to lower LDL. But according to Miriam Pappo, a registered dietician and director of Clinical Nutrition at Montefiore Medical Center, “There is conflicting evidence on this. Antioxidants in general have been shown to lower bad cholesterol and increase HDL,” also known as “good” cholesterol. She continued, “The antioxidant resveratrol, found in wine, might be the key ingredient in wine that helps prevent damage to blood vessels, reduce bad cholesterol or LDL, and increase good cholesterol HDL.” Much resveratrol research, however, has been performed on animals and in larger doses than would be found in normal wine consumption.

    Pappo pointed out that several major studies on this topic have produced different results. The 2005 “French Paradox” study showed that alcohol found in red wine increased HDL but did not decrease LDL. Researchers in Madrid, meanwhile, found that red wine could lower LDL levels by 9 percent in healthy people and by 12 percent in less-healthy people.

    “The key is moderation of one to two drinks a day, at most, along with a healthy balanced diet and exercise,” cautioned Pappo. “Three or more drinks per day can result in elevated serum triglycerides,” that is, fat in the bloodstream.

    Have a question about wine and healthy living? E-mail us.

    Have you ever topped off your glass of cabernet or pinot noir while saying, “Hey, it’s good for my heart, right?” This widely held impression dates back to a catchphrase coined in the late 1980s: the French Paradox.

    The French Paradox refers to the notion that drinking wine may explain the relatively low rates of heart disease among the French, despite their fondness for cheese and other rich, fatty foods. This theory helped spur the discovery of a host of beneficial plant compounds known as polyphenols. Found in red and purple grape skins (as well as many other fruits, vegetables, and nuts), polyphenols theoretically explain wine’s heart-protecting properties. Another argument stems from the fact that the Mediterranean diet, an eating pattern shown to ward off heart attacks and strokes, features red wine.

    However, the evidence that drinking red wine in particular (or alcohol in general, for that matter) can help you avoid heart disease is pretty weak, says Dr. Kenneth Mukamal, an internist at Harvard-affiliated Beth Israel Deaconess Medical Center. All of the research showing that people who drink moderate amounts of alcohol have lower rates of heart disease is observational. Such studies can’t prove cause and effect, only associations.

    Moderate drinking — defined as one drink per day for healthy women and two drinks per day for healthy men — is widely considered safe. But to date, the health effects of alcohol have never been tested in a long-term, randomized trial.

    Grape expectations

    Although some studies suggest wine is better for the heart than beer or hard liquor, others do not, according to a review article about wine and cardiovascular health in the Oct. 10, 2017, issue of Circulation. That’s not surprising, says Dr. Mukamal. “In many cases, it’s difficult to tease out the effect of drinking patterns from specific types of alcoholic beverages,” he explains. For example, people who drink wine are more likely do so as part of a healthy pattern, such as drinking a glass or two with a nice meal. Those habits — rather than their choice of alcohol —may explain their heart health.

    Also, the French Paradox may not be so paradoxical after all. Many experts now believe that factors other than wine may account for the observation, such as lifestyle and dietary differences, as well as earlier underreporting of heart disease deaths by French doctors. What’s more, Dr. Mukamal notes, heart disease rates in Japan are lower than in France, yet the Japanese drink a lot of beer and clear spirits, but hardly any red wine.

    Resveratrol reservations

    What about the polyphenols in red wine, which include resveratrol, a compound that’s heavily advertised as a heart-protecting and anti-aging supplement? Research in mice is compelling, says Dr. Mukamal. But there’s zero evidence of any benefit for people who take resveratrol supplements. And you’d have to drink a hundred to a thousand glasses of red wine daily to get an amount equivalent to the doses that improved health in mice, he says. Also, a 2014 study of older adults living in the Chianti region of Italy, whose diets were naturally rich in resveratrol, found no link between resveratrol levels (measured by a breakdown product in urine samples) and rates of heart disease, cancer, or death. As for the Mediterranean diet, it’s impossible to know whether red wine is an important part of why that eating style helps reduce heart disease, says Dr. Mukamal.

    If you enjoy red wine, be sure to limit yourself to moderate amounts. Measure out 5 ounces (which equals one serving) in the glass you typically use. Five ounces appears smaller in a large goblet than in a standard wine glass. Also, older men should be aware that both the National Institute of Alcohol Abuse and Alcoholism and the American Geriatric Society recommend that starting at age 65, men should limit their alcohol use to no more than a single drink per day. Age-related changes, including a diminished ability to metabolize alcohol, make higher amounts risky regardless of gender.

    Scientific studies, the media, and even some doctors tout the heart health benefits of red wine. But if controlling blood pressure is important to you, consider this the next time you raise your glass: A new study published online in Circulation Research suggests that non-alcoholic red wine may be better at lowering blood pressure than regular red wine. Powerful antioxidants in red wine called polyphenols may be more effective when there’s no alcohol to interfere with them.

    “It is a very interesting study with provocative findings,” says Dr. Deepak Bhatt, a cardiologist and professor of medicine at Harvard Medical School. I would like to believe the results. Of course, it is a small study with a limited duration of follow-up, so the findings do need to be confirmed in other, larger studies that follow patients for a longer period of time.”

    In vino veritas

    In wine there is truth, said Pliny the Elder in the first century AD. One truth about red wine is that too much can raise blood pressure and increase the risks of cancer, liver disease, and car accidents if you get behind the wheel after drinking.

    In moderation, however, drinking red wine increases HDL (“good” cholesterol). It also protects against artery damage, which may lower blood pressure and help prevent heart disease. Polyphenols, in particular, may protect the lining of blood vessels in the heart. But most studies about red wine’s antioxidants have been conducted on animals, and were not able to sort out the contribution from alcohol.

    The study

    A team of Spanish researchers recruited 67 men between ages 55 and 75, all with diabetes or cardiovascular risk factors. Each man drank red wine daily for four weeks, then drank non-alcoholic red wine daily for four weeks, then drank gin daily for four weeks. The daily amounts were moderate: 10 ounces of wine or three ounces of gin. That’s about two drinks a day.

    When the men drank non-alcoholic red wine, their systolic blood pressure (the top number of a blood pressure reading) decreased on average by 6 points. That’s enough to reduce heart disease risk by 14% and stroke risk by as much as 20%, according to the researchers. There was no change in blood pressure when the men drank gin, and only a small reduction in blood pressure when they drank regular red wine.

    Researchers also found that the men’s plasma nitric oxide levels went up when they drank non-alcoholic red wine. That’s a good thing, because nitric oxide relaxes blood vessel walls, allowing better blood flow. The NO levels went up only slightly when the men drank regular red wine, and not at all when they drank gin.

    The results of the study look like something to toast: you can get polyphenol and nitric oxide benefits without having to drink alcohol and risk the dangers that come with it. Not so fast, says Dr. Bhatt. “It makes scientific sense, but these findings really need to be confirmed in other studies,” he reminds us.

    What the study doesn’t tell us is how non-alcoholic red wine stacks up against regular red wine for preventing heart attacks or other cardiovascular problems. An excellent discussion of the benefits and risks of drinking red wine and other alcoholic beverages is available on The Nutrition Source, a website published by the Harvard School of Public Health’s Department of Nutrition.

    What you should do

    If you’re interested in lowering your blood pressure, Dr. Bhatt says drinking non-alcoholic red wine won’t hurt. “I wouldn’t ever make a clinical recommendation based on just one small study. However, if you happen to like non-alcoholic red wine and drink it anyway, it might be worthwhile to see if it helps your high blood pressure,” he says.

    But don’t count on non-alcoholic red wine to lower high blood pressure, also known as hypertension, cautions Dr. Bhatt. Most people need a combination of exercise, a healthy diet, and medications to control high blood pressure.

    Moderate exercise for 150 minutes per week and following the Dietary Approaches to Stop Hypertension (DASH) diet can powerfully lower blood pressure, sometimes making medicines unnecessary. DASH is an eating plan featuring more fruits, vegetables and whole grains; foods with nutrients known to help reduce blood pressure, like calcium, potassium and magnesium; and reduced sodium and saturated fat intake.

    High blood pressure is a big problem. The Centers for Disease Control and Prevention reported last week that a third of all Americans have high blood pressure, and the majority of them don’t have it under control.

    Those are sobering facts. If the Spanish study pans out, one possible solution won’t be too hard to swallow.

    By Stephanie Castillo, Prevention

    Any hardworking gal knows that kicking back with a girlfriend and a glass of red wine is a fabulous way to de-stress. The best part? Your red-wine habit also happens to come with some happy health benefits, such as protecting your ticker and even slimming your waistline. Check out these eight reasons why winding down with a glass of vino is a good call all around.

    1. Lower your cholesterol

    High-fiber Tempranillo red grapes—which are used to make certain red wines, like Rioja—may actually have a significant effect on cholesterol levels, according to a study from the Universidad Complutense de Madrid in Spain.

    Healthy study participants who consumed the same grape supplement found in red wine saw their LDL, or “bad cholesterol,” levels decrease by 9% among healthy. Participants with high cholesterol experienced a drop of 12%. What’s the big deal? Excess LDL ends up getting deposited in arterial walls and forming plaque, which causes arteries to stiffen and blood pressure to rise, ultimately leading to heart attacks, says Arthur Agatson, MD, an associate professor of medicine at the University of Miami and author of The South Beach Heart Program.

    12 Foods That Lower Cholesterol Naturally

    2. Protect your heart

    On top of lowering bad cholesterol, polyphenols—the antioxidants in red wine—can help keep blood vessels flexible and reduce the risk of unwanted clotting, says John Folts, PhD, a professor of cardiovascular medicine and nutrition at the University of Wisconsin–Madison.

    “They’re nearly as effective as aspirin,” says Folts. But be careful: Chronic heavy drinking damages the heart, so, as with most things, moderation is key.

    3. Control blood sugar

    Trending stories,celebrity news and all the best of TODAY.

    The skin of red grapes—a rich source of red wine’s natural compound resveratrol—may actually help diabetics regulate their blood sugar, finds recent research published in the journal Nutrition. Study participants who took a 250 mg resveratrol supplement once a day for three months had lower blood glucose levels than those who didn’t take the pill. Plus, resveratrol-takers also had significant decreases in total cholesterol and systolic blood pressure. Researchers suspect that resveratrol may help stimulate insulin secretion or activate a protein that helps regulate glucose and insulin sensitivity.

    4. Boost your brain

    Resveratrol may also be the key to keeping your memory sharp, says Philippe Marambaud, PhD, a senior research scientist at New York’s Litwin-Zucker Research Center for the Study of Alzheimer’s Disease and Memory Disorders. The compound has been shown to hamper the formation of beta-amyloid protein, a key ingredient in the plaque found in the brains of people with Alzheimer’s. Marambaud suggests flexing your noodle by doing crossword puzzles and brain teasers for an hour then cooling down with a glass of wine.

    5. Fight off a cold

    If you hate getting sick (and who doesn’t?), the antioxidants in red wine may help keep you healthy. A 2010 study in the American Journal of Epidemiology found that among 4,000 faculty members at five Spanish universities, those who drank more than 14 weekly glasses of wine for a year were 40% less likely to come down with a common cold. Why? According to the National Institutes of Health, antioxidants are believed to fight infection and protect cells against the effects of free radicals, which may play role in cancer and other diseases.

    Another antioxidant boost? They may also lower sex hormone levels to protect against breast cancer, says a study from Cedars-Sinai Medical Center in Los Angeles.

    6. Stop cancer

    According to researchers at the University of Virginia, the resveratrol you get from drinking one glass of red wine three or four times a week may be enough to starve any nascent cancer cells. The scientists dosed human cancer cells with resveratrol and found that the compound inhibited the key action of a cancer-feeding protein.

    7. Get slim

    Clearly, resveratrol is a bit of a limelight hog when it comes to the healthful compounds in vino. But research in the Journal of Biological Chemistry suggests piceatannol, the chemical compound our bodies convert from resveratrol, deserves some credit. This compound was shown to actually prevent the growth of fat cells in a series of lab tests. How? Researchers say that piceatannol binds to the insulin receptors of fat cells, essentially blocking the pathways necessary for immature fat cells to mature and grow.

    8. Jazz up dinner

    Who said your red wine consumption had to be limited to the glass? You can include the drink in your dinner, either as a sauce or complimentary ingredient, and still reap its benefits.

    More from Prevention:

    6 Sneaky Signs You Drink Too Much

    28 Days To A Healthier Heart

    The Ultimate Anti-Cancer Diet

    Is Your Drinking Habit Deadly?

    Red wine is good for gut health and can lower cholesterol, but you only need it once a fortnight, a new study has found.

    The first major research of its kind found significantly higher diversity of friendly bacteria in the gut among red wine drinkers, but not among drinkers of white wine, cider or beer.

    Scientists at King’s College London believe the beneficial effect is due to polyphenols found in the skin of grapes, which go into the red wine-making process, but are not used in white wine.

    These are packed with antioxidants which fuel the diversity of microbes in the gut.

    Despite the positive findings, the experts warned drinkers not to exceed recommended safe alcohol limits, saying the data showed a beneficial effect was possible even with as little as one glass of red wine a fortnight.

    Dr Caroline Le Roy, who led the study, said: “While we have long known of the unexplained benefits of red wine on heart health, this study shows that moderate red wine consumption is associated with greater diversity and a healthier gut microbiota that partly explain its long debated beneficial effects on health.”

    The microbiome is the collection of microorganisms in an environment and plays an important role in human health.

     Alcoholism and Health Issues: Cholesterol, Triglycerides, the Liver, and More

    Excessive drinking, binge drinking, and alcohol use disorder all damage the body.

    Acute problems from alcohol poisoning can put a person in the hospital, and consistent problem drinking of any kind, over many years, can damage nearly every organ system in the body. This can cause health consequences ranging from pain to behavioral disturbances to life-threatening cancers.

    How Alcohol Use Disorder Damages the Body

    Alcohol use disorder, heavy drinking, and binge drinking can all cause acute and chronic health issues. Some chronic health problems related to alcohol use disorder or problem drinking are listed below according to the specific disorder or system they affect.


    In moderate amounts – no more than one 5-ounce serving per day – red wine has been correlated with healthy cholesterol levels. Drinking more wine, beer, hard liquor, or mixed drinks, however, is likely to increase cholesterol. Problem drinking over years can lead to chronic high cholesterol. Also, damage to the pancreas, leading to chronic pancreatitis, can cause diabetes.


    These are fats found in the blood, which provide excess calories to help cells function; drinking alcohol, particularly beer or liquor, can increase the amount of these fats in a negative way. Too many triglycerides can lead to hardening of the artery walls, increasing the potential of heart disease or stroke.


    Alcohol interferes with the liver’s ability to release glucose, causing hypoglycemia or low blood sugar. This can induce diabetes in people who are prone to the condition, or it can make diabetes worse in people who are already receiving treatment.


    All kinds of excessive drinking can damage the heart. Types of heart damage include arterial fibrillation (a type of heart arrhythmia), cardiomyopathy (stretching and drooping of the heart muscle, so it does not beat very strongly), and inflammation (sometimes causing blood clots, which can lead to stroke or pulmonary embolism).

    Blood pressure:

    Changes to the sympathetic nervous system when a person drinks excessively can raise blood pressure. While this is a temporary situation, consistent heavy drinking regularly raises blood pressure, and eventually, the condition becomes chronic.


    Digestive problems are a side effect of drinking too much, since alcohol can change the pH balance of stomach acid. It can also irritate the stomach lining, especially if a person struggling with alcohol use disorder stops eating regular or healthy meals. Gastritis, or an inflammation of the stomach lining, indigestion or acid reflux, and ulcers are side effects of a chronic drinking problem. Changes in digestion can also affect how much vitamin B12, or thiamine, the body absorbs, which can harm other organ systems, especially the brain.


    Since the liver processes most of the alcohol that enters the body, it is one of the most affected organs. People who drink heavily, or struggle with alcohol use disorder, are more likely to develop liver damage. This includes alcoholic hepatitis (inflammation of the liver), hepatic steatosis (increased fat in the liver), cirrhosis (irreversible scarring or destruction to liver tissue) and liver cancer.


    After the liver filters most toxins out of the body, the kidneys are responsible for removing much of what is left. However, if the liver does not filter enough alcohol out of the body, it will reach the kidneys and damage that organ’s ability to process toxins. The kidneys are also responsible for keeping enough water in the body; when poisoned by too much alcohol, the kidneys are not able to prevent dehydration. Additionally, high blood pressure can damage the kidneys, along with other organs.


    Drinking too much also inflames the pancreas, leading to pancreatitis. Chronic inflammation of this organ interferes with digestion, causing abdominal pain and diarrhea, which often do not go away without medication.


    Excessive drinking can lead to osteoporosis, or the thinning of bone from loss of calcium. This can lead to a higher risk of bone fractures later in life. Alcohol use disorder can also damage bone marrow, preventing the production of red blood cells, and this can lead to problems clotting, or excessive bruising. Fewer red blood cells also leads to anemia, a condition in which oxygen is not carried through the body properly; this causes lightheadedness, shortness of breath, and fatigue.


    Chronic problem drinking can damage several areas of the brain, leading to neuropathy, or numbness in the extremities, as well as short-term memory loss, disordered thinking, and dementia. Low thiamine levels from alcohol use disorder can also lead to Wernicke-Korsakoff syndrome, commonly known as wet brain.Heavy drinking can also lead to seizures because it changes how GABA receptors function. When a person who is physically dependent on alcohol is not able to drink, or tries to stop drinking without medical supervision, those pathways are more easily excited, which can lead to anxiety, panic attacks, and seizures. Additionally, liver damage harms the brain by leading to hepatic encephalopathy, or swelling in the brain due to unfiltered toxins.

    Areas of the brain damaged by excessive drinking include the cerebellum (controls motor function), the limbic system (controls memory and emotional processing), and the cerebral cortex (controls the ability to think, plan, and interact with others).

    Mental health:

    Many people who struggle with alcohol use disorder display symptoms of depression. A 2005 study conducted in New Zealand found that, for many people struggling with alcoholism, their depression cleared up when they became sober.

    Can Damage from Excessive Drinking Be Reversed?

    If a person struggling with alcohol use disorder stops drinking via a professional medical detox program, enters a rehabilitation program based in therapy, and maintains sobriety while their symptoms are still in the early stages, they may be able to reverse much of the damage to their body. The brain, in particular, seems especially able to heal damage. Other systems, like the immune system and the pancreas, may not be as able to heal damage. However, even if a person is not able to reverse damage caused to their body by problem drinking, stopping alcohol consumption and managing the addiction can still stop the progression of the disease.

    Alcohol Consumption Raises HDL Cholesterol Levels by Increasing the Transport Rate of Apolipoproteins A-I and A-II

    HDL cholesterol (HDL-C) concentrations are well established as a major protective factor against coronary heart disease.1 Moderate alcohol intake has been associated with protection against coronary heart disease in observational studies, an effect that appears to be mediated in large part by alcohol-induced increases in HDL-C concentrations.2345678 Despite the potential importance of the association between alcohol consumption and increased HDL-C concentrations, the mechanism of this effect has not been established. Two previous turnover studies in human subjects had contradictory conclusions, perhaps because study subjects were few in number and were in a state of caloric excess while on alcohol.910

    The present study tested the hypothesis that the increase in HDL-C concentrations with moderate alcohol intake results from increased transport rate (TR) of the major HDL apolipoproteins apoA-I and -II. We measured the in vivo turnover of apoA-I and -II in paired HDL turnover studies in healthy men and women without and with alcohol consumption. We found that the increase in plasma HDL-C with moderate alcohol consumption is associated with an increase in the TR of apoA-I and -II, without a significant change in the fractional catabolic rate (FCR).


    Study Population

    Five women and nine men were recruited from the clinic of the Laboratory of Biochemical Genetics and Metabolism and via posted advertisements. Eligibility was confined to subjects ≥21 years old who consumed alcohol on a regular basis and had no personal or family history of alcoholism. Subjects were also excluded for significant systemic disease by history, physical examination, and laboratory screening and for use of tobacco or medications known to alter lipid concentrations, including birth control pills. Although there were no exclusions based on race or ethnic background, all subjects were white.

    Experimental Protocol

    All subjects underwent 2 study periods each of 4 weeks’ duration; the first 2 weeks served as an equilibration phase, and the turnover study was carried out during the second 2 weeks. Each subject consumed both a Western-type diet (control) and the same diet plus ethanol (EtOH), in varied order. The subjects were studied at the inpatient unit of The Rockefeller University Clinical Research Center and were encouraged to continue their usual physical activity. The Rockefeller University Institutional Review Board approved the study, and informed consent was obtained from each subject.


    The control diet was designed with use of the US Department of Agriculture Nutrient Data Base11 to conform to a high-fat diet often consumed in Western societies. The diet contained 15% protein, 43% carbohydrate, and 42% fat at a P/S ratio of 0.1, with 215 mg cholesterol/1000 Kcal consumed. The EtOH diet was identical to the control diet except that alcohol (as vodka) was substituted for carbohydrate in an isocaloric manner. The EtOH dose reflected the subject’s reported usual intake up to 1 mL · kg−1 · d−1. The EtOH was given in a single or divided dose according to the subject’s usual intake pattern and was consumed at the end of meals. The diets consisted of whole foods from common ingredients of known composition.11

    Kinetic Studies

    Both apoA-I and -II were prepared and radioiodinated as previously described.12 After the injection of labeled apolipoprotein, blood samples of 7 to 20 mL each were drawn at 10 minutes; 4, 12, 24, 36, and 48 hours; and then daily through day 14. Plasma was prepared, and 1-mL aliquots were used for the determination of the remaining 125I-apoA-I and 131I-apoA-II radioactivity. The plasma apoA-I and -II decay curves were normalized to the 10-minute sample and analyzed with the Matthews model.13 The model, fitted to each decay curve with SAAM II software,14 was used to estimate the FCR. The TR of each apolipoprotein was calculated as the product of its plasma concentration, its FCR, and the plasma volume (assumed to be 4.5% of the body weight), all divided by the body weight.

    Lipid and Lipoprotein Measurements

    Plasma samples anticoagulated with EDTA were obtained after a 12-hour overnight fast on days 1, 3, 7, 10, and 14 after isotope injection for the determination of lipid and lipoprotein concentrations. No temporal trends were observed, so the mean of all 5 determinations was used in the data analysis. Lipid and lipoprotein measurements were made with fresh specimens, and apolipoprotein determinations were made with aliquots of plasma stored at −70°C. Total cholesterol and triglyceride concentrations were determined with enzymatic methods with reagents from Boehringer-Mannheim. Lipoprotein cholesterol concentrations were determined after serial ultracentrifugation.15 Total and HDL-C values were standardized by the Lipid Standardization Program of the Centers for Disease Control and Prevention, supported by the National Heart, Lung, and Blood Institute.16 The apoA-I concentrations were measured with enzyme-linked immunosorbent assay.12 The apoA-II concentrations were determined in the Northwest Lipids Research Clinics laboratories based on a radial immunodiffusion assay.17

    Postheparin Lipase Activity

    On day 11 of each metabolic diet and 3 days before isotope injection, an intravenous bolus injection of heparin was administered at a dose of 60 U/kg body wt. Blood was drawn exactly 15 minutes later, and postheparin plasma was obtained and stored at −70° until assay for hepatic lipase (HL) and lipoprotein lipase (LPL) activity. The activity of LPL was determined with radioactive triolein in a glycerol-based assay.12 The activity of HL was measured in triplicate with a commercially available fluorometric assay (Progen)18 and adapted to a 96-well microtiter plate format. Lipase activities were expressed as μmol free fatty acids released · h−1 · mL postheparin plasma−1.

    Lipoprotein Size Determinations

    The average sizes of HDL, LDL, and VLDL were determined with proton NMR spectroscopy by Dr James Otvos (University of North Carolina ).19

    Statistical Analysis

    The present study was a standard 2-treatment, 2-period crossover trial. We compared mean differences between the 2 diets with a Wilcoxon signed-rank test. The null hypothesis for this test is that there is no difference between the 2 diets. The correlations between the dose of EtOH and the EtOH diet–induced changes in HDL and related parameters were examined with Pearson’s correlation, as were the correlations between changes in HDL-C and the changes in HDL turnover parameters. A similar analysis with Spearman’s rank order correlations gave similar results. The statistical software package S-Plus 3.4 for Windows was used for data analysis.


    Baseline characteristics, EtOH intake, and plasma lipid and lipoprotein values during the control and EtOH diets are shown for each subject in Table 1. The subjects varied in age from 21 to 70 years (mean±SD 53.3±15.9 years), in weight from 51.4 to 97.5 kg (75.7±14.6 kg), and in body mass index from 18.9 to 35.0 kg/m2 (25.6±4.2 kg/m2), and they consumed alcohol in an amount ranging from 0.20 to 0.81 g · kg−1 · d−1 (0.45±0.19 g · kg−1 · d−1). There was no significant change in weight or physical activity during and between the 2 turnover studies.

    The results of the paired HDL turnover studies with the control and EtOH diets are shown in Table 2. The apoA-I concentrations were 10% higher (P=0.048) with the EtOH compared with the control diet, associated with a 21% increase in apoA-I TR (P=0.041) but no significant change in apoA-I FCR (P=0.12). Similarly, apoA-II concentrations were 17% higher (P=0.005) with the EtOH compared with the control diet, with a 19% increase in apoA-II TR (P=0.016) but no significant change in apoA-II FCR (P=0.92). Thus, alcohol intake appears to increase HDL-C concentrations via an increase in the TR of the 2 major HDL apolipoproteins apoA-I and -II.

    Alcohol intake altered the activity of both endothelial lipases in directions believed to lower atherosclerosis risk. HL concentrations were 8% lower (P=0.01) on the EtOH diet, whereas LPL concentrations were 23% higher (P=0.001).


    Several observational studies suggest that moderate alcohol intake reduces the risk of atherosclerosis, and the major mechanism appears to be the well known ability of alcohol to raise HDL-C concentrations.52021222324 Despite this, the metabolic pathway or pathways by which alcohol increases HDL-C concentrations are not well understood. Because the liver is reported to be the major site of apoA-I synthesis25 and because alcohol increases apoA-I production in transformed human hepatocytes,262728 we hypothesized that alcohol raises HDL-C primarily by raising the TR of apoA-I and -II. In paired metabolic HDL apolipoprotein turnover studies, we found that dietary alcohol increases the TR of both apoA-I and -II, roughly to the same degree as the increase in their concentrations and in the HDL-C concentration. We also found that the amount of alcohol consumed predicted the degree of increase in the TR and that both correlated with the increase in HDL-C. These results suggest that the increase in TR is the major mechanism by which alcohol consumption raises HDL-C.

    Our results in part confirm and in part contradict the results of the only 2 published studies of which we are aware that explore the effects of alcohol consumption on HDL turnover in human subjects.910 Malmendier and Delcroix9 studied apoA-I metabolism in 7 healthy nonobese men before and during a 4-week intake of 60 to 70 g EtOH/d and found a 49% increase in the TR and a 30% increase in the FCR of apoA-I. Thus, we confirm their finding that a prominent effect of alcohol on HDL turnover is an increase in apoA-I TR. The fact that the degree of increase in apoA-I TR in their study was more than double that seen in the present study may be due to their use of twice as much alcohol (60 to 70 g/d versus 33 g/d mean in our study), especially given our evidence for a dose-response effect in the range of 13 to 51 g/d. Surprisingly, they saw no increase in HDL-C (2% rise, NS), which is inconsistent with almost all other human studies and perhaps due to confounding from the small number of subjects and the relative lack of dietary control. It might also reflect a counterbalancing of the increase in apoA-I TR by a significant 30% increase in the apoA-I FCR, although they did report a statistically significant 12% increase in plasma apoA-I concentrations. In a second, smaller study by Gottrand et al,10 5 normolipemic men received 50 g/d EtOH as red wine added to a metabolic diet, apparently without any compensating reduction in other caloric intake. Alcohol induced a 14% increase in HDL-C accompanied by 20% and 60% increases in apoA-I and -II concentrations, respectively. They reported no change in the TR of either apoA-I or apoA-II; although a trend to increased TR was observed (11% and 18%, respectively). They did not find a significant change in apoA-I FCR, which is in agreement with our result but not with those of Malmendier and Delcroix,9 whereas the 21% decrease in apoA-II FCR reported by Gottrand et al10 was found by neither Malmendier and Delcroix9 nor us. These apparent discrepancies may be explained by the very small numbers of subjects in the prior studies, their lesser dietary control, and, in the case of the study by Gottrand et al,10 the intake of the many nonalcoholic components of wine.

    The effect of alcohol intake on HDL turnover has also been studied in nonhuman primates.29 In squirrel monkeys, high-dose alcohol intake increased HDL-C and apoA-I concentrations.29 However, this was associated with a decrease in apoA-I FCR and no change in apoA-I TR. The possible reasons for the differences between the present results and those reported in squirrel monkeys cannot be assessed given the lack of information in this model about the effects of alcohol on lipase activities, HDL size, apoA-II turnover, and hepatocyte metabolism.

    The effect of alcohol consumption on the major HDL particle size or density subfractions, HDL2 and HDL3, is inconsistent among studies. Haskell et al21 found an increase in HDL-C and HDL3 mass, but not HDL2, on resumption of moderate drinking. In contrast, Contaldo et al30 reported that the increase in HDL-C after short-term alcohol intake was primarily an increase in HDL2. Two other studies have indicated that alcohol consumption is associated with increased concentrations of both HDL2 and HDL3.524 In agreement with these latter 2 studies and with a more detailed assessment of HDL size than in prior published studies, we found no significant change in HDL particle size distribution. Although some reports suggest that larger HDL subfractions may be more strongly related to low atherosclerosis risk, others have found that large and small HDL particles may be equally associated with decreased risks of myocardial infarction.5 Interestingly, the only study that simultaneously measured HDL size, alcohol intake, and atherosclerosis event rates found that increases in both large and small HDL particles contribute to the reduced risk of events with alcohol consumption.5

    We found that moderate alcohol consumption causes an increase in LPL and a decrease in HL activity, both of which would be expected to cause an increase in HDL particle size. The fact that there was no such increase is surprising and suggests the interesting possibility of a counterbalancing increase of smaller particles, which may have resulted from the increase in HDL apolipoprotein TR. Our previous work demonstrated that LPL and HL strongly predict apolipoprotein HDL FCR (inversely and positively, respectively).31 On this basis, we would have predicted that the alcohol-induced changes in LPL and HL both should have caused a reduction in HDL apolipoprotein FCR. Thus, the observed lack of change in FCR appears paradoxical, until one considers the lack of change in HDL particle size distribution. If HDL apolipoprotein FCR is primarily a function of HDL particle size rather than a direct function of LPL or HL activity, the observed lack of change in FCR would be expected as a result of the lack of change in HDL size.

    The major mechanism of the alcohol-induced increase in HDL apolipoprotein TR is likely an increase in hepatic production, because the liver is estimated to be the site of synthesis of ≈90% of plasma apoA-I in humans.25 Although on the basis of our studies we cannot rule out an effect of alcohol on intestinal apoA-I production, this is unlikely, because alcohol intake is associated with increased postprandial lipemia32 and decreased HDL2 concentrations.33 Studies of HepG2 cells, a transformed human hepatocyte cell line, have shown that alcohol increases the synthesis and secretion of apoA-I, causing an increase in cholesterol efflux ability.26 Furthermore, the increase with chronic exposure to alcohol appears to be specific for apoA-I compared with some other apolipoproteins,27 although apoA-II data were not reported. Interestingly, this in vitro effect is dose dependent (0.05% to 0.5%),28 reminiscent of our finding of dose-dependency of the TR effects. The molecular mechanism of the increased apolipoprotein synthesis is not known and cannot be readily addressed in humans in vivo. In hepatocyte culture, this effect appears to involve the microsomal EtOH-oxidizing system27 and is speculated to be due to intracellular increases in phospholipid and cholesterol.28

    In conclusion, we demonstrated that moderate alcohol consumption results in dose-dependent increases in plasma concentrations of the major HDL components (HDL-C, apoA-I and -II) through an increase in the HDL apolipoprotein TR, without a change in FCR or HDL particle size distribution.

    Figure 1. Relationships between changes in HDL-C (mg/dL) and apoA-I TR (mg · kg−1 · d−1) with EtOH intake (g · kg−1 · d−1). Results are plotted as change in levels (EtOH minus control diet values) versus EtOH intake, with Pearson’s correlation coefficient and significance.

    Figure 2. Relationships between changes in HDL-C (mg/dL) with changes in apo A-I TR (mg · kg−1 · d−1) and apoA-I FCR (pools/d). Results are plotted as change versus change in levels (EtOH minus control diet values), with Pearson’s correlation coefficient and significance.

    BMI indicates body mass index; T-Chol, total cholesterol; TG, triglycerides.

    1Missing value.

    2>90th percentile adjusted for age/sex.

    3<10th percentile adjusted for age/sex.

    4Wilcoxon matched-pairs test.

    1Missing value.

    2Wilcoxon matched-pairs test.

    This work was supported by General Clinical Research Center grant M01-RR-00102 from the National Center for Research Resources, a Clinical Investigator Award (HL-02034) from the National Institutes of Health, and a Merit Review Award from the Department of Veterans’ Affairs (to Dr Brinton). We thank the nutrition research and nursing services of the General Clinical Research Center of the Rockefeller University Hospital. We thank Katie Tsang for technical assistance and all study participants for their cooperation.


    Correspondence to Jan L. Breslow, Laboratory of Biochemical Genetics and Metabolism, Box 179, The Rockefeller University, 1230 York Ave, New York, NY 10021-6399. E-mail

    • 1 Gordon DJ, Probstfield JL, Garrison RJ, et al. High-density lipoprotein cholesterol and cardiovascular disease: four prospective American studies. Circulation.1989; 79:8–15.CrossrefMedlineGoogle Scholar
    • 2 Gaziano JM, Manson JE. Diet and heart disease: the role of fat, alcohol, and antioxidants. Cardiol Clin.1996; 14:69–83.CrossrefMedlineGoogle Scholar
    • 3 Stampfer MJ, Colditz GA, Willett WC, et al. A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. N Engl J Med.1988; 319:267–273.CrossrefMedlineGoogle Scholar
    • 4 Rimm EB, Giovannucci EL, Willett WC, et al. Prospective study of alcohol consumption and risk of coronary disease in men. Lancet.1991; 338:464–468.CrossrefMedlineGoogle Scholar
    • 5 Gaziano JM, Buring JE, Breslow JL, et al. Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction. N Engl J Med.1993; 329:1829–1834.CrossrefMedlineGoogle Scholar
    • 6 Pearson TA. Alcohol and heart disease. Circulation.1996; 94:3023–3025.CrossrefMedlineGoogle Scholar
    • 7 Suh I, Shaten BJ, Cutler JA, et al. Alcohol use and mortality from coronary heart disease: the role of high-density lipoprotein cholesterol: the Multiple Risk Factor Intervention Trial Research Group. Ann Intern Med.1992; 116:881–887.CrossrefMedlineGoogle Scholar
    • 8 Schaefer EJ, Lamon-Fava S, Ordovas JM, et al. Factors associated with low and elevated plasma high density lipoprotein cholesterol and apolipoprotein A-I levels in the Framingham Offspring Study. J Lipid Res.1994; 35:871–882.MedlineGoogle Scholar
    • 9 Malmendier CL, Delcroix C. Effect of alcohol intake on high and low density lipoprotein metabolism in health volunteers. Clin Chim Acta. 1985;152;281–288:.Google Scholar
    • 10 Gottrand F, Beghin L, Duhal N, et al. Moderate red wine consumption in healthy volunteers reduced plasma clearance of apolipoprotein A-II. Eur J Clin Invest.1999; 29:387–394.CrossrefMedlineGoogle Scholar
    • 11 United States Department of Agriculture, Agricultural Research Service. USDA Nutrient Data Base for Standard Reference, Release 9. Hyattsville, Md: United States Department of Agriculture, Agricultural Research Service ;1990.Google Scholar
    • 12 Brinton EA, Eisenberg S, Breslow JL. Elevated high density lipoprotein cholesterol levels correlate with decreased apolipoprotein A-I and A-II fractional catabolic rate in women. J Clin Invest.1989; 84:262–269.CrossrefMedlineGoogle Scholar
    • 13 Matthews CME. The theory of tracer experiments with 131-I labelled plasma proteins. Physics Med Biol.1957; 2:36–53.CrossrefMedlineGoogle Scholar
    • 14 SAAM Institute. SAAM II User Guide 1998. Seattle, Wash: SAAM Institute, Inc; 1998.Google Scholar
    • 15 Warnick GR, Benderson J, Albers JJ. Dextran sulfate-Mg2+ precipitation procedure for quantitation of high-density-lipoprotein cholesterol. Clin Chem.1982; 28:1379–1388.MedlineGoogle Scholar
    • 16 Clinical Chemistry Standardization Section. Lipid Standardization Programs of the Centers for Disease Control. Atlanta, Ga: Center for Environmental Health, Centers for Disease Control, Department of Health and Human Services; December 1985.Google Scholar
    • 17 Cheung MC, Albers JJ. The measurement of apolipoprotein A-I and A-II levels in men and women by immunoassay. J Clin Invest.1977; 60:43–50.CrossrefMedlineGoogle Scholar
    • 18 De Oliveira e Silva ER, Kong M, Han Z, et al. Metabolic and genetic determinants of HDL metabolism, and hepatic lipase activity in a metabolic ward study of normolipidemic females. J Lipid Res.1999; 40:1211–1221.MedlineGoogle Scholar
    • 19 Otvos JD, Jeyarajah EJ, Bennett DW, et al. Development of a proton nuclear magnetic resonance spectroscopic method for determining plasma lipoprotein concentrations and subspecies distributions from a single, rapid measurement. Clin Chem.1992; 38:1632–1638.MedlineGoogle Scholar
    • 20 Fraser GE, Anderson JT, Foster N, et al. The effect of alcohol on serum high density lipoprotein (HDL): a controlled experiment. Atherosclerosis.1983; 46:275–286.CrossrefMedlineGoogle Scholar
    • 21 Haskell WL, Camargo C Jr, Williams PT, et al. The effect of cessation and resumption of moderate alcohol intake on serum high-density-lipoprotein subfractions: a controlled study. N Engl J Med.1984; 310:805–810.CrossrefMedlineGoogle Scholar
    • 22 Crouse JR, Grundy SM. Effects of alcohol on plasma lipoproteins and cholesterol and triglyceride metabolism in man. J Lipid Res.1984; 25:486–496.MedlineGoogle Scholar
    • 23 Taskinen MR, Nikkila EA, Valimaki M, et al. Alcohol-induced changes in serum lipoproteins and in their metabolism. Am Heart J. 1987;113(2 pt 2):458–464.Google Scholar
    • 24 Clevidence BA, Reichman ME, Judd JT, et al. Effects of alcohol consumption on lipoproteins of premenopausal women: a controlled diet study. Arterioscler Thromb Vasc Biol.1995; 15:179–184.CrossrefMedlineGoogle Scholar
    • 25 Ikewaki K, Zech LA, Kindt M, et al. Apolipoprotein A-II production rate is a major factor regulating the distribution of apolipoprotein A-I among HDL subclasses Lp A-I and A-II in normolipidemic humans. Arterioscler Thromb Vasc Biol.1995; 15:306–312.CrossrefMedlineGoogle Scholar
    • 26 Amarasuriya RN, Gupta AK, Civen M, et al. Ethanol stimulates apolipoprotein A-I secretion by human hepatocytes: implications for a mechanism for atherosclerosis protection. Metabolism.1992; 41:827–832.CrossrefMedlineGoogle Scholar
    • 27 Tam S-P. Effect of ethanol on lipoprotein secretion in two human hepatoma cell lines, HepG2 and Hep 3B. Alcohol Clin Exp Res.1992; 16:1021–1028.CrossrefMedlineGoogle Scholar
    • 28 Dashti N, Franklin FA, Abrahamson DR. Effect of ethanol on the synthesis and secretion of apo A-I and apo B-containing lipoproteins in HepG2 cells. J Lipid Res.1996; 37:810–824.MedlineGoogle Scholar
    • 29 Hojnacki JL, Cluette-Brown JE, Dawson M, et al. Alcohol delays clearance of lipoproteins from the circulation. Metabolism.1992; 41:1151–1153.CrossrefMedlineGoogle Scholar
    • 30 Contaldo F, D’Arrigo E, Carandente V, et al. Short-term effects of moderate alcohol consumption on lipid metabolism and energy balance in normal men. Metabolism.1989; 38:166–171.CrossrefMedlineGoogle Scholar
    • 31 Brinton EA, Eisenberg S, Breslow JL. Human HDL cholesterol levels are determined by apoA-I fractional catabolic rate, which correlates inversely with estimates of HDL particle size: effects of gender, hepatic and lipoprotein lipases, triglyceride and insulin levels, and body fat distribution. Arterioscler Thromb.1994; 14:707–720.CrossrefMedlineGoogle Scholar
    • 32 Wilson DE, Schreibman PH, Brewster AC, et al. The enhancement of alimentary lipemia by ethanol in man. J Lab Clin Med. 1970;75;264–274.Google Scholar
    • 33 Patsch JR, Karlin JB, Scott LW, et al. Inverse relationship between blood levels of high density lipoprotein subfraction 2 and magnitude of postprandial lipemia. Proc Natl Acad SciU S A.1983;80:1449–1453.Google Scholar


    By now the cardiovascular benefits of a daily glass of wine are well known. But many teetotalers wonder whether they can reap the same rewards from wine’s unfermented sibling, or are they simply left out altogether.

    Grape juice may not provide much buzz, but you can still toast to good health when it comes to its ability to avert heart disease. Alcohol in moderation can relax blood vessels and increase levels of HDL, the “good” cholesterol. But the substances believed to provide much of red wine’s heart benefits — resveratrol and flavonoids — are also found in grape juice, especially the variety made from red and dark purple Concord grapes.

    Image Credit…Leif Parsons

    Independent studies have found that like alcohol, grape juice can reduce the risk of blood clots and prevent LDL (“bad” cholesterol) from sticking to coronary arteries, among other cardiac benefits. One, conducted by scientists at the University of Wisconsin and published in the journal Circulation, looked at the effects of two servings of Concord grape juice a day in 15 people with coronary artery disease. After two weeks, the subjects had improved blood flow and reduced oxidation of LDL. Oxidized LDL can damage arteries.

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *