They function by reducing the effects of the fight-or-flight hormones on the heart. Many of these natural beta-blockers can also improve your overall heart health. Consider eating more of or supplementing with these natural options.

Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. VIEW ALL HISTORY. Beta-blockers are a type of medication that's traditionally used to treat heart conditions.

Sometimes, beta-blockers are prescribed for off-label use…. Beta-blockers are often prescribed for irregular heartbeats, high blood pressure, and after heart attacks. Learn more about how they work.

In a study of older adults living in long-term care, researchers randomly assigned facilities to use either a potassium-rich salt substitute or…. A recent study has found that tai chi was more effective compared to aerobic exercise in lowering blood pressure among prehypertension patients.

Portopulmonary hypertension is a progressive complication of high blood pressure in the veins that lead to your liver. Renal parenchymal disease is a group of conditions that can develop in the parts of your kidney that filter your urine and produce the hormone….

According to new research, adding salt at mealtime, using a salt shaker for example, is associated with an increased risk of developing kidney disease,. Baroreflex failure is a rare condition. People with this condition experience sharply rising blood pressure during exercise, pain, and stress, and can….

New research examined the benefits and differences between three types of medications used to treat high blood pressure. A Quiz for Teens Are You a Workaholic?

How Well Do You Sleep? Health Conditions Discover Plan Connect. Are There Natural Beta-Blockers? Medically reviewed by Jennie Olopaade, PharmD, RPH — By Eleesha Lockett, MS — Updated on June 13, Other supplements.

Are there risks to trying natural beta-blockers? The takeaway. How we reviewed this article: Sources. Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations.

We avoid using tertiary references. You can learn more about how we ensure our content is accurate and current by reading our editorial policy. Jun 13, Written By Eleesha Lockett, MS.

Apr 5, Medically Reviewed By Jennie Olopaade, PharmD, RPh. Share this article. Read this next. Can Beta-Blockers Help Your Anxiety? Medically reviewed by Lindsay Slowiczek, PharmD. Everything to Know About Beta-Blockers.

Medically reviewed by Alan Carter, Pharm. Want to Lower Your Blood Pressure? Tai Chi May Work Better Than Aerobics A recent study has found that tai chi was more effective compared to aerobic exercise in lowering blood pressure among prehypertension patients.

READ MORE. Overview of Portopulmonary Hypertension. Medically reviewed by Mia Armstrong, MD. Overview of Renal Parenchymal Disease. Medically reviewed by Avi Varma, MD, MPH, AAHIVS, FAAFP. Foods of animal origin provide most of the carnitine in American diets. A typical omnivorous diet provides about 24 to mg carnitine daily for a person weighing pounds.

In contrast, a vegan diet provides about 1. Endogenous carnitine synthesis does not appear to be affected by dietary carnitine intake or carnitine excretion and is sufficient to meet the carnitine needs of healthy people [ 1 ]. A person weighing lb who follows a strict vegetarian diet, for example, synthesizes approximately Carnitine status is not routinely assessed in clinical practice, but it can be determined by measuring circulating carnitine.

The ratio of acyl-L-carnitine ester to free L-carnitine can also be used to assess carnitine status because under normal conditions most carnitine is in the free unesterified form. A ratio of 0. Healthy children and adults do not need to consume carnitine from food or supplements because the liver and kidneys synthesize sufficient amounts to meet daily needs [ 10 , 11 , 12 ].

In , the Food and Nutrition Board FNB of the National Academies of Sciences, Engineering, and Medicine concluded that carnitine is not an essential nutrient [ 12 ]. Therefore, the FNB did not establish Dietary Reference Intakes DRIs for carnitine [ 13 ].

Carnitine is present in animal products, especially red meat [ 1 ]. Poultry, fish, and dairy foods also provide some carnitine, but vegetables, fruits, and grains provide negligible amounts [ 1 , 12 , 14 ].

The bioavailability of acetyl-L-carnitine has not been well studied [ 15 ]. Data on the carnitine content of specific foods are limited.

The U. Table 1 lists several foods and their approximate carnitine content per serving, based on several small studies. Carnitine is available in dietary supplements containing only carnitine or a combination of carnitine and other ingredients [ 17 ].

The two main forms of carnitine in dietary supplements are L-carnitine and acetyl-L-carnitine, and amounts range from about 3 mg to 5, mg [ 17 ]. Two types of carnitine deficiency states exist.

Primary carnitine deficiency is a genetic disorder of the cellular carnitine transporter system that causes a shortage of carnitine within cells. Primary carnitine deficiency usually presents during infancy or early childhood.

It can result in epilepsy and encephalopathy in infants; seizures, irregular heartbeat, and breathing problems in adolescents and young adults; and myopathy, rhabdomyolysis, cardiomyopathy, or sudden death in older people.

Although some individuals with primary carnitine deficiency do not have symptoms, all affected people have an increased risk of heart failure, hepatic disorders, and coma [ 18 ]. Secondary carnitine deficiency results from certain disorders such as chronic renal failure that reduce endogenous carnitine synthesis or increase its excretion or from chronic use of pivalate-containing medications that reduce carnitine absorption or increase its excretion [ 10 , 19 ].

Signs and symptoms of secondary carnitine deficiency include hyperammonemic encephalopathy malaise, seizures, and decreased consciousness caused by elevated ammonia levels , hypoglycemia, hypoketonemia low level of ketones in the blood , dicarboxylic aciduria increased concentrations of dicarboxylic acids in the urine , hyperuricemia excess uric acid in the blood , muscle weakness, myoglobinuria excess myoglobin in the urine , cardiomyopathy, and sudden death [ 20 ].

Babies born prematurely have high growth demands but have low carnitine stores and an inadequate ability to synthesize this nutrient [ 24 ]. Premature infants may require supplemental carnitine in addition to that supplied in breast milk and fortified infant formula [ 1 ]. Many enteral and parenteral formulas for premature infants are fortified with L-carnitine to improve lipid metabolism and promote weight gain [ 1 ].

However, a Cochrane Review of six randomized clinical trials in newborns requiring parenteral nutrition many of whom were premature did not support the use of parenteral carnitine to improve lipid utilization or weight gain [ 25 ].

Carnitine homeostasis in individuals with renal diseases can be impaired by reduced synthesis and increased elimination of carnitine by the kidneys. Renal diseases can also reduce carnitine intake from food because patients often have poor appetite and consume fewer animal products [ 20 ].

Many patients with end-stage renal disease, particularly those on hemodialysis, become carnitine insufficient. Low levels of carnitine in blood and muscle stores can contribute to anemia, muscle weakness, fatigue, altered levels of blood fats, and heart disorders.

Numerous studies suggest that high doses of supplemental carnitine often injected administered to patients on maintenance hemodialysis can correct some or all of these symptoms [ 26 ]. However, most of these studies had small numbers of participants and were not double-blind clinical trials.

The authors of a meta-analysis of these studies concluded that carnitine supplements might help patients manage their anemia but not their blood-lipid profiles, and that the effects of these supplements on exercise capacity and heart disorders were inconclusive [ 26 ].

Clinical and psychometric assessment scores were better, and improvements determined by clinicians were greater in supplement users than in the placebo groups [ 30 ].

In contrast, a Cochrane Review of 15 clinical trials including 13 of those in the meta-analysis described above had somewhat different findings [ 29 ]. The results showed that the supplementation decreased symptom severity at 12 and 24 weeks but not at 52 weeks.

Similarly, acetyl-L-carnitine supplements improved scores on the Mini Mental State Examination at 24 weeks but not at 12 or 52 weeks and had no effect on the severity of dementia, functional ability, or overall clinical global impression scores.

The authors of the Cochrane Review noted that results from studies conducted more recently were less positive than those from earlier studies; they concluded that the routine clinical use of acetyl-L-carnitine supplements to treat the signs and symptoms of dementia was not justified.

Carnitine plays a role in transporting long-chain fatty acids in the myocardial mitochondria, where they are metabolized via oxidation for energy. It is also involved in moderating oxidative stress [ 33 , 34 ] and might decrease markers of inflammation [ 35 ].

During ischemic events, carnitine prevents fatty acid ester accumulation, which can lead to fatal ventricular arrhythmias [ 34 ]. For these reasons, researchers are examining whether carnitine affects cardiovascular health.

Clinical trials examining the effects of carnitine supplements on CVD have had mixed results. A meta-analysis of 13 clinical trials included a total of 3, adults with acute myocardial infarction who took either L-carnitine from 2. The study found that L-carnitine significantly reduced rates of all-cause mortality, ventricular arrhythmias, and new-onset angina but did not affect risk of heart failure or myocardial reinfarction [ 34 , 36 ].

The carnitine dose and duration of the clinical trial did not appear to affect outcomes. These benefits did not vary by supplement dose or study duration. However, L-carnitine did not affect rates of all-cause mortality or performance on a timed walking test.

Other research has raised concerns about the negative cardiovascular effects of chronic exposure to carnitine. A study that included 2, adults age 54—71 years undergoing elective cardiac evaluation found that L-carnitine is metabolized by intestinal microbiota to trimethylamine-N-oxide TMAO , a proatherogenic substance that is associated with increased CVD risk [ 38 ].

Because of differences in intestinal bacteria composition, omnivorous study participants produced more TMAO than vegans or vegetarians after consumption of L-carnitine.

The study also found dose-dependent associations between fasting plasma L-carnitine concentrations and risk of coronary artery disease, peripheral artery disease, and CVD, but only in participants with concurrently high TMAO levels. A clinical trial also found potentially deleterious outcomes in individuals age 58 to 75 years with metabolic syndrome who received 1 g supplemental L-carnitine or placebo twice a day for 6 months [ 39 ].

Although the results showed no differences in total plaque volume between groups, total cholesterol and low-density lipoprotein cholesterol levels were higher in participants taking L-carnitine.

L-carnitine supplementation was also associated with 9. Peripheral artery disease is a vascular disorder usually caused by atherosclerosis and its resulting arterial stenosis and occlusion. It is prevalent among older adults, although it is often underdiagnosed [ 40 , 41 ].

Researchers have examined whether propionyl-L-carnitine, an acyl derivative of L-carnitine, mitigates the cramping leg pain of intermittent claudication, the main symptom of peripheral artery disease, but findings from studies have been mixed. In one trial, participants supplemented with propionyl-L-carnitine had improved peak walking times walking until pain could not be tolerated , self-reported improvements in walking distance and speed, and decreased pain.

The other two trials showed no benefit of propionyl-L-carnitine on peak walking time compared with placebo. Insulin resistance plays an important role in the development of type 2 diabetes. Because insulin resistance may be associated with mitochondrial dysfunction and a defect in fatty-acid oxidation in muscle [ 43 , 44 , 45 , 46 ], carnitine supplementation has been studied for its possible effects on insulin resistance and diabetes.

A meta-analysis of 41 randomized clinical trials examined the effects of L-carnitine supplementation on glycemic markers in 2, men and women age 18 years and older [ 47 ].

Most participants had health conditions such as type 2 diabetes, obesity, polycystic ovary syndrome, or nonalcoholic fatty liver disease. L-carnitine supplements at doses of 0. Other meta-analyses have had a narrower focus, examining only studies in specific populations.

The L-carnitine improved measures of insulin resistance, and the benefits at 12 months exceeded those at 3 months. A systematic review and meta-analysis of four randomized clinical trials all of which were included in the meta-analysis described above with a total of adults with type 2 diabetes compared the metabolic effects of L-carnitine with those of placebo [ 44 ].

Additional clinical trials with larger samples are needed to determine whether L-carnitine supplements can reduce the risk of diabetes or the severity of its clinical manifestations. Carnitine might play a role in sperm maturation, sperm motility, and spermatogenesis [ 49 ].

It might also reduce oxidative stress, which could improve oocyte growth and maturation [ 50 ]. Therefore, researchers are examining whether supplemental carnitine improves sperm count, concentration, and motility as well as pregnancy rates.

Carnitine also helps transport some toxic compounds out of the mitochondria [ 4 ]. Carnitine is concentrated in tissues that oxidize fatty acids as a dietary fuel [ 1 , 5 ]. Most of the remainder is stored in the liver and kidney, and circulating plasma contains only about 0.

Excess plasma carnitine is excreted in urine [ 6 ]. Foods of animal origin provide most of the carnitine in American diets. A typical omnivorous diet provides about 24 to mg carnitine daily for a person weighing pounds. In contrast, a vegan diet provides about 1.

Endogenous carnitine synthesis does not appear to be affected by dietary carnitine intake or carnitine excretion and is sufficient to meet the carnitine needs of healthy people [ 1 ]. A person weighing lb who follows a strict vegetarian diet, for example, synthesizes approximately Carnitine status is not routinely assessed in clinical practice, but it can be determined by measuring circulating carnitine.

The ratio of acyl-L-carnitine ester to free L-carnitine can also be used to assess carnitine status because under normal conditions most carnitine is in the free unesterified form. A ratio of 0. Healthy children and adults do not need to consume carnitine from food or supplements because the liver and kidneys synthesize sufficient amounts to meet daily needs [ 10 , 11 , 12 ].

In , the Food and Nutrition Board FNB of the National Academies of Sciences, Engineering, and Medicine concluded that carnitine is not an essential nutrient [ 12 ]. Therefore, the FNB did not establish Dietary Reference Intakes DRIs for carnitine [ 13 ]. Carnitine is present in animal products, especially red meat [ 1 ].

Poultry, fish, and dairy foods also provide some carnitine, but vegetables, fruits, and grains provide negligible amounts [ 1 , 12 , 14 ].

The bioavailability of acetyl-L-carnitine has not been well studied [ 15 ]. Data on the carnitine content of specific foods are limited.

The U. Table 1 lists several foods and their approximate carnitine content per serving, based on several small studies. Carnitine is available in dietary supplements containing only carnitine or a combination of carnitine and other ingredients [ 17 ].

The two main forms of carnitine in dietary supplements are L-carnitine and acetyl-L-carnitine, and amounts range from about 3 mg to 5, mg [ 17 ]. Two types of carnitine deficiency states exist. Primary carnitine deficiency is a genetic disorder of the cellular carnitine transporter system that causes a shortage of carnitine within cells.

Primary carnitine deficiency usually presents during infancy or early childhood. It can result in epilepsy and encephalopathy in infants; seizures, irregular heartbeat, and breathing problems in adolescents and young adults; and myopathy, rhabdomyolysis, cardiomyopathy, or sudden death in older people.

Although some individuals with primary carnitine deficiency do not have symptoms, all affected people have an increased risk of heart failure, hepatic disorders, and coma [ 18 ].

Secondary carnitine deficiency results from certain disorders such as chronic renal failure that reduce endogenous carnitine synthesis or increase its excretion or from chronic use of pivalate-containing medications that reduce carnitine absorption or increase its excretion [ 10 , 19 ].

Signs and symptoms of secondary carnitine deficiency include hyperammonemic encephalopathy malaise, seizures, and decreased consciousness caused by elevated ammonia levels , hypoglycemia, hypoketonemia low level of ketones in the blood , dicarboxylic aciduria increased concentrations of dicarboxylic acids in the urine , hyperuricemia excess uric acid in the blood , muscle weakness, myoglobinuria excess myoglobin in the urine , cardiomyopathy, and sudden death [ 20 ].

Babies born prematurely have high growth demands but have low carnitine stores and an inadequate ability to synthesize this nutrient [ 24 ]. Premature infants may require supplemental carnitine in addition to that supplied in breast milk and fortified infant formula [ 1 ].

Many enteral and parenteral formulas for premature infants are fortified with L-carnitine to improve lipid metabolism and promote weight gain [ 1 ]. However, a Cochrane Review of six randomized clinical trials in newborns requiring parenteral nutrition many of whom were premature did not support the use of parenteral carnitine to improve lipid utilization or weight gain [ 25 ].

Carnitine homeostasis in individuals with renal diseases can be impaired by reduced synthesis and increased elimination of carnitine by the kidneys. Renal diseases can also reduce carnitine intake from food because patients often have poor appetite and consume fewer animal products [ 20 ].

Many patients with end-stage renal disease, particularly those on hemodialysis, become carnitine insufficient. Low levels of carnitine in blood and muscle stores can contribute to anemia, muscle weakness, fatigue, altered levels of blood fats, and heart disorders.

Numerous studies suggest that high doses of supplemental carnitine often injected administered to patients on maintenance hemodialysis can correct some or all of these symptoms [ 26 ]. However, most of these studies had small numbers of participants and were not double-blind clinical trials.

The authors of a meta-analysis of these studies concluded that carnitine supplements might help patients manage their anemia but not their blood-lipid profiles, and that the effects of these supplements on exercise capacity and heart disorders were inconclusive [ 26 ].

Clinical and psychometric assessment scores were better, and improvements determined by clinicians were greater in supplement users than in the placebo groups [ 30 ].

In contrast, a Cochrane Review of 15 clinical trials including 13 of those in the meta-analysis described above had somewhat different findings [ 29 ]. The results showed that the supplementation decreased symptom severity at 12 and 24 weeks but not at 52 weeks.

Similarly, acetyl-L-carnitine supplements improved scores on the Mini Mental State Examination at 24 weeks but not at 12 or 52 weeks and had no effect on the severity of dementia, functional ability, or overall clinical global impression scores. The authors of the Cochrane Review noted that results from studies conducted more recently were less positive than those from earlier studies; they concluded that the routine clinical use of acetyl-L-carnitine supplements to treat the signs and symptoms of dementia was not justified.

Carnitine plays a role in transporting long-chain fatty acids in the myocardial mitochondria, where they are metabolized via oxidation for energy. It is also involved in moderating oxidative stress [ 33 , 34 ] and might decrease markers of inflammation [ 35 ].

During ischemic events, carnitine prevents fatty acid ester accumulation, which can lead to fatal ventricular arrhythmias [ 34 ].

For these reasons, researchers are examining whether carnitine affects cardiovascular health. Fortified foods, including some brands of eggs, yogurt, juices, milk, soy drinks, and infant formulas, may also have omega-3s.

To say that taking a fish oil pill will cure all of your ailments, or even cure all of your heart-related ailments, is a stretch. Preventive care — including regular check-ups, a healthy diet, and exercise— is your best bet.

But when it comes to dietary supplements, omega-3s have the potential to lower risk of heart disease, though supplementation has not yet been shown to do so in any population other than individuals who have had recent cardiovascular events. As with any supplement, you should also be aware that they are not regulated by the Food and Drug Administration and may contain toxins such as mercury and unwanted ingredients such as saturated fatty acids.

The Penn Heart and Vascular blog provides the latest information on heart disease prevention, nutrition and breakthroughs in cardiovascular care. The Truth About Fish Oil, Omega-3 Fatty Acids, and Heart Health May 24, Topics: Fitness and Nutrition Preventive Heart Care.

Request an Appointment. Gum Disease and Heart Disease ICDs and Pacemakers. About this Blog The Penn Heart and Vascular blog provides the latest information on heart disease prevention, nutrition and breakthroughs in cardiovascular care.

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Find a Program or Service. Public or penny scales became available in the s, and private bathroom scales were available from Insurance companies also participated in the quantitative approach with their ideal and desirable weight charts, introduced in , reissued with lower weights in , then periodically thereafter—until replaced in the s by the Body-Mass Index BMI as the table of choice.

As the cult of youth became a national imperative later in the century, the idea of a lifelong stable weight, supported by statistical and medical research, gained more credence.

Bodies should not get heavier with age, and hence men and women of all ages should weigh the same as they had at eighteen or twenty-five. This notion of weight stability is, however, contested.

Statisticians at the U. Centers for Disease Control and Prevention CDC have recently challenged this idea, providing data to show that being slightly overweight is health-promoting, especially in older people.

The main point here is that the low-fat diet for weight reduction was already well in place before physicians and scientists began promoting it for cardiovascular health in the s. The low-fat diet was part of our dieting tradition before the ideology of low fat conquered America.

But until the s, the low-fat approach did not rise to the level of an ideology—the faith-inspiring and widely accepted notion that a low-fat diet was good for all Americans. A century-long preference for slim bodies and the well-entrenched practice of reducing weight by using a low-calorie, low-fat diet explains how the ground was already prepared for the widespread acceptance of the diet-heart hypothesis introduced shortly after mid century.

Yet, even though Americans were familiar with the low-fat, low-calorie diet, and some Americans followed it for weight reduction purposes, at mid century the typical middle-class American did not eat a low-fat diet. Rather there was more emphasis on meat, less on fruits and vegetables.

Even before the era of fast food dating from the s, Americans were consuming high-fat all-American favorites, such as meat stews, creamed tuna, meat loaf, corned beef and cabbage, mashed potatoes with butter, breaded and fried veal cutlets, deep-fried vegetables, French fries, lamb chops, liver, cheesecake, butter, and whole milk.

Americans preferred marbled beef from cattle that were grain—not grass—fed, not free-ranging but fattened up in feed lots to produce tender, succulent, high-fat meat. In the South at mid century, popular foods included greens and beans with ham hocks, fried chicken, country ham, biscuits and cornbread with butter or gravy, sausages, and sausage gravy.

Desserts were a staple, including homemade pies of all sorts, ranging from fruit to chocolate, banana cream, coconut, and pecan. Barone grew up with values shared by many Americans that predisposed her to a certain kind of fat-promoting eating.

The quality of produce available in supermarkets was uniformly low, a situation that explained the preference for canned fruit and vegetables. By contrast, the quality of desserts was high: homemade cakes, pies, and cookies abounded.

Within the context of a regionally diverse American diet, popular attitudes toward food, and technological changes, medical researchers began by the late s to recommend the low-fat diet. But by the s, the preaching of the low-fat diet began to be directed to all Americans as a general preventive measure.

In the s, coronary heart disease was the leading cause of death in the United States. Scientists and physicians sought to identify the causes of heart disease in an effort to promote preventive measures. to localized studies, both in the United States and abroad, suggested a strong correlation between diets high in saturated fats and cholesterol and increased incidence of cardiovascular disease.

In short, the diet-heart hypothesis held that diets high in saturated fats and cholesterol were a major cause of coronary heart disease.

In the s, Keys and others promoted a low-fat diet—a special variety of which Keys labeled the Mediterranean diet—with less meat, more grains, vegetables, fruits, and some olive oil. The AHA did not recommend a low-fat diet for all. Subscribing to low fat in the s and s was in fact a modest proposal.

This report was important because it also singled out overweight Americans as a group that should lower the fat content of the diet as a way of reducing calories.

Daniel Levy, current director of the Framingham Heart Study, maintains that in spite of the AHA's recommendations, there was no sense of national urgency concerning the relationship of dietary fat to heart disease until That year, the U.

Dietary Guidelines. For the first time, the federal government told Americans to eat more fruits, vegetables, whole grains, poultry, and fish, to eat fewer high-fat foods, and to substitute nonfat for whole milk. Even though many diet-heart studies focused on high-risk patients, and although the proposed massive Diet-Heart study of the late s and the early s was abandoned for lack of money and methodological problems, a host of scientific studies supported the low-fat approach.

By , the scientific consensus was that the low-fat diet was appropriate not only for high-risk patients, but also as a preventive measure for everyone except babies. From through the s, dietary fat was increasingly blamed not only for coronary heart disease but also for overweight and obesity.

Although some scientists and physicians remained unconvinced by the data, the argument in favor of the low-fat diet for all carried the day, following the recommendations of the Consensus Report. Here was a chance for the food industry to profit from scientific research and for Americans to participate in the reigning health crusade.

government has been telling people what to eat for more than a century…. This history of federal involvement in the American diet is essential for understanding how low fat conquered America in the s and s. The United States Department of Agriculture USDA , established in , had two main duties: to ensure a sufficient and reliable food supply and to provide information on subjects related to agriculture, the latter charge being interpreted to mean making dietary advice available to citizens.

In , the agency laid out five basic food groups: fruits and vegetables, meats and other protein foods, cereals and other starchy foods, sweets, and fatty foods. In , the Food and Nutrition Board of the U. Academy of Sciences introduced Recommended Daily Allowances, or RDAs, and from the department has produced revised versions at regular intervals.

In , the Senate appointed George McGovern to chair a Select Committee on Nutrition and Human Needs mandated to look into the problem of hunger in America. This committee, which met until , was instrumental in the federal government's promotion of low-fat diets.

During the nine years of hearings, the committee's focus shifted from its initial emphasis on hunger and the poor to chronic disease and diet. Committee members became convinced that Americans were not only eating too much, but were also eating the wrong foods.

The committee's work culminated in its early report, Dietary Goals for the United States , which promoted increased carbohydrate and reduced fat consumption along with less sugar and salt. The report recommended that Americans eat more fruits, vegetables, whole grains, poultry, and fish, less meat, eggs, and high-fat foods, and that they substitute nonfat for whole milk.

Critics, both scientific and industrial, called the diet-heart hypothesis unproved and the dietary recommendations disputable. Under pressure from many constituencies, but especially the food industry, the committee revised and reissued its report later in the year.

With the publication of the Dietary Goals , the federal government officially supported the low-fat approach. In —79, the American Society of Clinical Nutritionists, the AHA, and the National Cancer Institute fell in line with their own low-fat recommendations. By , a scientific consensus was emerging that a low-fat diet was needed to prevent the two leading causes of death, coronary heart disease and cancer.

Federal government support for low fat continued with each official government publication from the Surgeon General's Healthy People to the Dietary Guidelines for Americans , first issued in and every five years thereafter a joint effort of the Department of Health and Human Services HHS and the USDA.

Thus, by the s, in spite of protests from the food industry and skeptical scientists, federal agencies forged a consensus on dietary advice at the same time that a growing scientific consensus advocated low fat for everyone.

By the end of the decade, both the controversial Surgeon General's Report on Nutrition and Health and the World Health Organization WHO were promoting low fat. Although the food industry had initially worried about the low-fat approach, by the s food producers had begun to realize that low fat could provide profit-making opportunities.

In , after much controversy and negotiation, the USDA released its first and long-awaited food pyramid that lent full support to the ideology of low fat. Wide press coverage gave the pyramid much publicity, and it quickly became an icon.

Food companies would pay to label their foods with the AHA seal of approval. By , endorsed food products started to appear in grocery stores, but there was a problem: fresh foods were not labeled. This exclusion could suggest to consumers that processed foods were the heart-healthiest.

Following protests, the AHA withdrew the program, but reinstated it in By , fifty-five companies were participating with over products certified, many of which were cereal products, including Kellogg's Frosted Flakes, Fruity Marshmallow Krispies, and Low-Fat Pop-Tarts.

Supermarket chicken with AHA Seal of Approval. Four ounces contain mg of sodium. Approving meats injected with salt seems to be at odds with the AHA's long-standing efforts to reduce hypertension. Some hyptertensives are known to be salt-sensitive. Photo taken by me in Blacksburg, Virginia, summer Was low fat the only thing that mattered for good health?

Had the ideology of low-fat taken such a hold that that sugar-laden refined processed foods qualified for AHA approval as heart-healthy? No wonder consumers were confused and assumed that low fat was what really counted in terms of health.

It was possible to think that if a food were low fat, one could eat to appetite. We begin to see how a profusion of products low in fat but high in sugar and calories might ironically promote the fattening of America, even while being labeled heart-healthy.

The tradition of low-calorie, low-fat diets, and scientific and federal promotion of low fat could not have conquered America without the participation of the popular press. Two popular health sources, namely, Prevention magazine f.

Both have subscribed to and promoted the low-fat diet since the s. One of the main contributions of popular magazines, such as Prevention , the Ladies' Home Journal , and Family Circle , was to include numerous advertisements for low-fat foods, one of the main ways American women learned about low-fat products.

Prevention promoted the low-fat diet for both heart health and weight reduction in the s and s. Jane Brody, personal health columnist for The New York Times since , whose articles have appeared in at least other American newspapers, also promoted the low-fat diet for heart health and weight loss, following the USDA Federal Dietary Guidelines.

The attack on dietary fat and cholesterol dominated the s, as scientific studies implicated the American diet as a major cause of coronary heart disease. The first step in the program was the low-fat diet.

Scientific studies suggested that those who ate foods low in animal fat and cholesterol had less cholesterol in their blood. Yet, there was no proof that a low-fat diet would reduce heart disease. Dean Ornish had shown that lifestyle changes could halt or reverse atherosclerosis.

Participants in his program reversed atherosclerosis, and cholesterol levels fell from an average of to , with low-density lipoproteins LDL reduced from to Even though Ornish's study involved only twelve participants, his results buttressed the dominant scientific belief that a low-fat diet could prevent, and might even reverse, heart disease.

Scientists wondered if all Americans should try to lower their cholesterol levels. But were these goals appropriate for all Americans? Another consideration was that studies up to then had been done only on middle-aged men, the group most afflicted by heart disease.

Scientists had studied neither women nor the elderly in clinical trials of cholesterol reduction. Thus, the AHA, the AMA, and experts at the NIH and the NHLBI endorsed not only the general program to lower cholesterol, but also the low-fat diet as the way to do it.

Two studies helped scientists begin to answer the question concerning the general applicability of the low-fat diet as the way to lower cholesterol. The second attributed lower death rates to drug-induced cholesterol reduction.

Scientists interpreted these findings to mean that lowering cholesterol levels by any means had clear benefits for preventing heart attacks. But the studies did not show that lowering cholesterol levels increased longevity, and so long-term outcomes remained unclear.

Throughout the s and s, Prevention 's dominant diet recommendation was the low-fat, high complex-carbohydrate diet, labeled the Prevention diet. This long-standing association of low fat with low calorie would soon be upended, however, as the food industry flooded the market with low-fat—but fattening—foods.

In many of these foods, sugar replaced fat so that low fat became high calorie. The early s saw a move from low fat to no fat on the part of some popular health writers. Reflecting the influence of the Ornish studies, the message presented in Prevention in the early s in editorials, columns, and ads was that if low fat was good, no fat was better.

In December , Editor Mark Bricklin introduced a new generation of nonfat foods. The nonfat cookies were a prime example of how, according to some scientists and science writers, low fat made Americans fatter. The low-fat diet reigned supreme in the late s, as scientists, the federal government, and popular health writers declared the low-fat, high-carbohydrate diet the gold standard for heart health and weight control.

Prevention writers warned of the dangers of the popular high-protein diets, even while acknowledging that people overdid the low-fat, high-carbohydrate foods.

It seemed that too many Americans thought they could eat as much as they wanted as long as it was low or no fat. They had followed the advice to count fat grams and not calories—with the result that some had gotten fat on low and no-fat foods.

Researchers studied diets in countries where heart disease and obesity were rare to see if Americans could learn from other cultures. Subscribing to a universalizing model, they assumed that all human bodies functioned in the same way.

The idea was that we could observe what other people ate, for example, the Chinese or the Japanese, see what effect their diets had on heart health and weight, and then, if need be, emulate them.

Investigators reasoned that if a diet worked for the Japanese or the Chinese, it should also work for Americans. Nutritional researchers gathered interesting data from these two Asian diets, leading them to suggest that Americans ate too much fat and protein to the neglect of vegetables.

A healthier diet would be vegetable based, with only modest amounts of fat and animal protein. But sometimes they departed from this dominant positivistic position.

Brody, for example, recognized sex differences in her discussion of how women's pattern of heart disease differed from that of men.

In the early s, scientists found that males and females experienced heart disease differently. She reported on a study of , older adults that had found that losing weight had no effect on life span. Although weight loss helped individuals manage diabetes and hypertension, the study found that obesity—and this term was not spelled out in the study—had few effects on mortality as people aged.

By the age of seventy-four, there was no relationship between being obese and a higher risk of dying. A major challenge to the use of diet as a way to reduce weight came from set-point theory. In the early s, Brody began to question the low-fat dogma on these grounds.

According to set-point theory, each person's weight has a fairly stable set point that resists gain or loss of weight. Although the set point may change with age and in some people can be overridden, the set point means that permanent weight loss is extremely demanding—if not impossible—for many people.

Drawing on scientific studies, she explained that it was not clear that people could lose weight and keep it off. In a break with her long-standing recommendation of the low-fat diet, she called for an individualized approach, suggesting that a one-size-fits-all diet might not be the most effective for all.

She had not lost faith in the low-fat diet, but as scientists continued to complicate the issues involved in weight loss and maintenance, Brody and others began to moderate their low-fat-for-all message. Increasing knowledge of dietary fats also complicated the low-fat agenda.

Again, Brody's solution was a low-fat diet for both heart health and weight loss. Meanwhile, challenges to low fat diet for heart disease prevention came from two other fronts: success with drug therapy and scientific dissent about the efficacy of the diet for heart health.

In the s, statins' ability to reduce cholesterol levels suggested that drugs might be more effective than diet, thus challenging the hegemony of the low-fat diet as a recommendation for heart health.

The statins—with four on the market by —promised to change the emphasis on the low-fat diet as the major therapy for cholesterol reduction. Although statins, available since , had been shown to lower cholesterol, until the mids, it was not clear that they saved lives.

But in , a scientific study showed that Merck's simvastatin not only reduced the risk of coronary heart disease, but also saved lives. Kolata suggested that this finding would encourage more aggressive drug treatment of high cholesterol in patients at risk for coronary heart disease and could result in a major change in medical practice.

As far back as the s, a minority of scientists and popular health writers had questioned the low-fat diet. Some scientists had argued that it was the kind of fats—not the total amount—that mattered. This skepticism emerged full-blown in the s. He explained that because the scientific community had recommended the diet, people assumed there was proof that the diet worked, even though there was none.

One leading obesity researcher, Dr. Jules Hirsch, physician-in-chief at Rockefeller University and one of the principal contributors to the notion of set-point theory, raised a different challenge.

Willett noted that substituting carbohydrates for fats could reduce high-density lipoproteins HDL levels while raising triglyceride levels. With such challenges, could the ideology of low fat maintain its position of authority? Responding to these critiques, Brody began to modify her recommendations.

This diet was high in monounsaturated fat, but low in saturated fat, emphasizing beans, grain, vegetables and fruits, small amounts of yogurt and cheese, fish, eggs, poultry, and a little red meat. At the end of the decade, Kolata wrote about the low-fat diet for heart disease prevention and therapy, noting that there was no longer scientific consensus on the heart-healthiest diet.

Although the official recommendation since the s had been that carbohydrates replace fats in the diet, some scientists disagreed.

Willett, for example, consistently argued that it was not total fats that mattered, but the type of fat. He recommended that Americans forget low-fat diets and embrace good fats such as olive oil and nuts. At the same time, the Atkins diet resurfaced, generating renewed interest in this high-protein, high-fat, low-carbohydrate diet, with over five million copies of the paperback edition in print.

The Atkins diet had become a national phenomenon in the s, with ten million copies of Dr. Atkins Diet Revolution sold. Brody dismissed the diet, noting that no long-term studies had been done and arguing that much of the initial weight loss was water.

She suggested that as the diet became boring and unpalatable, dieters consumed fewer calories—and lost weight. Brody opposed this diet, reporting that with sensible eating and regular exercise she had lost thirty-five pounds.

Her success convinced her that willpower and a low-calorie approach, along with exercise, could produce weight loss and maintenance. Eat more calories than your body uses and you will gain weight.

Eat fewer calories and you will lose weight. The body, which is, after all, nothing more than a biochemical machine [my emphasis], knows no other arithmetic. Simple carbohydrates, much loved by Americans, were at fault, Atkins maintained: white flour, sugar, and potato products, those de-fatted processed products that had fattened America.

By the end of the century, Brody was moderating her low-fat position to declare that fat can be a friend! Scientific studies had vindicated some fats, showing that avocados, walnuts, salad dressings with oil, sautéed vegetables, fatty fish, and some margarine were heart-healthy.

Recounting the history of low-fat diet advice, Brody noted a major shift within the scientific community. Following the findings of Willett and others, scientists were now claiming that it was not the total amount of fat but the kind of fat that mattered.

Brody was converting to this point of view. The key to heart health now seemed to be reducing saturated and trans fats hydrogenated plant fat , but not all fats. Ignoring scientific studies that supported set-point theory, she argued that if low fat was not the answer to weight loss, we must count calories and exercise.

The twenty-first century ushered in new enemies and new approaches. Prevention readers were advised that if they wanted to be thin, they must cut out sugar and manage stress.

Scientists showed that stress-induced cortisol promoted abdominal fat—declared the most dangerous kind of fat. The index offered a scientific way for readers to choose healthful carbohydrates that proponents maintained would not promote weight gain.

In the new millennium, there was little agreement on which diet was the best either for heart disease prevention or weight reduction. It makes no difference if these calories are in fats or vegetables or cake or ice cream. Change was at hand on the diet front.

In a breakthrough article , Brody moved away from the one-size-fits-all low-fat diet that she had promoted with a religious fervor for more than twenty years to suggest that perhaps different diets worked for different people.

Addressing the widespread confusion about fat and fats, she noted that no consensus existed among experts. She proposed that a one-size-fits-all approach no longer worked in a society as ethnically and culturally diverse as ours.

It was becoming more and more apparent that the public health message promoting the low-fat diet had had unintended consequences: it had led some people to adopt an unhealthy diet—just as long as it was low fat.

Writing about the high-fat, low-fat controversy in , Brody emphasized the importance of a balanced diet. She pointed out that after three decades of popularity of the Atkins diet, scientists had still not tested it for long-term safety and effectiveness. She argued that the high-protein diet attracted those who failed on the low-fat diet.

Brody maintained that it was not low fat that was fattening Americans, but more calories. Americans were eating on average calories more per day, and they had not reduced their fat consumption—if one used the higher total calorie count to figure percentages. Brody reiterated that it was just calories that mattered—no matter what kind.

The Mediterranean diet found new followers as critics challenged the low-fat diet in the face of what many scientists and physicians were calling an obesity epidemic.

Low-fat proponents had not foreseen that Americans would overindulge in refined low-fat carbohydrates. One of the unanticipated consequences of industrial food technology was the ability of the food industry to flood the market with highly processed low-fat—but fattening—foods.

They argued that substituting refined carbohydrates for fats was not the answer, explaining that refined carbohydrates—whether low fat or not—raise triglyceride levels and lower both good and bad cholesterol. They maintained that there was no evidence from clinical trials to show that reducing dietary fat would by itself lead to weight loss.

Rather, ignoring set-point theory, they maintained that it was too many calories and too little physical exercise that led to weight gain.

So, by , the most recent research challenged the low-fat ideology that had held sway for so long, but at least some research affirmed Brody and Kolata's position that what counted was calories consumed and energy expended. Finally, in , the results of long-term studies on low-carbohydrate, high-protein, high-fat diets, such as Atkins, were published.

But it turned out that many people who succeeded on the diet were vindicated. People lost weight—and for many for whom low-fat or low-calorie diets had not worked, it was the first time they had lost weight. So what if the first 5—7 pounds were water?

Many lost far more than this. The studies found that, contrary to expectations, the diet did not damage heart and blood vessels; in fact, in some patients readings improved.

As proponents had claimed, cholesterol levels did not rise, triglyceride levels fell, and HDLs improved. At the end of a year, however, both the low-fat and the low-carbohydrate diets produced about the same results in terms of weight loss.

This was the same argument opponents of the low-fat diet had used when they argued that the fattening of America coincided with the decades in which the low-fat diet reigned as nutritional orthodoxy. After explaining why some people lost weight on the Atkins diet, Brody reiterated that it was only calories that mattered.

Both the writers for Prevention and the science writers for The New York Times carefully reported on scientific studies.

They reflected a great faith in the validity of the studies and the value of reporting them to the wider public. They were not reluctant, however, to include their own point of view, comparing and interpreting these studies for readers.

These writers reflect the larger American—journalistic—faith in science during these years before many questions were raised concerning the reliability of such clinical, epidemiological, and laboratory studies.

The popular media, in short, played a pivotal role in preaching the low-fat message, and, then, in more recent years, in questioning it. Several developments that came together in the s and s help explain how the ideology of low fat conquered America in those decades.

The dietary context was an established tradition of low-calorie, low-fat dieting for weight reduction that predisposed Americans to accept what was promoted as a heart-healthy diet. A plethora of diet-heart studies carried out by scientists and physicians suggested that a low-fat diet might prevent heart disease.

These studies drew on research that had been done from the s through the s. By the late s, the federal government started promoting the low-fat diet, and shortly thereafter the food industry began to make low-fat products available and to advertise them widely.

The second one is Meridia as the brand name, or sibutramine. It can increase blood pressure. So for people who already have heart disease , they should not use this product. And blood pressure needs to be monitored carefully with the use of this product. Election We'll notify you here with news about.

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By Becky Upham. Fact Checked. Caffeine can help you burn fat by boosting your metabolism and helping you burn more fat as fuel. You can get caffeine from natural sources like coffee and green tea. Green tea extract is simply a concentrated form of green tea.

Green tea extract is also rich in caffeine and the polyphenol epigallocatechin gallate EGCG , both of which are compounds that can help you burn fat 12 , In addition, these two compounds complement each other and can help you burn fat through a process called thermogenesis. In simple terms, thermogenesis is a process in which your body burns calories to produce heat 14 , 15 , In another study, scientists compared the effects of a placebo, caffeine, and a combination of green tea extract and caffeine on burning fat.

They discovered that the combination of green tea and caffeine burned roughly 65 more calories per day than caffeine alone and 80 more calories than the placebo Keep in mind that in these studies the participants took green tea extract in combination with additional caffeine.

Therefore, this does not definitively show that green tea extract alone has these same effects. Studies have shown that while no detrimental effects have been reported from green tea itself, the excess consumption of green tea extract may prove to be harmful to the liver, particularly if taken on an empty stomach.

Do not exceed the recommended dosage Green tea extract is simply concentrated green tea. It contains epigallocatechin gallate EGCG and caffeine, which can help you burn fat through thermogenesis.

Protein is incredibly important for burning fat. A high protein intake can help you burn fat by boosting your metabolism and curbing your appetite. It also helps your body preserve muscle mass 20 , 21 , For instance, a study involving 60 participants with overweight and obesity found that a high protein diet was almost twice as effective as a moderate protein diet at burning fat Protein can also curb your appetite by increasing the levels of fullness hormones like GLP-1, CCK, and PYY while reducing levels of the hunger hormone ghrelin 20 , While you can get all the protein you need from protein-rich foods, many people still find it challenging to eat enough protein daily.

Options include whey, casein, soy, egg, and hemp protein powders. Keep in mind that calories are still important. Protein supplements should simply replace snacks or part of a meal, rather than be added on top of your diet. The recommended daily intake of protein will vary based on your activity levels, age, sex, weight, height, etc.

That said, the Recommended Dietary Allowance RDA for protein is 0. Protein supplements are a convenient way to increase your protein intake. There are two different types of fiber : soluble and insoluble.

Soluble fiber absorbs water in your digestive tract and forms a viscous gel-like substance Interestingly, studies have shown that soluble fiber can help you burn fat by curbing your appetite 26 , 27 , It can also help reduce levels of the hunger hormone ghrelin 26 , 27 , In addition, soluble fiber helps slow down the delivery of nutrients to the gut.

When this happens, your body takes more time to digest and absorb nutrients, which can leave you feeling full for longer While you can get all the soluble fiber you need from food, many people find this challenging.

Soluble fiber supplements can help you burn fat by curbing your appetite and possibly reducing how many calories you absorb from food. Some great soluble fiber supplements include glucomannan and psyllium husk.

Yohimbine is a substance found in the bark of Pausinystalia yohimbe , a tree found in Central and Western Africa. These receptors normally bind adrenaline to suppress its effects, one of which is encouraging the body to burn fat for fuel.

A study involving 20 elite soccer players found that taking 10 mg of yohimbine twice daily helped them shed 2. Keep in mind that these athletes were already quite lean, so a 2.

Further research is needed on the long-term effects of yohimbine. Nonetheless, more information is needed on yohimbine before it can be recommended as a go-to fat-burning supplement.