Functions of Insulin in the Body: Good Guy or Bad Guy?

The functions of insulin in the body are widely misunderstood. In this article, we will explore the actions of insulin on a cellular level to gain a better appreciation for all it does as well as a clearer understanding of how to keep this hormone functioning in balance and at its optimal capacity.

Insulin is perhaps the most important compound circulating in our bodies. It is involved in more than 60 key biological processes. Impairments in insulin function affect many facets of health and well-being and, if left uncorrected, are ultimately fatal. Despite its paramount importance, the functions of insulin in the body are widely misunderstood.

Insulin is an anabolic hormone, meaning it acts to promote synthesis and building, as opposed to catabolic hormones that break down and deconstruct bodily tissues and compounds. Given its vital importance, it is curious that insulin is sometimes portrayed as the bad guy. Consider, for instance, how we cast insulin as the villain responsible for the development of adverse health conditions: type 1 and type 2 diabetes, metabolic syndrome, polycystic ovary syndrome, and even certain types of cancer.

In this article, we will explore the basic functions of insulin in the body to gain a better appreciation for all it does as well as a clearer understanding of how to keep this hormone functioning in balance and at its optimal capacity.

What Is Insulin?

In technical terms, insulin is a peptide hormone produced by pancreatic beta cells located in the islets of Langerhans. As touched on in the introduction, insulin is the primary anabolic hormone found in the human body.

It governs the metabolic processes your body uses to digest and absorb carbohydrates, proteins, and fats, playing a particularly prominent role in the absorption of carbohydrates—specifically, the movement of glucose from the bloodstream into the liver, muscle, and fat cells throughout the body. Insulin acts on receptors located on the membranes of cells in the liver, other organs, and muscles to promote the uptake of glucose from the blood into the tissue where it is used as fuel or stored as glycogen for later use. Once insulin has successfully engineered the absorption of glucose into the cells, blood glucose levels return to the healthy, baseline range within a few hours.

This touches on the function of insulin that’s most familiar to the average person: its role in regulating blood glucose levels, also called blood sugar levels. Blood glucose or sugar serves as fuel for all the muscles, tissues, and organs of the body. Most importantly, it is the primary fuel for the brain. As such, it is extremely important that blood glucose levels be maintained within a very narrow range.

Low blood sugar, or hypoglycemia leaves us shaky, irritable, weak, and unable to focus or think clearly. Very high blood sugar levels wreak havoc on our organs and can even induce a coma. Insulin is released by the beta cells in the pancreas when blood sugar levels increase in response to ingestion of carbohydrates and other nutrients. When blood glucose levels are low, the secretion of insulin is inhibited.

Insulin is not only anabolic with regard to delivering fuel and building glucose stores. It also promotes muscle building and fat storage. Depending on your diet and exercise regimen, insulin can work to build muscle and improve body composition. Alternatively, if calories are consumed in excess, creating a positive energy balance, insulin works to clear excess circulating fatty acids in the blood by promoting their storage in adipose cells.

It’s important to understand that the relationship between insulin and glucose goes both ways. When insulin levels in the blood are high, the liver’s production and secretion of glucose decreases and systems throughout the body prioritize the growth and development of new cells. When levels are low, those effects are reversed, and widespread catabolism (the process by which cells are broken down to release the energy they contain) sets in. The catabolic effect associated with low insulin levels has a particularly prominent impact on stores of body fat.

When beta cells become damaged, insulin synthesis as well as insulin secretion become impaired. One example of this would be the autoimmune reaction that results in type 1 diabetes mellitus, the primary symptoms of which are abnormally high blood glucose concentrations as well as excessive catabolism through the body. Type 2 diabetes mellitus stems from the same cause—the destruction of beta cells—however, it’s differentiated from type 1 diabetes in that damage is not spurred by an autoimmune reaction and is less severe.

A Timeline of Key Discoveries About Insulin

Because of the vital importance of insulin as a diabetes treatment, it has been intensely studied for close to a century.

In the early 1920s, a team of researchers from the University of Toronto hit on a method for extracting insulin from the pancreases of animals and purifying it to make it safe to administer to humans as a treatment for diabetes. This discovery earned them the Nobel Prize in 1923.

As an interesting side note, an eminent Romanian scientist named Nicolae Paulescu successfully extracted insulin and demonstrated its efficacy as a diabetes treatment prior to the Canadian team, however, his extract could not be used on humans. No mention of Paulescu’s work was made when the Nobel Prize was awarded, which has since been viewed as a “historic wrong,” in the words of Ian Murray, a professor of physiology, vice-president of the British Association of Diabetes, and founding member of the International Diabetes Foundation.

In 1955, biochemist Fred Sanger determined the order of the amino acids in insulin, making it the first protein to be sequenced. His work with insulin, which he found was made up of two chains of amino acids (the A chain containing 21 amino acids and the B chain 30) linked by disulphide bonds, led to the knowledge that all proteins found in the human body are composed of varying sequences of some or all of the same set of amino acids. This work resulted in another Nobel Prize, which was awarded to Sanger in 1959.

Insulin spurred another major scientific breakthrough in 1963 when it became the first protein to be chemically synthesized. However, it was not yet possible to produce it on a large scale, meaning that individuals with diabetes had to continue to use animal insulin, which causes side effects such as immune responses in some patients.

In 1969, Dorothy Hodgkin (also a Nobel Prize winner), used X-ray crystallography to map the molecular structure of insulin. This allowed researchers to learn more about the functions of insulin in the body as well as how it’s produced.

The form of insulin used for diabetes care today dates back to 1978, when scientists used genetic modification to get bacteria to generate the A and B chains of insulin, then developed a chemical process to link the chains together. This allowed synthetic human insulin to be mass produced and diabetes to be treated far more effectively.

7 Key Discoveries About Insulin

The 4 Different Types of Insulin

At this time, insulin therapy involves the use of four primary types of insulin differentiated by how rapidly the effect of insulin sets in, when the effect reaches its peak, and how long the effect lasts.

The four types are:

  1. Rapid-acting insulin
  2. Short-acting insulin
  3. Intermediate-acting insulin
  4. Long-acting insulin

Per information provided by the American Diabetes Association, the first type, rapid-acting insulin, can be detected in the bloodstream within 15 minutes of injection, reaches peak concentrations in the blood between 30 and 90 minutes, and continues to be detectable for approximately 5 hours.

Short-acting insulin can be detected within 30 minutes, reaches peak concentrations about 2 to 4 hours after injection, and remains present for between 4 and 8 hours.

Intermediate-acting insulin reaches the bloodstream between 2 and 6 hours after injection, peaks between 4 and 14 hours after, and stays in the blood for around 14 to 20 hours.

Long-acting insulin does not reach the bloodstream for 6 to 14 hours, reaches peak concentrations shortly after, and remains in the blood for between 20 hours and a full day.

Every diabetic has individual insulin needs and responses, and there’s no single type that’s universally best. Rather, it’s important to tailor insulin therapy to a patient’s specific needs. It’s even possible to use two types mixed together to access a range of different delivery times, peaks, and durations.

What You Should Know About the 4 Types of Insulin

Insulin’s Role in the Development of Adverse Health Conditions

Experts have found that abnormal insulin levels as well as changes to the body’s ability to detect the presence of insulin contribute to the development of several health conditions, including:

  • Diabetes mellitus: The symptoms of both type 1 diabetes and type 2 diabetes stem from insulin abnormalities resulting in hyperglycemia (high blood sugar levels).
    • Type 1 diabetes is an autoimmune condition that causes the body to destroy the pancreatic beta cells that produce insulin, ultimately resulting in complete insulin deficiency.
    • Type 2 diabetes results from either impaired insulin production, insulin resistance, or a combination of both. The mechanisms that cause type 2 diabetes have yet to be fully comprehended, but contributing factors seem to include a lack of physical activity and imbalanced diet.
  • Metabolic syndrome: This accounts for a cluster of conditions including high blood pressure, high cholesterol and triglycerides, and abdominal obesity, all of which seem to originate from insulin resistance. Metabolic syndrome often precedes the development of type 2 diabetes as well as heart disease.
  • Polycystic ovary syndrome (PCOS): This hormonal disorder affects women during their reproductive years, resulting in elevated levels of androgen and poorly functioning ovaries. It’s common for PCOS to involve insulin resistance. Once insulin resistance sets in, the body increases its insulin production, which in turn leads to increased production of androgens.
  • Cancer: Insulin promotes extremely rapid cell division, which can cause cancer to metastasize. High levels of insulin also appear to trigger dangerous changes to DNA regulatory genes that can result in cancer. Furthermore, tumors of the beta cells (whether cancerous or noncancerous) result in a condition called insulinoma that causes high levels of insulin as well as reactive hypoglycemia.

Let’s get into some specifics about the role insulin plays in the development of these conditions.

Diabetes

Type 1 diabetes occurs because the beta cells of the pancreas stop producing insulin. The condition is either present from birth or from an early point in childhood. The treatment of type 1 diabetes necessitates careful monitoring of blood sugar levels in combination with regular insulin injections to keep those levels stable.

Type 2 diabetes, once called adult-onset diabetes, though it’s now becoming quite common among adolescents and children, transpires when the body begins to require higher and higher levels of insulin in order for that protein to carry out its essential functions. This happens due to insulin resistance—though a sufficient amount of insulin is present in the bloodstream, the body cannot detect it, meaning it must continue to produce more and more and more. At a certain point, the demand for insulin exceeds the beta cell’s ability to produce it, and synthetic human insulin must be introduced in order to regulate blood sugar levels.

As has been noted already, without enough insulin, physiological disturbances occur that result in unpleasant symptoms such as:

  • Low energy levels
  • Frequent infections
  • Impaired eyesight
  • Numbness or tingling in the extremities
  • High levels of thirst
  • Poor healing of cuts and bruises

As this transpires, the cells of the body shift away from glucose metabolism—since a reliable supply of glucose is no longer available—and begin the breakdown of fat stored as an emergency energy source. If the cells remain in this fat-fueled mode long enough, they begin producing ketones.

As a side note, individuals adhering to the keto diet intentionally pursue the production of ketones by strictly restricting carbohydrates in order to force the body to switch from glucogenesis to ketogenesis as its mode of energy production. In this resulting state of ketosis, the body burns off fat stores at a much higher rate than usual. Intentionally induced nutritional ketosis can be beneficial in terms of weight loss and other potentially positive physiological changes, however, diabetic ketoacidosis is not beneficial at all and is instead quite harmful. In addition to the question of intention, the two states can be differentiated by blood ketone levels. The blood ketone threshold for nutritional ketosis is 0.6 mmol/L. When those levels exceed 1.5 mmol/L, a person is at high risk of ketoacidosis. When left untreated, ketoacidosis can result in severe illness, coma, and even death.

Metabolic Syndrome

Sometimes referred to as insulin resistance syndrome, metabolic syndrome involves the presence of at least three of the following five conditions:

  1. High blood pressure
  2. Low levels of high-density lipoprotein (HDL) cholesterol
  3. High triglyceride levels
  4. High fasting blood glucose levels
  5. Abdominal obesity

A growing consensus among experts holds that insulin resistance is the catalyst behind the development of metabolic syndrome. “Once acquired, those with a genetic predisposition would develop all the other aspects of the disorder,” they claim.

Other researchers believe insulin resistance arises from a sedentary lifestyle, but whether or not the insulin resistance comes first, it’s clear that it plays a pivotal role in the pathogenesis of metabolic syndrome.

Polycystic Ovary Syndrome (PCOS)

Polycystic ovary syndrome results from imbalanced reproductive hormones. It can involve the presence of a fluid-filled cyst inside the ovaries, but the name is somewhat misleading as it’s entirely possible for individuals to have PCOS without developing cysts.

It’s also possible for PCOS to produce very little disruption to a person’s life. In other cases, however, it leads to more serious health problems including type 2 diabetes and metabolic syndrome.

As touched on above, insulin resistance drives the development of PCOS. Some risk factors that lead to insulin resistance can’t be controlled, but others relate to lifestyle such as diet and physical activity. Proactive steps can help prevent insulin resistance, and making adjustments can also help to reverse this condition.

Cancer

Insulin has been implicated as a factor in overall cancer risk—specifically, high levels of circulating insulin appear to raise your odds of developing cancer.

Because insulin is a growth factor, hyperinsulinemia promotes extremely rapid cell division, which is not desirable when it comes to cancer cells. Cancer cells exposed to high insulin concentrations can proliferate and migrate aggressively.

DNA regulatory genes are also influenced by chronically elevated insulin and blood sugar, which can trigger changes or mutations in the cell. These alterations can lead to cancers in different tissues and organs in the body.

Last but not least, with insulinoma, the tumors (which can be noncancerous) constantly secrete insulin, thereby causing hypoglycemia (low blood sugar).

How Insulin Leads to the Development of These 4 Conditions

Understanding the Functions of Insulin in the Body

As touched on previously, the presence of glucose stimulates the body to secrete insulin. However, other macronutrients, hormones, and biological compounds also stimulate insulin secretion. The primary function of insulin, as well as its counterpart, glucagon, is to regulate blood glucose concentrations.

Basal Insulin Secretion

A very comprehensive article published in the Clinical Biochemist Reviews establishes the healthy basal level of insulin secretion when the body’s in a fasting state as 0.25 to 1.5 units of insulin per hour. In healthy individuals, basal secretion maintains fasting insulin concentrations in the bloodstream of between 3 and 15 mlU/L. This allows for insulin-dependent entry of glucose into the cells of the body, prevents excessive breakdown of triglycerides, and minimizes glucogenesis, all of which ensures that blood sugar levels remain stable.

Glucose-Stimulated Insulin Secretion

When all is operating as it should, glucose-stimulated insulin secretion occurs in two distinct phases. The first phase is a rapid response, resulting in insulin secretion within 1 minute of glucose entering the bloodstream. This phase peaks in 3 to 5 minutes and only lasts for about 10 minutes.

The second phase has a slower onset. It’s not apparent until 10 minutes after glucose reaches the bloodstream (at which point the first phase will be over, or close to over). The phase involves continuous secretion of insulin for the duration of the time that blood sugar levels remain elevated. The amount of insulin secreted is proportional to the concentration of glucose in the bloodstream.

The first phase involves insulin that has already been synthesized and stored, while the second phase requires the use of newly synthesized insulin.

The Release of Insulin in Response to a Meal

The neat and tidy insulin responses described above only occur in laboratory settings. In the real world, the secretion of insulin stimulated by food intake proves far more difficult to predict due to the multitude of variables involved, such as:

  • Presence of specific nutrients, including amino acids
  • Physical makeup of the foods
  • Rate of gastric emptying
  • Speed of gastrointestinal motility

Furthermore, neural input as well as other digestive hormones such as incretin affect insulin response.

Specific nutrients produce distinct insulin responses. For instance, non-esterified fatty acids (NEFA),  which may come directly from high-fat foods or from the synthesis of excess carbohydrates, lead to increased output of glucose and reduce insulin sensitivity. There’s some indication, too, that they alter glucose-stimulated insulin secretion—in the short-term, elevated levels of NEFA in the blood have been linked to increased glucose-stimulated insulin secretion, but chronically high levels of NEFA result in decreased glucose-stimulated insulin secretion as well as decreased insulin synthesis.

The Role of Insulin Receptors

First described by scientists in 1971, insulin receptors contain special proteins called insulin responsive substrates (IRS) that mediate the effects of insulin on the body’s cells.

Four distinct IRS proteins have been identified and named (rather prosaically): IRS 1, IRS 2, IRS 3, and IRS 4.

IRS 1 controls most actions of insulin in the skeletal muscle cells. IRS 2 handles the liver as well as peripheral insulin signals and the development of pancreatic beta cells. The roles of IRS 3 and 4 remain somewhat more mysterious. IRS 3 can be found in fat cells as well as in beta cells and in the liver, while IRS 4 appear in the thymus, brain, and kidneys.

How Insulin Functions on a Cellular Level

The primary functions of insulin in the body’s cells have to do with the metabolism of carbohydrates, fats, and amino acids from protein as well as the transcription and translation of mRNA.

  • Carbohydrates: Insulin contributes to carbohydrate metabolism at many points during the process. It facilitates the diffusion of glucose from carbohydrates into fat and muscle cells, signals the presence of an abundance of intracellular energy, and more.
  • Fats: Insulin instigates the synthesis of fatty acids in adipose tissue (fat) as well as in the liver and in the mammary glands during lactation. It also affects the metabolism of phospholipids.
  • Protein: Insulin stimulates protein synthesis throughout the body. It also contributes to the transcription of mRNA as well as aiding translation of mRNA into ribosomal proteins.

In a big-picture sense, insulin’s role has to do with the regulation of the body’s cellular energy supply and the balance of micronutrients. When the body is in a fed, as opposed to fasting, state, insulin orchestrates the anabolic processes that lead to muscle growth (so long as a sufficient quantity of amino acids are available), tissue healing, and more. Insulin signals an abundance of energy, indicating to the body that it can halt the breakdown of fat stores and instead carry out fat synthesis.

How Does Insulin Function in the Body?

How to Enhance Insulin Function

Aside from the nutritional strategy of minimizing large spikes in blood glucose, the most effective way to enhance insulin function is to stay physically active.

It makes sense that insulin is an important factor in making sure the body is properly fueled for physical activity. Insulin helps deliver glucose from the blood into the muscle cell. Once in the muscle, glucose is metabolized to produce energy to support physical exertion. Insulin also stores excess glucose as glycogen so that it can be used for energy at a later time.

Dietary protein and amino acids can also stimulate insulin release. Consuming a balance of carbohydrate and protein during exercise has been proven to stimulate more insulin than carbohydrate alone, resulting in faster delivery of glucose to working muscles.

Insulin is also needed to optimize recovery of muscles from a hard workout. Immediately after exercise, the muscle is primed to replenish fuel stores like glycogen and to rebuild and repair muscle proteins. During this period, insulin accelerates the rate at which glycogen and protein synthesis proceeds, up to 2 to 3 times the normal rate as long as carbohydrate and protein are ingested and made available.

Insulin likes to do these jobs, and can carry them out quite efficiently. However, for individuals who live sedentary lifestyles, the muscles use very little stored fuel, resulting in an abundance of excess fuels, carbohydrates, fats, and amino acids in circulation. The good news is, just a single bout of exercise can wake up the insulin receptors and enhance their sensitivity and functioning.  This helps rebalance the body’s energy utilization and storage processes.

Tips for Enhancing Insulin Function

Conclusion

In summary, insulin is an amazing hormone dedicated to ensuring that the food we eat is properly routed to where it is needed and when it is needed. A poor diet high in processed carbohydrates, excess energy intake, and lack of physical activity all tax the ability of insulin to do its job properly.

The overproduction of insulin, as it tries to overcome these challenges, has led to an interpretation that insulin in some way contributes to metabolic dysfunction and health complications. While it’s true that abnormal insulin levels as well as changes to the body’s ability to detect the presence of insulin can lead to the development of adverse health conditions such as diabetes, metabolic syndrome, polycystic ovary syndrome, and even cancer, insulin itself is not to blame.

Rather, the true instigating factors in the development of these conditions can be traced back to a person’s genes, lifestyle choices, environment, or a combination of all the above. By supplying your body with a properly balanced diet and prioritizing physical activity as much as your other commitments and overall health allow, you can build a foundation for proper insulin function that will keep this crucial hormone operating as a “good guy, not a “bad” one.

Body Repair After Quitting Drinking: How to Naturally Promote Recovery from Alcohol

What is involved in body repair after quitting drinking, and what can you do to help support recovery and detox? Find out how to minimize withdrawal symptoms and recover better from excessive alcohol use. 

Whether alcohol use has reached the level of alcohol addiction, or regular heavy drinking has simply started to take its toll, quitting alcohol is one of the healthiest decisions anyone can make to improve health and quality of life. Drinking too much alcohol can have damaging physical, psychological, and interpersonal effects that could be disastrous or even fatal, but alcohol recovery isn’t easy either. If you or a loved one has decided to be alcohol-free, the question now is how to speed up body repair after quitting drinking? How long does it take to detox from the effects of alcohol, and what can you do to minimize withdrawal symptoms and improve the body’s health? Read on for natural solutions.

The Symptoms of Alcohol Withdrawal

Depending on your personal level of alcohol dependence, withdrawal symptoms could be mild or severe. In the worst case scenarios, alcohol withdrawal syndrome can include:

  • Anxiety
  • Nausea
  • Tremors
  • Headache
  • Vomiting
  • Rapid heart rate
  • Irritability
  • Confusion
  • Sweating
  • Elevated blood pressure
  • Insomnia
  • Nightmares
  • Fever
  • Seizures
  • Extreme agitation and confusion
  • Visual, auditory, and/or tactile hallucinations

These symptoms could start occurring as soon as 6 hours after your last drink and potentially last for weeks. The severest symptoms are part of delirium tremens (DT), the most dangerous level of alcohol withdrawal that should be undergone only in a hospital or rehab setting as part of a substance abuse recovery process.

The National Institute on Alcohol Abuse and Alcoholism has an online questionnaire to help you evaluate your level of alcohol use and better decide your body’s ability to quit “cold turkey” or with the aid of a treatment center. This post-acute withdrawal phase is often the hardest part, and the more recovery resources you have, the better your chances of maintaining sobriety and not relapsing the next day because the withdrawal symptoms are too overwhelming.

The Symptoms of Alcohol Withdrawal

Body Repair After Quitting Drinking: How To Minimize Withdrawal Symptoms and Recover Faster

What happens to your body when you stop drinking? Is it just one endless hangover? Will the damage done to the stomach lining, kidneys, and liver eventually reverse? Here are the areas you may notice the most dramatic side effects and recovery benefits, and how you can support your recovery after you’re done drinking alcohol.

1. Repair Skin Damage

The cartoon image of a drunk is someone hiccuping bubbles and sporting rosy cheeks and a big, red nose. Part of that picture is actually true: regular overconsumption of alcohol damages your skin, making you look older and causing tissue inflammation. There are a few reasons for this.

  • Dehydration: Because it’s a diuretic, alcohol dehydrates your skin, leading to less elastic skin that can become dry, flaky, and painful.
  • Inflammation: The facial flush that occurs when you drink isn’t the rosy glow of healthy skin but an inflammatory reaction to poison, almost like a mild allergic rash. While that inflammation will subside when you sober up, repeated inflammation to the area will damage the skin over time and leave a lasting redness. It’s also been associated with a higher risk of cancer.
  • Aging: New research indicates drinking alcohol prematurely ages your cells, including your skin cells, causing visual signs of premature aging.

Alcohol has long been associated with bad skin, including what was once known as a “drinker’s nose” or rhinophyma. Rhinophyma is not directly linked to alcohol as a cause and is in fact a form of rosacea. However, there is research showing that there’s a high prevalence of alcohol use among patients with inflammatory skin diseases, and a possible increased risk of basal cell carcinoma linked to alcohol consumption.

The conclusion: alcohol use causes skin damage and premature aging, may worsen other skin conditions, and could increase the risk of skin cancer.

The Solution

Once you quit drinking, what does your skin need most to recover? The first step is adequate, regular hydration, and perhaps a daily moisturizing facial lotion with SPF to protect against sun damage. The second step is to make sure your body has the proper supplies to regenerate new skin and tissue cells, which means amino acids for skin tightening, especially the collagen amino acids that can restore supple, youthful skin. Whether you get them from diet or supplementation, you can’t repair or regenerate new tissue without the necessary amino acids.

2. Reduce Risk of Heart Attack

Excessive alcohol consumption has a serious impact on your cardiovascular health, increasing your risk of pulmonary (lung) conditions and heart disease. Heart failure affects up to five million Americans, and the risk of heart failure is nearly doubled for those who drink heavily.

In the previously linked systematic review of studies, the risk of alcohol abuse was found to be so dangerous, the researchers’ conclusion stated that although “the current literature provides some evidence for a lower risk of heart failure with light-to-moderate consumption of alcohol […] it would be premature to recommend light-to-moderate drinking as a means to lower the risk of heart failure, given the possible risk of abuse and resulting consequences.”

For all the articles that get passed around about the benefits of drinking red wine for heart health, the risk of over-consuming alcohol is so much greater than the small amount of potential benefit from moderate consumption that it is not recommended.

The conclusion: by quitting alcohol entirely, you significantly reduce your risk for heart disease, heart attack, heart failure, and other cardiovascular and pulmonary conditions.

The Solution

According to the American Heart Association, alcohol use and abuse endangers the heart by increasing the amount of fat (triglycerides) in our bloodstreams. Once you’ve quit drinking, there are natural ways to help lower cholesterol and blood lipid levels, and aid in your body’s clean-up of these substances.

3. Reverse Liver Damage

Our livers are unique organs, able to heal from damage in ways that our hearts (for example) cannot. Because alcohol is an intoxicant, it’s up to our livers to process it in order to detox the body, which is why liver disease is a dangerous risk of chronic alcohol abuse.

Consuming large amounts of alcohol can lead to fatty liver disease, alcoholic hepatitis, cirrhosis of the liver, and ultimately liver failure and death. At a certain point the scarring on the liver is so advanced it is irreversible, but there is a large and vitally important window of time when, if you can quit drinking, you can stop the damage in its tracks and allow the liver to heal completely.

The conclusion: alcohol damages the liver, but abstaining can stop the damage and possibly allow it to be reversed.

The Solution

Once alcohol is out of your system, you can help the liver detox and repair itself in a few simple ways: by consuming a liver-flush diet, knowing which key vitamins, supplements, and amino acids aid in liver support, and avoiding intoxicants like alcohol, unnecessary drugs, or exposure to industrial chemicals and preventable diseases like hepatitis. Your liver and kidneys are the only truly natural detoxifiers you have, and in a heavy drinker they are often fatally overtaxed. By quitting alcohol, you can cure your detox organs.

4. Lose Weight and Improve Body Composition

Alcohol leads to higher fat levels in the blood, and therefore alcohol consumption is also associated with higher body weight gain, obesity, and the symptoms that can accompany excess weight like type 2 diabetes, high blood pressure, and metabolic syndrome. Alcohol itself contributes to high calorie consumption, but the calories in alcohol are empty, with no nutritional benefit. Alcohol is processed and stored just like sugar, and like a diet high in refined sugar, it’s closely associated with dangerous weight gain and obesity.

While there’s no direct correlation between the amount of alcohol consumed and the amount of weight gained due to each of us having our own individual metabolism rates, it’s nevertheless true that reducing or eliminating alcohol intake helps lead to successful weight loss and long-term weight-loss management in those with diabetes, as well as avoiding weight gain in the first place.

The conclusion: alcohol can contribute to weight gain and obesity, while abstaining can aid in weight loss.

The Solution

Once you’re sober, proper diet and exercise are still the first and foremost ways to safely lose weight and maintain a healthy body composition. You’ll also want to control for hunger cravings, especially if alcohol addiction is at play. Eating can be an addiction much like drinking, the main difference being that you have to eat every day, while those who are addicted to other substances can remove the temptation entirely. By eating nutritionally dense and filling meals full of the protein and amino acids necessary to build muscle and lose weight, you can avoid the dangers of obesity and regain your optimal fitness.

5. Support Energy and Sleep

Energy levels and proper rest are two sides of the same coin. Because alcohol acts like sugar in the body, the comedown from sobering up can lead to fatigue and energy crashes not unlike drops in blood sugar. This encourages people to overeat or return to drinking despite their best intentions to quit—it’s an effort to correct that crash and regain the rush.

On the flip side, because alcohol also interrupts the brain activity associated with rest, memory creation, and waking, it disrupts normal sleep patterns. Just as so-called “blackout drunks” can be manically active and then wake up with no memory of what they did or said, even more moderate drinkers will experience poor sleep quality due to conflicting brain activities that prevent them from entering into deep REM sleep.

The conclusion: While drinking, you sleep without getting the benefits of “dream sleep” and the neurological function it provides. When newly sober, one of the most maddening side effects can be sometimes long-lasting insomnia that further depletes already low energy levels.

The Solution

While there are sleep aids you can take to chemically induce sleep, they are not recommended for those whose sleep issues are due to coming down from a chemical alcohol dependence in the first place. There are certain natural nutrients and amino acids for insomnia you can explore, pre-bed rituals you can adopt to retrain your brain for regular sleep, and even more amino acids to help boost your daily energy as your body recalibrates to a non-toxic state.

The Amazing Attributes of Abstinence

Now you have an idea of what the body must go through to repair itself once you quit drinking, plus the various ways you can support a natural recovery. Keep in mind that alcohol’s effects don’t stop at damage to your body, and thus quitting drinking can improve even more aspects of your life: alcohol detox and abstinence can save you money, can save your relationships from the consequences of binge drinking, and can help save your overall emotional and mental health going forward.

Get the Facts About Hyperlipidemia: 4 Crucial Questions, Answered

Hyperlipidemia (high cholesterol) can stem from genetic causes, but the majority of the time, it results from lifestyle choices and environmental factors. As it causes no symptoms itself, it’s vital that health care practitioners routinely screen for this silent condition. Lifestyle changes involving diet and physical activity form part of any successful hyperlipidemia treatment plan, and the use of proven supplements can be a highly effective complementary treatment.

More frequently referred to as high cholesterol, hyperlipidemia is the medical term used to describe unusually elevated blood levels of lipids (fat molecules). Though it’s possible to inherit hyperlipidemia, most cases can be traced back to lifestyle choices and environmental factors. Hyperlipidemia itself causes no symptoms, but it does adversely impact your health—most notably by increasing your risk of developing coronary artery disease.

Read on to learn how hyperlipidemia develops, 14 risk factors for hyperlipidemia, how doctors diagnose hyperlipidemia (as well as the different types), and natural treatments for hyperlipidemia.

1. How Does Hyperlipidemia Develop?

To understand how high cholesterol develops, you must first have a basic grasp of some essential facts about cholesterol itself. Cholesterol, a type of fat made in the liver, makes vital contributions to the functioning of the human brain, development of membranes surrounding cells, production of hormones, and storage of vitamins.

In order to travel through the bloodstream, cholesterol pairs with proteins to form lipoproteins. There are two forms of lipoproteins—high-density lipoproteins (HDL) and low-density lipoproteins (LDL)—each of which carry out different functions.

  • Low-density lipoproteins (LDL): Because LDL cholesterol has been linked to the development of cardiovascular disease, it’s known as “bad cholesterol.” LDL cholesterol moves cholesterol molecules through your arteries, and when levels get too high, fatty deposits begin to build up on the walls of your arteries. This leads to atherosclerosis, the hardening or narrowing of the arteries, which in turn raises your risk of heart disease.
  • High-density lipoproteins (HDL): HDL cholesterol, or “good cholesterol,” can actually counterbalance the negative effects of LDL cholesterol. That’s because HDL transports unused cholesterol molecules back to the liver, where they can be excreted. This prevents the development of high blood cholesterol levels and the associated adverse health outcomes, such as heart attack and coronary heart disease.

If your doctor elects to perform a lipid profile, they will likely measure your triglyceride levels too. Your body stores any calories not required for immediate energy needs in the form of triglycerides. Regularly consuming more calories than necessary to fuel your body, particularly if you consume a diet high in carbohydrates, is likely to result in high triglyceride levels (technically speaking, hypertriglyceridemia).

High cholesterol levels in the blood, as touched on in our discussion of LDL cholesterol, causes deposits of fat to accumulate in the blood vessels. As these deposits grow, they can restrict blood flow through the arteries. If a deposit spontaneously breaks loose, it can create a clot that triggers a heart attack or stroke.

This makes it important to monitor and manage your cholesterol levels. For HDL cholesterol, this means keeping your levels at or above a certain threshold while for LDL cholesterol, it means making sure they do not rise too high. Optimal levels for total, HDL, and LDL cholesterol as well as triglycerides are impacted by whether or not you have heart disease, diabetes, or other conditions that put you at higher risk of developing high cholesterol.

The guidelines for each category are as follows:

  • Overall cholesterol
    • Optimal: Under 200 milligrams per deciliter (mg/dL)
    • Concerning: 200-239 mg/dL
    • High: 240 mg/dL and higher
  • HDL cholesterol
    • Optimal: 60 mg/dL and higher
    • Adequate: 50-59 mg/dL for women and 40-59 mg/dL for men
    • Low: Under 50 mg/dL for women and 40 mg/dL for men
  • LDL cholesterol:
    • Optimal for those with heart disease or diabetes: Under 70 mg/dL
    • Optimal for those at risk of heart disease: Under 100 mg/dL
    • Adequate for those with no heart disease, concerning for those with heart disease: 100-129 mg/dL
    • Concerning for those with no heart disease, high for those with heart disease: 120-159 mg/dL
    • High for those with no heart disease, very high for those with heart disease: 160-189 mg/dL
    • Very high: 190 mg/dL and higher
  • Triglycerides:
    • Optimal: Under 150 mg/dL
    • Concerning: 150-199 mg/dL
    • High: 200-499 mg/dL
    • Very high: 500 mg/dL and higher

Making Sense of Your Cholesterol Levels

2. What Factors Raise Your Risk of Hyperlipidemia?

As we covered in the last section, hyperlipidemia results from an unbalanced ratio of LDL cholesterol to HDL cholesterol. While certain types of hyperlipidemia have a genetic component (meaning it’s important for you to know if you have a family history of hyperlipidemia), most result from lifestyle choices.

According to a study published in 2017, both age and sex influence a person’s likelihood of developing high levels of LDL cholesterol or triglycerides. The cross-sectional study, which enrolled 2,000 individuals, also found correlations between hyperlipidemia and lifestyle choices such as smoking, physical inactivity, and the consumption of fatty meats. Meanwhile, individuals who ate more fruits and vegetables were less likely to develop high cholesterol.

Research points to other risk factors as well, such as having a large waist circumference and consuming excessive quantities of alcohol. There are also links between elevated cholesterol levels and several health conditions, such as: kidney disease, polycystic ovary syndrome (PCOS), and decreased thyroid activity. Certain medications affect cholesterol levels too, like steroids, progestin, retinoids, diuretics, and in some cases, beta blockers.

Other factors shown to raise your risk of developing hyperlipidemia include:

  • Sedentary lifestyle: Failing to engage in physical activity on a routine basis can skew your cholesterol levels. It appears that exercise increases production of HDL cholesterol and increases the size of LDL cholesterol molecules, rendering them less harmful.
  • Use of tobacco products: Scientists have observed that smoking cigarettes injures blood vessel walls, which increases the odds that fat will build up on them. Smoking also appears to adversely impact HDL cholesterol levels.
  • Consumption of saturated and trans fats: Studies show that regularly eating foods that contain saturated fats (for instance, fatty meats) and trans fats (commonly included in processed foods like crackers, microwave popcorn, cookies, and more), leads to higher cholesterol levels.
  • Blood sugar levels: Analysis reveals a connection between high blood sugar and high levels of very-low-density lipoprotein (VLDL), a particularly unhealthy type of cholesterol, as well as lower levels of HDL cholesterol.
  • Body fat percentage: Researchers have also found a link between how much body fat a person has and their likelihood of having hyperlipidemia.
  • Overall physiology: As you age, your liver becomes less effective at removing LDL cholesterol, making you more likely to develop hyperlipidemia.

14 Hyperlipidemia Risk Factors

3. How Do Doctors Diagnose Hyperlipidemia?

Hyperlipidemia itself causes no noticeable symptoms, which is why it’s important for doctors to routinely check cholesterol levels, particularly for individuals who have a higher risk of developing the condition.

They do this, as touched on previously, with a test called a lipid panel. This simple blood test allows doctors to measure your total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. In order to ensure accurate results, your physician may ask that you fast for between 8 and 12 hours leading up to the blood draw.

However, recent research trends toward a consensus that fasting may not be necessary. According to a study published in JAMA Internal Medicine in 2019, fasting prior to a lipid profile produced negligible differences to total, LDL, and HDL cholesterol levels. Triglyceride levels were consistently slightly higher for participants who did not fast.

The study enrolled close to 8,300 participants, all of whom had documented cardiovascular risk. Each participant had fasting and nonfasting lipid profiles done with a minimum of 1 month’s time in between the tests. The fasting protocol used required them to abstain from eating or drinking anything except water for 8 hours before the test. By following participants for a median of 3 years, the authors were able to determine that whether or not individuals fasted prior to the lipid profile did little to impact doctors’ ability to predict their risk of future health problems. This is exciting news not only because just about everyone dreads fasting, but more significantly, because fasting can cause issues for older individuals as well as those with diabetes.

5 Different Types of Hyperlipidemia

Experts have categorized the different types of hyperlipidemia that have a genetic component based on the different fats involved in each as well as how each affects the body.

  1. Type I, hyperlipidemia familial lipoprotein lipase deficiency: This inherited condition interferes with the mechanisms by which the body breaks down fats. It can cause abdominal pain, chronic pancreatic infections, and swelling of the liver and the spleen. It’s one of the more severe types of hyperlipidemia, and tends to develop during childhood.
  2. Type IIa, familial hypercholesterolemia, and type IIb, familial combined hyperlipidemia: Both type IIa and type IIb lead to elevated levels of LDL cholesterol. As the names of these types indicate, they do have a genetic component. They’re also one of the few types that can cause visible symptoms—specifically, deposits of fat under the skin and near the eyes. Both types put individuals at increased risk of heart problems.
  3. Type III, familial dysbetalipoproteinemia: This type involves increased total cholesterol and triglyceride levels in combination with decreased HDL levels. It, too, can cause visible symptoms—orange or yellow discoloration of the palms and the development of yellowish deposits of lipids in the skin over the elbows and knees. This type also raises your risk of cardiovascular disease.
  4. Type IV, familial hypertriglyceridemia: This type is differentiated from the others by the fact that it involves elevated levels of triglycerides, not cholesterol. It has been linked to obesity, high blood glucose, and high insulin levels. Typically, this condition remains unnoticed until early adulthood.
  5. Type V, mixed familial hyperlipoproteinemia: This type is quite similar to type I, but it also involves elevated levels of VLDL cholesterol. It’s quite common among patients diagnosed with metabolic syndrome.

Hyperlipidemia without a genetic component, also known as acquired hyperlipidemia, tends to mimic the forms described above.

4. Are There Natural Treatments for Hyperlipidemia?

There are a variety of prescription drugs on the market that can decrease cholesterol and triglyceride levels, such as:

  • Statins
  • Bile-acid-bindingresins
  • Cholesterol absorption inhibitors
  • Fibrates
  • Niacin

While these drugs do effectively treat hyperlipidemia, they can cause seriously unpleasant side effects. Statins, the first option most doctors will try, have been known to cause muscle aches, digestive upset and mental cloudiness. In rare cases, they can also cause liver damage and rhabdomyolysis, a serious condition that results in intense muscle pain, liver damage, and if left untreated, kidney failure and death.

Depending on which type of hyperlipidemia you have, as well as the results of your lipid profile, it’s possible that lifestyle changes and natural cholesterol treatments will allow you to avoid the use of potentially harmful prescription drugs. And even if a drug is necessary to manage your risk of more serious health problems like a heart attack or stroke, lifestyle shifts will still be an important part of your overall treatment plan.

Here are five lifestyle changes and natural treatments that can bring your cholesterol and triglyceride levels into the healthy range.

1. Develop a Healthy Diet

There’s no one right way to eat, but there are certain science-backed elements you can use to build a healthy diet that works for you.

When it comes to lowering bad cholesterol levels and raising good ones, the fats you eat make a big difference. Saturated fats found in red meat, bacon, and sausage and trans fats found in fried and processed foods are particularly problematic. Omega-3 fatty acids, on the other hand, have a wealth of heart-health benefits. Fatty cold-water fish like salmon and mackerel contain plenty of these good fats, as do walnuts and flaxseeds.

It’s also important to consume plenty of soluble fiber, which has been shown to lower LDL cholesterol levels. Load up on fiber-rich vegetables and fruits, legumes, and oats.

2. Engage in Physical Activity

Researchers have found that your physical activity levels have a pronounced impact on your HDL cholesterol levels. The more you exercise, the better those levels will be. And the less you exercise, the lower they’ll drop.

It appears that for cholesterol-management purposes, you should shoot for 40 minutes of moderate to vigorous exercise on 3 or 4 days of the week. Aim for a minimum of 150 minutes of exercise total per week.

If you have the time necessary to try swimming laps at the pool or joining a game of pick-up basketball, that’s wonderful. But finding ways to incorporate exercise into your daily routine, like biking to work or picking up the pace when you take your dog for a walk, can also help you hit that physical activity threshold.

3. Stop Smoking

As mentioned earlier, smoking causes HDL cholesterol levels to fall and triglyceride levels to rise. Furthermore, it independently increases your risk of developing heart disease. If you’re a current smoker, no matter which type of high cholesterol you have, quitting will be an important part of your treatment plan.

As you’re almost certainly aware, it can be quite a challenge to quit. It may be helpful to talk to your doctor about strategies for doing so, like using a nicotine patch, or to seek support from others who have successfully kicked the habit.

4. Evaluate Your Weight

There can be a connection between body weight (particularly fat mass) and cholesterol levels. Research has shown that by adopting dietary strategies designed to produce sustainable weight loss, individuals were able to raise their HDL cholesterol levels and lower their LDL cholesterol levels.

Learn more about strategies for pursuing healthy weight loss here.

5. Incorporate Proven Supplements

If you’re committed to pursuing natural methods of lowering your cholesterol, you can find more in-depth advice about proven methods for doing so, as well as the rationale behind choosing a natural approach, in this article.

For our purposes, it will suffice to say that supplements can play a very important role in naturally addressing hyperlipidemia.

For instance, compelling research has revealed that taking an essential amino acid supplement can produce highly desirable results on cholesterol levels.

Studies have shown that essential amino acids, which stimulate the synthesis of the proteins that transport lipids out of the liver as well as those that flush fatty acids into safe storage areas, can lower levels of total cholesterol, LDL cholesterol, VLDL cholesterol, and triglycerides in the liver as well as the bloodstream. These results have been seen with a dosage schedule of two 11-gram doses, twice a day.

These all-natural, completely safe compounds bring benefits for your overall health and—it’s important to note—they can be combined with statins without any ill effects. In fact, they actually make them more effective, per the findings of an Italian research team.

If you’re curious about amino acid supplementation, this primer is a great place to begin.

5 Natural Ways to Address Hyperlipidemia

Conclusion

Hyperlipidemia is the medical term for high blood levels of lipids. It can stem from genetic causes, but the majority of the time, it results from behavior choices and environmental factors such as an overly sedentary lifestyle, the use of tobacco products, or excessive alcohol consumption.

As it causes no symptoms itself, it’s vital that health care practitioners routinely screen for this silent condition, which has been linked to an increased risk of cardiovascular disease.

There are a variety of prescription medications available that can be used to get cholesterol levels under control, but they can cause unpleasant side effects. And even if the benefits of using one of those drugs outweighs the risks, it’s still important to make lifestyle changes such as developing a healthy diet that facilitates lower levels of LDL cholesterol and higher levels of HDL cholesterol as well increasing physical activity. It can also be quite valuable to incorporate supplements with proven benefits for bringing cholesterol levels into a healthy range, such as essential amino acids.

How to Lengthen Telomeres—and Why You Should

Shortening of telomeres plays a vital role in cellular division and the aging process, which has led to intense interest in how to lengthen telomeres. Research indicates that both telomerase therapy and RNA treatments could possibly be effective interventions, however, it will likely be some time before those treatments become available to the public. In the meantime, a new study points to amino acids as a possible method for enhancing the health of your telomeres. 

“Telomeres”—have you encountered that term yet? It seems that interest in telomere length and how to lengthen telomeres is reaching somewhat of a fever pitch.

Researchers describe telomeres as the cellular equivalent of the plastic tips placed on the ends of shoelaces to prevent fraying. The material telomeres keep intact, however, is your DNA.

When a cell divides and replicates, the replication does not include the full length of the DNA strand—a small section from the ends does not get copied. Telomeres cap the ends, ensuring nothing vital gets left out of the replicated cell. Each time a cell divides, a little bit of the telomeres at its ends gets left behind. So, over time, telomeres become shorter and shorter. When they get too short, the cell they’re attached to stops replication and enters senescence. The accumulation of senescent cells in the body is thought to contribute to the development of many age-related health conditions, such as:

A wealth of research indicates linkages between length of telomeres and overall health. While some have interpolated that to mean that short telomeres indicate a short lifespan, others feel it’s more complex than that.

Here’s what you should know about telomeres, the vital role of an enzyme called telomerase, and how to lengthen telomeres (including a very accessible option).

10 Quick Facts About Telomeres

What Are Telomeres?

The word telomere is derived from Greek (as many medical terms are)—specifically, the word “telos,” which means end, and the word “meros,” which means part. Scientists suspect that short telomeres may be a contributing factor to the development of many chronic diseases, while geroscientists think it’s possible that the shortening of telomeres may drive the entire aging process.

Telomere shortening can be thought of as the lighting of a fuse attached to a cell. With each cell division, telomeres grow shorter until (to continue the metaphor) the flame gets too close to valuable genetic information, triggering cellular senescence or apoptosis (cell death).

Technically speaking, telomeres are repeated sequences of DNA that keep our chromosomes stable during cellular division and protect our genetic information. Thus, shorter telomeres correlate with an increased risk of cancer and other diseases linked to genetic malfunctions. Telomeres also regulate the cellular aging process, dictating how many times a cell can safely divide. Scientists used to believe that cells could replicate indefinitely, and research into telomeres has been a vital component of efforts to better understand cellular replication and its effect on human health.

The Science of Telomeres

Pioneering scientists Hermann Muller (who gave telomeres their name) and Barbara McClintock were the first to recognize that telomeres appeared to have a protective function. After their groundbreaking work in the 1930s, however, it would take several more decades for researchers to comprehend how telomeres functioned in relation to cellular aging.

One reason for that was the persistent assumption that cells could divide endlessly, an incorrect belief that was shattered at last in 1961 when two scientists from the Wistar Institute of Anatomy and Biology in Philadelphia, Pennsylvania discovered that cells can only divide a limited number of times. For the lung cell cultures they observed that limit appeared to be set around 40 or 50 divisions.

The next decade ushered in the work of Elizabeth Blackburn, an icon in the field of human telomere research. At Yale University in the 1970s, she became the first to identify a telomere sequence.

Another major breakthrough took place in 1998 when a research team based in Menlo Park, California found that artificially extending the length of the telomeres attached to cells could allow them to continue dividing indefinitely, thereby officially “establishing a causal relationship between telomere shortening and in vitro cellular senescence.”

Then, in 2009, Elizabeth Blackburn, Carol Greider, and Jack Szostak won a Nobel Prize for their discovery of telomerase, an enzyme that lengthens telomeres and which remains shut off in most cells after the early phases of growth.

Since then, telomeres have become a hot topic among those interested in healthy aging. “Once telomeres became popular knowledge, all sorts of people came out of the woodworks selling nutraceuticals, natural products, claiming that it was the fountain of youth,” explained Jerry Shay, a biologist at the University of Texas Southwestern Medical Center who specializes in telomeres, in an interview.

Understanding the Role of Telomerase

As touched on briefly in the preceding section, the enzyme telomerase is responsible for telomere lengthening. When it restores length to telomeres, it bestows the cells those protective caps that are correlated with a longer lifespan. Because of this, some experts in the field of geroscience believe that increasing the body’s supply of telomeres can safeguard—and even restore—the length of our telomeres. This, in turn, will help to prevent the development of age-related diseases.

While a number of different proteins contribute to telomere upkeep, telomerase carries out the most important role—it rebuilds the ends that get shortened during cellular division.

As established earlier, the cells of the body can’t replicate indefinitely. To be more precise, however, somatic cells can’t replicate like that. Stem cells, however, are immortal. To continue dividing without compromising genetic code, stem cells use telomerase to rebuild the ends of their telomeres. With perpetually long telomeres in place, they can carry on dividing, and dividing, and dividing. Telomerase keeps their telomeres at a consistent length regardless of how many times they divide, allowing them to continue with their vital work, which includes tissue growth and regeneration.

It is because ordinary, somatic cells do not use telomerase that they can only divide a limited number of times.

So, you might be thinking that supplementing with telomerase would have to be the most effective anti-aging treatment ever. And in a sense, you’d be right. But scientists worry this approach could come with serious adverse side effects. You see, there’s another type of cell that uses telomerase—cancer cells. That’s why they’re able to replicate so ruthlessly. Experts worry that if telomerase levels rise too high, that could fuel the growth of cancer.

How to Lengthen Telomeres

Because of the potential risks associated with telomerase therapy, research so far has been conducted with rodents. That said, the results have been highly encouraging.

A 2012 study published in EMBO Molecular Medicine found that the use of telomerase gene therapy in adult mice successfully extended lifespans without increasing cancer risk. They found that higher levels of telomerase translated to “remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging.” Even more impressive, however, were the increases to lifespan—an increase of 13% for 2-year-old mice and 24% for 1-year-old mice.

While this seems to indicate telomerase therapy could be an effective anti-aging tool, allowing us to live longer, healthier lives, it’s important to remember more research is needed to corroborate those findings. There are (obviously) many differences between humans and mice, including that mice have longer telomeres than humans at baseline.

That said, the results of in-vitro, test-tube studies have also shown that adding telomerase makes it possible for cells to continue to replicate long past the point at which they would typically undergo senescence or apoptosis.

Another interesting approach to lengthening telomeres is the use of RNA therapy. Dr. John Cooke, department chair of cardiovascular sciences at Houston Methodist Research Institute, led a team in analyzing whether RNA therapy could lengthen the telomeres of human cells, albeit in test tubes.

To do so, Cook and his team harvested cells from children living with progeria, a condition that causes such rapid aging, most who have it die in their teens. Earlier studies had already established that children with progeria have markedly short telomeres.

Before the RNA treatment, the harvested cells multiplied poorly and died quickly. Once the RNA was inserted, “cells proliferated normally,” stated Cooke. “It was a dramatic improvement.“ He noted, too, that the RNA treatment rolled back other indicators of aging, like the presence of inflammatory proteins.

A More Accessible Option

While findings on the use of telomerase and RNA are certainly exciting, it’s unlikely that most people will have access to these treatments in the near future. Luckily, there’s a more accessible way you can directly impact the health of your telomeres.

Vicki Lundblad, a professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Sciences, led a team who identified a key protein group that helps lengthen telomere ends. Through analysis of the structure of human telomerase, Lundblad uncovered three EST proteins—known as Est1, Est2, and Est3—that make major contributions to telomerase activity. Est2, along with RNA, does the cellular heavy lifting necessary for reconstructing telomeres, while Est1 and Est3 ensure that process progresses smoothly. Both Est1 and Est3 make unique contributions. Est 1 transports telomerase to the telomeres. “Without Est1, telomerase cannot get to the ends of chromosomes, and thus telomeres shorten,” Lundblad stated.

Ongoing analysis is centered on clarifying the role of Est3. What the team knows so far is that it uses specific amino acids to interact with telomerase. When the team inactivated those amino, shorter telomeres were produced, indication that telomerase activity had been measurably impaired.

In other words, without amino acids, the body cannot utilize telomerase. Yet another reason to ensure your body always has a ready, more-than-adequate supply of essential amino acids.

Conclusion

Telomeres ensure that the cellular division process does not result in the loss of genetic material. Instead, each time your cells divide, a section of your telomeres gets left behind. When telomeres become too short, cells stop dividing and become inactive.

This has led to intense interest in how to preserve and lengthen telomeres. Research indicates that both telomerase therapy and RNA treatments could possibly be effective interventions. However, it will likely be some time before those treatments become available to the public.

In the meantime, a new study points to amino acids as a possible method for enhancing the health of your telomeres. Given the many benefits associated with amino acids, this seems like a telomere-lengthening strategy worth trying.

When It Comes to Early Treatment of Fatty Liver, Ultrasound Detection Could Be Key

Fatty liver disease poses a serious public health challenge, in part due to the fact that it remains largely asymptomatic until the later stages. This makes identifying a noninvasive method for early detection of fatty liver disease a top clinical priority. Read on to learn why experts agree ultrasound has many advantages as a method for screening the general population for fatty liver disease.

Experts estimate that approximately 100 million individuals in the United States meet the criteria for non-alcoholic fatty liver disease, though most of them don’t know it. That’s because the early stages of fatty liver are often asymptomatic, meaning that a person has no indication they do not have a healthy, normal liver until the disease has progressed into more advanced stages. A key element of reversing this trend is finding ways to incorporate screening for fatty liver into routine clinical practice. Of the methods currently available for detecting fatty liver, ultrasound stands out as a noninvasive assessment option that efficiently and reliably detects the disease.

What Is Fatty Liver?

The liver, the largest internal organ, metabolizes nutrients and filters toxins from the bloodstream. It plays an especially active role not only in how your body digests fat, but also in how it produces and utilizes it. When the balance between those activities becomes skewed, fat builds up in the liver. As fat accumulates in the liver, it creates inflammation in the liver cells, which can lead to impaired liver function and scarring of liver tissue. If the disease is allowed to progress unchecked, it can ultimately progress to liver failure.

There are two primary types of fatty liver: alcoholic fatty liver disease (AFLD) and non-alcoholic fatty liver disease (NAFLD). The former refers to the development of fatty liver in individuals with high levels of alcohol use, and the latter refers to the disease when it develops without heavy alcohol consumption.

In the absence of excessive alcohol intake, the most common underlying cause of fatty liver is insulin resistance. A number of factors can impair the body’s sensitivity to insulin, such as:

  • Increased body weight
  • Aging
  • Family history of type 2 diabetes
  • Large fat deposits in the abdominal area

If the body cannot appropriately detect the presence of insulin, then it increases its own insulin production. Rising levels of insulin can cause other issues such as:

  • Increased blood pressure
  • High triglyceride levels
  • Accumulation of fat in the liver

Typically, individuals in the early stages of fatty liver disease have no perceptible symptoms. If the liver becomes sufficiently enlarged, they may begin to sense a mild ache or tenderness where it’s located in the upper-right abdomen.

The Link Between Insulin Resistance and Fatty Liver Disease

If individuals are able to address the insulin resistance that causes fat to build up in the liver, then it’s typically possible to restore full liver health without any lasting serious consequences. However, if the condition is not detected, then it can progress to a more serious form of fatty liver—non-alcoholic steatohepatitis (NASH). This is the stage at which inflammation of the liver as well as liver fibrosis (scarring) occur. This form of fatty liver can then cause cirrhosis and even liver failure.

What Happens When Fatty Liver Progresses to Cirrhosis?

As touched on above, fatty liver usually causes no noticeable symptoms. However, once it progresses from NAFLD to NASH to cirrhosis, symptoms begin to appear. Cirrhosis demarcates the point at which liver scarring becomes quite severe. Hallmark symptoms of cirrhosis include:

  • Weakness and fatigue
  • Decreased appetite
  • Weight loss
  • Jaundice (yellowing of the eyes and skin)
  • Itchiness
  • Nosebleeds
  • Spider veins (clusters of blood vessels that resemble spider webs)
  • Confusion and difficulty focusing
  • Ascites (abdominal pain and swelling)
  • Edema (swelling of the legs)
  • Gynecomastia

In most  cases, cirrhosis develops because of a long-term viral hepatitis C infection or ongoing alcohol abuse. However, untreated NAFLD can also progress to cirrhosis.

If cirrhosis is not effectively treated, it progresses to end-stage liver disease, which will prove fatal if a liver transplant does not occur in time. While it’s not possible to reverse the scarring that occurs, you can minimize its impact and prevent future scarring from taking place. The key to doing so is taking every possible opportunity to cleanse your liver and support its health and functioning. To learn more about managing a cirrhosis diagnosis, read this article.

11 Symptoms of Cirrhosis

For Early Detection of Fatty Liver, Ultrasound Could Be Key

Studies show that ultrasound images offer a reliable, efficient method for diagnosing fatty liver. According to a 2018 hospital-based, cross-sectional study published in the Journal of International Medical Research, ultrasound’s “sensitivity and specificity in detecting moderate to severe fatty liver are comparable to those of histology [liver biopsy],” a far more invasive procedure.

Preventing NAFLD from progressing to cirrhosis and even liver failure requires effective risk stratification and the development of strategic treatment plans. In order to do that, doctors need to evaluate:

  • How much fat has accumulated in the liver
  • Whether the liver is inflamed, and if so, to what degree
  • Whether scarring is present, and if it is, how severe

Liver biopsy has historically been the preferred method for confirming a diagnosis of fatty liver and developing a treatment plan. However, non-invasive imaging methods like ultrasound allow doctors to screen individuals who do not yet show signs of liver disease, allowing those in the early stages of NAFLD to access treatment faster.

Both B-mode ultrasonography (US) as well as ultrasound elastography (USE) can be used for this purpose. Ultrasound elastography even allows doctors to evaluate degrees of inflammation and scarring, vital pieces of information relevant to disease progression and treatment selection.

Medical professionals have determined that imaging tests like liver ultrasound have multiple advantages over both liver biopsy and blood tests to measure serum biomarkers, such as:

  • Non-invasiveness
  • Evaluation of a greater volume of fat accumulation in the liver
  • Less variability
  • More quantitive data

Ultrasonography

Conventional ultrasonography (US) is widely available, affordable, and noninvasive. Because of this, it’s common for US to be the first method used to clinically evaluate fatty liver, particularly when doctors want to screen for suspected NAFLD.

Key features found on ultrasound images that indicate fatty liver disease include:

  • Hepatomegaly, meaning the liver is visibly enlarged
  • Increased echogenicity, indicating the surface bouncing the echo can reflect increased sound waves
  • Intrahepatic vascular blurring, referring to blurred images of blood vessels in the liver

Ultrasound Elastography

Ultrasound elastography (USE), like conventional ultrasound, is widely available and relatively inexpensive. It’s attracted a high level of interest due to utility as a noninvasive method of assessing liver stiffness.

The theory supporting its use is that tissue stiffness can be used as a measure of the presence and degree of liver fibrosis, which in turn indicates how far the disease has progressed.

Currently available USE methods can be divided into two general groups: first, transient elastography, an ultrasound-based technique that does not rely on images and second, and elastography techniques that do use images.

Diagnosing Fatty Liver Disease with Ultrasonography and Ultrasound Elastography

Conventional liver ultrasound and ultrasound elastography can be seen as complementary screening measures as they provide different data points, all of which can be combined to form a diagnosis and treatment plan.

Research on the Use of Ultrasound to Detect Fatty Liver

The Journal of International Medical Research study cited earlier drew its findings from the analysis of 390 health histories, 226 from patients who were diagnosed with fatty liver after master health checkups and 164 who were not. The goal was to determine whether the diagnoses of fatty liver made using ultrasound findings correlated to laboratory blood test parameters for the disease. This, then, would show whether it’s valuable to include ultrasound screening for fatty liver in routine health checkups.

Patients whose ultrasound examinations showed fatty liver were classified as cases and those whose ultrasounds did not were classified as controls. Diagnostic findings from blood tests—lipid profiles [total cholesterol, triglycerides, high-density lipoprotein (HDL), and low-density lipoprotein (LDL)], serum GOT [aspartate transaminase (AST)], serum GPT [alanine transaminase (ALT)], and HbA1c levels—were obtained for both cases and controls when available. HbA1c levels were available for 311 patients, serum GPT levels for 266, and serum GOT for 261.

The authors found that lipid, liver enzyme, and HbA1c levels were all substantially elevated for cases compared to controls. Overall, the findings were consistent with previous studies in that they showed NAFLD to be the most common cause of high blood levels of GPT and GOT. The authors note, too, that NAFLD should not be viewed as “an isolated or random event in metabolic syndrome,” but instead treated as a component of the condition. Furthermore, they state that NAFLD should be regarded as a risk factor for the development of:

They note, too, that ultrasound can help to diagnose fatty liver in patients where it could otherwise be easily overlooked due to an absence of clinical markers that would raise suspicion. For instance, individuals from South Asian countries who develop fatty liver disease often maintain lower body mass indexes than those in European and American countries with the disease. This can cause the results of blood pressure tests to be misleading, as they may show normal levels despite the presence of increased liver fat. Ultrasound screening can be used for mass screening that will identify patients who might otherwise slip through the diagnostic cracks.

Because fatty liver disease tends to be asymptomatic, developing reliable screening methods to identify high-risk NAFLD patients is of paramount importance to managing the disease. Liver biopsy is reliable for diagnostic purposes, but impractical as a screening tool. Ultrasound, however, appears to be near-equal in terms of reliability and it’s far better suited for screening purposes.

How to Prevent, or Treat, Fatty Liver Disease

At this time, no medications exist for the treatment of fatty liver disease. However, it can be both prevented and treated with lifestyle changes. Depending on the underlying cause of the disease as well as a person’s overall health, doctors may recommend adjustments such as:

  • Limiting alcohol consumption
  • Eating more nutrient-rich foods and avoiding highly processed ones
  • Increasing physical activity

For individuals at risk of developing NAFLD, as well as those with NAFLD, adopting a fatty liver diet will be a crucial part of an effective treatment plan. Unsurprisingly, a central tenet of this diet is limiting consumption of both saturated and trans fats. It also involves completely cutting out alcohol, limiting salt and sugar, eating plenty of high-fiber plant foods, like whole grains and legumes, and upping your intake of fruits and vegetables.

Experts recommend the following foods as ideal components of a fatty liver diet:

  • Green vegetables: Broccoli, spinach, kale, and other green vegetables can help prevent liver fat buildup while supporting weight loss and enhancing your overall health.
  • Fish: Salmon, trout, tuna, and sardines contain omega-3 fatty acids that can actually lower liver fat levels and decrease liver inflammation.
  • Walnuts: Like fish, walnuts contain concentrated amounts of omega-3 fatty acids, which can improve your liver disease prognosis, liver function, and health.
  • Dairy: Studies show that whey protein can protect liver cells from damage linked to NAFLD.
  • Olive oil: This staple of the Mediterranean diet can lower liver enzyme levels and bodyweight, perhaps due to the omega-3 fatty acids it contains.
  • Green tea: Research indicates green tea can enhance liver function and decrease liver fat storage.
  • Coffee: This popular beverage can prevent liver damage associated with fatty liver disease as well as lower levels of liver enzymes.
  • Tofu: Soy proteins found in tofu can reduce the accumulation of fat in the liver.

There’s also some evidence to support the use of certain supplements, including vitamin E, to prevent or treat fatty liver disease. Studies indicate that milk thistle, which has anti-inflammatory and antioxidant properties, can have a positive effect on liver health. And turmeric, a potent antioxidant, can quell inflammation throughout the body, which can help to reduce your risk of liver disease as well as manage liver disease. To learn more about natural methods for detoxifying the liver, read this article.

Perhaps the most consequential choice you can make to protect or improve your liver health is to supplement with amino acids. According to the work of a team of scientists based in Kyoto, Japan, taking branched-chain amino acids (BCAAs) can slow, and potentially halt, the progression of chronic liver disease. After 11 weeks, blood samples showed that rats given BCAAs had liver enzyme levels that were 22% lower than the control group. The researchers also found that levels of the CTGF protein, which correlates to liver fibrosis, were an average of 75% higher in the control group. Even more significantly, markers that indicate rates of cell death, an enzyme called caspase 3 and a protein called albumin, were 100% and 80% higher in the control group.

Studies done with human subjects support the conclusion that amino acid supplements are an effective natural method for treating liver disease.

How to Treat and Prevent Fatty Liver Disease

Key Takeaways About Fatty Liver Disease and Ultrasound

Non-alcoholic fatty liver disease (NAFLD) is becoming an ever more pressing public health challenge, in part due to the fact that it remains largely asymptomatic until the later stages of the disease, and the determinants of the disease have yet to be fully understood. Once the disease reaches the later stages, in which liver fibrosis progresses toward cirrhosis, severe complications can ensue. This makes identifying a noninvasive method for detecting fatty liver disease a top clinical priority. Ultrasound has many advantages as a method for screening the general population for fatty liver disease. It’s efficient, widely available, and has been shown to be as accurate as biopsies, the gold standard for diagnosing liver disease.

Acute Fatty Liver of Pregnancy: How to Recognize Symptoms and Improve Outcomes

Find out about this preventable cause of maternal mortality, how to recognize its symptoms, and what is needed for both mother and child to survive acute fatty liver of pregnancy.

Acute fatty liver of pregnancy (AFLP) is a rare disorder that occurs in the late-stage second and third trimester of pregnancy. It is a life-threatening but preventable cause of maternal mortality whose risk factors are better understood in gynecology and obstetrics every year. This article has the details of what causes this condition, the symptoms of AFLP, and how to improve maternal outcomes and fetal survival rates.

What Is Acute Fatty Liver of Pregnancy?

Though uncommon, acute fatty liver of pregnancy is particularly dangerous because its clinical presentation allows it to be misdiagnosed as other conditions like HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count) and preeclampsia. In fact nearly half of AFLP cases are mistaken for preeclampsia, delaying treatment and increasing the risk to both mother and baby.

AFLP occurs in about 0.25% to 0.5% of U.S. pregnancies each year, and though physicians are not yet sure why, it more frequently involves twin pregnancies rather than single pregnancies, and male fetuses rather than female ones. Though “liver” is in the name, severe cases can come with multisystem involvement that includes acute renal failure, gastrointestinal bleeding, encephalopathy, coagulopathy, pancreatitis, and (more rarely) transient diabetes insipidus.

Women may have preeclampsia alongside AFLP, making both conditions harder to distinguish and treat, as researchers believe AFLP, preeclampsia, HELLP syndrome, and thrombotic thrombocytopenia purpura may all be “a spectrum of the same illness.” AFLP is typically diagnosed later in pregnancies just before the time of delivery, but diagnosis may not happen until directly after delivery, when the proper aid is most critical.

What Is the Cause of AFLP?

Acute fatty liver of pregnancy is caused when either the mother or the baby has a genetic disorder affecting the mitochondrial beta-oxidation of fatty acids. In simpler terms, that means the mitochondria in their cells are not able to break down fatty acids into their smaller molecular components, leading to a dangerous accumulation of fat in the liver cells, kidney, placenta, or other areas.

If the buildup leads to an interruption in the mother’s liver function, it puts both her and the fetus at risk; the liver removes toxins for both bodies, and the symptoms of dysfunction can be very slow and subtle in their development. This makes identifying the issue difficult for both the patient and her doctor.

Evolutionary Theories

While the exact reason acute fatty liver of pregnancy affects otherwise healthy women in the last stages before birth is unknown, researchers have theorized that it has to do with our evolution. In times of famine our bodies have mechanisms in place to allow us to switch from sugar energy (glucose) derived from carbohydrates to ketone energy sourced from our fat stores.

If you’ve ever heard of the ketogenic diet, it’s built on this same premise: if you deny the body carb intake via dietary restriction, it will trigger this secondary metabolism and lead to rapid body fat loss. This metabolic pathway is not unique to humans. It’s also what allows certain animals to hibernate all winter and migratory birds to cover long distances in nonstop flights.

During pregnancy, the mother’s body starts utilizing stored fat for energy. Why this happens is unclear; it could be due to needing extra energy for the potentially long duration of labor, or it could be because the body is now prioritizing carbohydrate energy for the nutrition and growth of the fetus (or both). Whatever the exact biological stimulus behind it, fat is being burned in the late stages of pregnancy, and if there is a previously unknown genetic disorder that inhibits the breakdown of fat and leads to liver buildup of fat, acute fatty liver disease of pregnancy could be the result, leading potentially to liver failure and an increased fetal mortality rate. In the most severe cases, a new mother may need a liver transplantation due to fulminant hepatic failure, and the newborn baby may require monitoring in the neonatal intensive care unit (NICU) to survive.

What Is Acute Fatty Liver of Pregnancy (AFLP)?

Signs and Symptoms of Acute Fatty Liver of Pregnancy

The increase in energy demands during the late stages of pregnancy lead to a heavier reliance on fat for energy. Researchers theorize that this is why AFLP occurs more typically at the end of pregnancy.

Early diagnosis of AFLP is crucial, because while a liver biopsy showing microvesicular steatosis of hepatocytes makes a sure diagnosis, it is not safe for the patient to undergo in the late stages of pregnancy. Rather, the blood test differences between AFLP and HELLP and preeclampsia, while subtle, have been carefully differentiated so that a determination could be made on blood tests as soon as possible without need of biopsy.

As liver function is compromised, the patient begins to go from healthy to extremely sick. The most commonly associated symptoms of AFLP are:

  • Loss of appetite
  • Mental confusion
  • Extreme sleepiness and fatigue
  • Abdominal pain and specifically epigastric (upper right abdomen) distress
  • Nausea or vomiting
  • Jaundice (an advanced symptom)

As you can see, most of these symptoms could easily be attributed to the usual symptoms of pregnancy until suddenly a woman finds herself jaundiced and in extreme danger. In the most tragic cases, diagnosis is only made after the fetus has died in utero.

The Difference Between AFLP and HELLP Syndrome

Acute fatty liver of pregnancy is distinct from HELLP syndrome and various other preeclampsia conditions by its development. While the symptoms are similar, a lab test is able to verify the distinction between the abnormal clotting conditions associated with AFLP and the decreased platelet count of HELLP syndrome.

Other differences include these HELLP symptoms:

  • Higher blood pressure
  • No acidosis (acid buildup in the blood)
  • No abnormality in blood glucose levels
  • No sensorium changes or compromised brain function
  • Normal uric acid levels
  • Less severe results from liver function tests

Other distinctions include subtle indications, like AFLP is more commonly associated with compromised kidney function than HELLP syndrome is, AFLP has a greater likelihood of bilirubin increase in lab testing than HELLP syndrome does, and hypertension is less present in AFLP, but AFLP patients frequently have proteinuria (protein in the urine).

Signs and Symptoms of Acute Fatty Liver of Pregnancy (AFLP)

The Diagnosis of AFLP

The diagnosis of acute fatty liver of pregnancy based on the symptoms alone is almost impossible. Sometimes the condition is not discovered and diagnosed until such time as an emergency cesarean section is called for due to fetal distress. Lab tests include looking for combinations of:

  • Evidence of liver problems
  • High serum ammonia
  • Abnormal clotting issues
  • Very low blood sugar
  • Uric acid
  • Signs of kidney damage

Clinicians will also rule out any other potential causes of liver failure, including potential exposure to various forms of hepatitis in third-world endemic areas, drug-induced liver damage, malaria exposure, and potential acute viral hepatitis B infection.

The Treatment of an AFLP Mother

Currently the management strategies of this condition involve facilitating a prompt delivery (via cesarean section if necessary) of the infant and anticipating the potential complications of acute liver failure, including having the appropriate blood product and plasma exchange material on hand. The sooner this condition is recognized, the better prepared the medical team can be for quickly and effectively treating both mother and child.

Depending on the mother’s condition after the placenta has been removed, she may need an enhanced level of postpartum care, including up to several weeks in an intensive care facility with round-the-clock multidisciplinary health care professionals (hepatology, obstetrics, hematology, anesthesia, and neonatology) to treat liver dysfunction and other related side effects.

Though it’s an incredibly serious condition, most mothers with AFLP exhibit rapid improvement after delivery, with follow-up tests showing liver functions reverting to normal.

The Care of an AFLP Baby

The first step in caring for a baby born to a mother with AFLP is to assign the child to a clinical geneticist and a neonatologist to check for any fatty acid oxidation defects like LCHAD (long-chain 3-hydroxyacyl-coenzyme A dehydrogenase) deficiency. Between 15% and 20% of all AFLP pregnancies result in children with LCHAD deficiency.

Children with fatty acid oxidation defects can range anywhere from asymptomatic to severely compromised with cardiomyopathy or encephalopathy. The child could also suffer from sudden infant death. That is why immediate expert evaluation is required.

Newborns with medium-chain fatty acid oxidation defects are 12 times more likely to have maternal liver disease, while newborns with LCHAD defects are 50 times more likely. This analysis revealed that out of 63 pregnancies resulting in 28 LCHAD-deficient births, 31% of those were associated with AFLP, HELLP syndrome, and preeclampsia, while 10% were linked to intrahepatic cholestasis (a pregnancy-associated disorder that impairs bile release from the liver cells). No links were found in pregnancies that resulted in healthy births.

Children born to mothers with AFLP may carry the same genetic defect as the mother, and may be more at risk of nonketotic hypoglycemia (a life-threatening inherited condition that inhibits the breakdown of amino acids). Other AFLP children may have dilated cardiomyopathy (a serious condition that involves swelling in the heart chambers) or progressive neuropathy (a worsening nerve disorder). All babies and mothers who have experienced acute fatty liver of pregnancy require testing for short-, medium-, and long-chain abnormalities in relation to the mitochondrial beta-oxidation of fatty acids.

Future Pregnancies

Having survived acute fatty liver of pregnancy once, it’s only reasonable to be concerned that this condition could affect you again. Unfortunately, there is no hard data on the exact likelihood of recurrence. Anyone who has undergone an AFLP pregnancy should be under the care of a maternal-fetal medicine sub-specialist for any future pregnancies, and should take special care to monitor for the symptoms of AFLP in all subsequent pregnancies.

The Diagnosis of Acute Fatty Liver of Pregnancy

AFLP Prognosis

Keep in mind that acute fatty liver of pregnancy is an incredibly rare condition worldwide. Nevertheless, because it’s such a dangerous condition with so few identifying symptoms, the diagnostic criteria has been carefully honed to detect it as soon as possible to prevent maternal and fetal mortality rates. By increasing yours and others’ awareness of this preventable cause of maternal mortality, you may help promote survival.

Plasma Exchange Therapy (Plasmapheresis): What Is It and What Can It Help Treat?

Plasma exchange therapy or plasmapheresis is not unlike undergoing dialysis and can help treat otherwise debilitating autoimmune disorders. Find out how it works.

Plasmapheresis, or plasma exchange therapy, involves removing the blood’s plasma via a blood withdrawal, cleaning it up, and transfusing it back. Similar in many ways to kidney dialysis, therapeutic plasma exchange can be used to treat certain autoimmune conditions by way of fluid replacement. We have the details on how this process works and which conditions it can help successfully treat.

What Is Plasma Exchange Therapy?

According to the American Society for Apheresis (ASFA), therapeutic plasma exchange (TPE) involves passing a patient’s blood through an apheresis machine, removing the filtered plasma volume, and then reinfusing the red blood cells back in, along with replacement fluid like fresh frozen plasma or albumin.

While the terms apheresis, plasmapheresis, and plasma exchange (PE) are quite often used interchangeably, there are some distinctions in their definitions that we’ll address first.

  • Apheresis: This is a general term that describes the removal of blood from a patient, after which some portion of the blood is separated and retained by the doctor while the rest is returned to the donor. If you’ve ever donated plasma, you have interacted with an apheresis machine.
  • Plasmapheresis: This process removes less than 15% of the donor’s blood volume, which is an amount so small it does not need to be replaced with other fluids (much like when you make a whole blood donation and you do not need any replacement substances other than a juice box and a cookie).
  • Plasma Exchange (PE): This therapeutic apheresis removes a large amount of plasma from the person’s blood flow, so much so that if it is not replaced immediately, he or she might experience hypovolemia (a decreased volume of circulating blood) and vasomotor (blood pressure) or circulatory collapse. In this instance replacement fluid is necessary.

The plasma fluid of those sick with autoimmune disorders could be full of antibodies that are attacking the immune system. By separating the red cells from the rest of the liquid part of blood with a cell separator and centrifugation machine, a health care professional can help remove these antibodies, alleviate autoimmune symptoms, and possibly improve quality of life.

What Does Plasma Exchange Therapy Treat?

Certain forms of neuropathy (diseases of the nervous system) and some complications of sickle cell disease can be treated with therapeutic apheresis. Other conditions that have shown clinical improvement from plasma exchange therapy include:

  • Guillain-Barre syndrome (GBS): Also known as acute inflammatory demyelinating polyneuropathy (AIDP), Guillain-Barre syndrome can cause weakness and paralysis of the limbs, and has shown strong evidence of treatment thanks to plasmapheresis in clinical practice, from severe to mild presentations of the condition. IV immunoglobulin (IVIg) is an alternative treatment for Guillain-Barre syndrome patients, with neither IVIg or plasma exchange therapy showing any superiority in clinical trials over the other.
  • Chronic inflammatory demyelinating polyneuropathy (CIDP): This neurological disorder is characterized by impaired sensory functions as well as progressive weakness in the limbs. There is strong evidence that plasma exchange therapy is effective as a short-term treatment alongside immunosuppressants, steroids, and IVIg.
  • Myasthenia gravis: This chronic autoimmune disease translates literally to “grave (serious) muscle weakness.” It afflicts the skeletal muscles of the limbs and body, including those needed for breathing. While clinical results are mixed, plasma exchange treatment is nevertheless considered a treatment option.
  • ANCA-associated rapidly progressive glomerulonephritis: This is inflammation of the tiny filters or glomeruli of the kidneys. Glomerulonephritis also plays a role in other autoimmune disorders like Goodpasture’s syndrome and systemic lupus erythematosus, both of which can be helped with the use of therapeutic apheresis in clinical practice.

Each of these conditions involves antibodies in the plasma of the blood which, instead of attacking foreign invaders like viruses, target healthy cells with important functions. This is true in conditions like multiple sclerosis (MS) in which the immune cells attack the protective sheathing on nerve cells. In more recent years plasma exchange therapy is being studied in relation to conditions like thrombotic thrombocytopenic purpura (TTP), a blood disorder characterized by low platelet levels and dangerous blood clots, and Wilson’s disease, a genetic disorder characterized by copper buildup in the body.

Plasmapheresis is also used as a first-line therapy in cases of hyperviscosity syndrome (too much viscosity in the blood) and cryoglobulinemia (the presence of abnormal proteins in the blood that can thicken in cold temperatures).

What is plasma exchange therapy?

How Is Plasma Exchange Therapy Administered?

Plasma exchange therapy may be administered on either an in-patient or out-patient basis. The patient will rest on a bed or cot while a needle and catheter (the tube) are inserted in the best vein possible (if not in the arm then in the shoulder or possibly the groin). This is the outtake tube, whereas the reinfusion line will be inserted in the other arm or possibly the foot.

Those who are donating plasma may be done in as little as 90 minutes, while those receiving plasma exchange therapy may find the procedure takes as long as 4 hours up to 5 times per week depending on the state of their overall condition and any side effects or exacerbations which may arise.

How Should You Prepare for Plasmapheresis?

Rest assured that the process is relatively painless. Outside of the discomfort associated with needles and sitting still for a long period of time, the general recommendations for optimal comfort during this procedure include:

  • Getting a good night’s rest the day before.
  • Drinking plenty of fluids well in advance (keep in mind that you can’t get up to pee during this procedure).
  • Eating a solid meal before this procedure to reduce the risk of becoming light-headed or fainting.
  • Wearing comfortable clothing and bringing a blanket if you tend to get cold.
  • Bringing a novel, electronic device, or book of puzzles to stay entertained during the duration.

Potential Risks of Plasma Exchange Therapy

Outside of the faintness, dizziness, and cold feelings most people know are associated with donating blood (and a drop in blood pressure), other risks of undergoing plasmapheresis include stomach cramps, blurred vision, and possible infection, blood clotting, or an allergic reaction.

If you worry about infection, talk with your doctor to make sure you’re up on your vaccinations. You may be prescribed an anti-coagulant for blood clots, and if there is an allergic reaction to the solution your plasma is replaced with, health care professionals will be on hand to help you safely through it.

How Is Plasma Exchange Therapy Administered?

It’s in Your Blood

Along with immunosuppression drugs, plasma exchange therapy can help treat and drastically improve certain autoimmune disorders by cleaning your blood. Talk to your doctor or another qualified health care professional about your treatment options and whether plasma exchange therapy could improve your condition.

What Everyone Should Know About B-Type Natriuretic Peptide and Congestive Heart Failure

B-type natriuretic peptide is a hormone produced by the heart ventricles in response to pressure changes linked to heart failure. By testing BNP levels, doctors can screen for heart disease and assess the efficacy of heart disease treatments. Learn what to expect from a test and how to keep your BNP levels in the healthy range.

Brain natriuretic peptide, commonly called B-type natriuretic peptide or, even more succinctly, BNP, is a hormone produced by the heart ventricles (the pumping chambers of the heart) in response to pressure changes linked to heart failure. Since its discovery in the late 1980s, it has earned a place of prominence in the medical world, as it can be used as a biomarker to facilitate the diagnosis of congestive heart failure (CHF).

Researchers have found that B-type natriuretic peptide measurements can be used not only to help with the diagnosis of heart failure, but also to predict future cardiovascular events and the risk that such events will prove fatal. This is part of what’s known in clinical practice as risk stratification: the separation of patients into low risk, rising risk, and high risk in order to develop the most effective treatment plan possible.

According to an article published in Circulation, a journal published by the American Heart Association, BNP levels are “a powerful marker” for cardiovascular risk stratification. “In a recent study of 78 patients referred to a heart failure clinic, BNP showed a significant correlation to the heart failure survival score,” the authors wrote. “In addition, changes in plasma BNP levels were significantly related to changes in limitations of physical activities and were a powerful predictor of the functional status deterioration.” They mention, too, that measurements of BNP levels taken when patients came in through the emergency department could be used to predicate how patients would fare once they were discharged, with higher BNP levels strongly associated with worse prognoses.

There’s some evidence as well that B-type natriuretic peptide concentrations have predictive value for other cardiac conditions, such as acute coronary syndromes and pulmonary embolism.

It’s rare that a relatively new diagnostic measurement results in such rapid and widespread changes to clinical practice. Read on to learn exactly what B-type natriuretic peptide is and how measurements of BNP levels, which can be analyzed with a simple blood test, allow doctors to evaluate complicated elements of cardiovascular health.

What Is B-Type Natriuretic Peptide?

In scientific terms, B-type natriuretic peptide (BNP) is a polypeptide made of 32 different amino acids. When the muscles of the heart stretch excessively in response to changes in blood volume caused by heart failure, they release BNP along with its inactive, 76-amino acid synthetic byproduct, known as N-terminal prohormone BNP, or NT-proBNP.

BNP is one of four natriuretic peptides. All the members of this protein hormone family are secreted by components of the circulatory system. Atrial natriuretic peptide (ANP) is secreted by the atria of the heart (the upper pumping chambers), as its name indicates. BNP comes from the larger, stronger lower chambers, while C-type natriuretic peptide (CNP) is generated primarily in the blood vessels. The highest levels of dendroaspis natriuretic peptide, or D-type natriuretic peptide (DNP), the most recently discovered member of the family, have been found in blood plasma but are believed to be secreted by the heart.

All four natriuretic peptides appear to help regulate circulation. So far, experts have compiled the most data on the actions of ANP and BNP, which are jointly known as the cardiac natriuretic peptides. Both cause the blood vessels to dilate, allowing more blood to flow through them and lowering the risk of clot formation. They also help the kidneys flush out higher quantities of water as well as salt (a process called natriuresis).

Furthermore, researchers have found that ANP and BNP downshift the production of hormones like adrenaline, angiotensin, and aldosterone that narrow blood vessels, increase fluid retention, or elevate the heart rate.

The overall effect of the actions of ANP and BNP—namely, relaxing blood vessels, thereby lowering blood pressure, and improving renal function—ensures that the heart does not have to overtax itself. That’s why when the heart is under stress, the body increases levels of these protective peptides.

What is B-Type Natriuretic Peptide?

How B-Type Natriuretic Peptide Relates to Heart Disease

As touched on in preceding sections, pressure changes inside the heart stimulate release of both B-type natriuretic peptide (BNP) and N-terminal (NT)-pro hormone BNP (NT-proBNP). Because those pressure changes tend to be indicative of either heart failure or some other type of cardiac malfunction, experts have proposed that both BNP and NT-proBNP levels might have prognostic value as a simple, inexpensive method of screening for cardiovascular diseases, particularly chronic heart failure.

The Effects of Chronic Heart Failure on the Body

Chronic heart failure, also called congestive heart failure (CHF), occurs when the ventricles (the walls of the heart chambers) become either too weak or too tense to properly pump blood throughout the body. Two of the top underlying causes are coronary artery diseases and high blood pressure. Other causes include heart valve diseases and, less frequently, diseases of the heart muscle (cardiomyopathies).

The heart’s purpose is to draw in the blood that has been circulating through the veins and push it back out into the arteries. As the muscles weaken, the hearts of individuals with CHF cannot contract enough to fully pump blood back into the arteries. As a result, blood begins to collect in the lungs, then the veins, and the tissues of the body do not receive the supply of oxygenated blood they need.

Because of this lack of sufficient oxygen in their bodily tissues, individuals with CHF often feel fatigued and unable to exert themselves physically. Renal function becomes impaired—sometimes permanently—exacerbating the fatigue and making treatment more challenging. The brain suffers from this lack of oxygen-rich blood as well, causing confusion.

The blood collected in the lungs and veins produces its own set of symptoms, beginning with lung function. Shortness of breath is the definitive symptom of CHF. Initially, it only sets in during physical exertion, but as the disease progresses, it transpires while individuals are resting. Advanced CHF can make it impossible for individuals to sleep lying flat—when they do, their shortness of breath can intensify to the point where they are awakened by it. Other ways CHF shows up in the respiratory system include wheezing, coughing, and increased susceptibility to pneumonia. The most severe presentation is acute pulmonary edema, a buildup of fluid in the lungs that requires emergent medical attention.

Other symptoms of CHF include:

  • Weakness
  • Loss of appetite
  • Fluid retention in the feet and legs
  • Abdominal bloating
  • Swelling of the scrotum and penis
  • Frequent nighttime urination
  • Diminished urine output throughout the day and night
  • Weight loss (cardiac cachexia)

People of all ages can develop chronic, congestive heart failure—even children!  Statistics show close to 5 million Americans currently have CHF, and around 555,000 new diagnoses are made each year.

This serious condition can be fatal, and it’s common for death to occur suddenly. Individuals with CHF experience sudden death at a rate that’s between 9 and 10 times that of the population at large! This makes it vital for doctors to have the means to rapidly and accurately diagnosis CHF.

13 Symptoms That Can Indicate Chronic Heart Failure (CHF)

Using B-Type Natriuretic Peptide to Diagnose Chronic Heart Failure

When it comes to diagnosing CHF in the advanced stages, doctors have a plethora of screening tests at their disposal. By that point, the symptoms will be quite clear, and chest X-rays, electrocardiograms (EKGs), or certain blood tests can confirm a doctor’s suspicion.

Earlier presentations of CHF can be harder to catch, however, as symptoms overlap with those of a number of lung, liver, and kidney diseases. In order to determine the root cause of a patient’s symptoms, doctors historically used an ultrasound test called an echocardiogram, or an echo for short. This safe, typically painless test allows doctors to see the heart muscles at work and to determine its ejection fraction, a measurement of the quantity of blood pumped by the left ventricle with each contraction. The healthy range for ejection fractions is between 50% and 70%.

The downside to echocardiograms is that they can be expensive and may not be available under all circumstances. This is where the value of BNP tests becomes clear. These simple, low-cost blood tests can be carried out bedside in an emergency department if need be. According to experts in the field, about 98% of the times that a BNP test reveals normal levels, it’s accurate to rule out CHF as a diagnosis. This suggests to doctors that they should focus their attention on alternate explanations for shortness of breath or other symptoms that could indicate CHF.

At most facilities, a test revealing BNP levels below 100 picograms per milliliter (pg/ml) is grounds for eliminating CHF as a potential diagnosis. If patients are experiencing kidney failure, the threshold rises to 200 pg/ml.

When tests show high BNP levels, next steps become less certain. This alone does not fully support a CHF diagnosis, as there are other factors that can affect BNP levels, such as:

  • Age
  • Sex
  • Lung, kidney, and liver health
  • Blood pressure
  • Thyroid function
  • Cortisol levels
  • Some uncommon tumors
  • Brain hemorrhages
  • Body weight

Certain medications, including diuretics, beta blockers, ace inhibitors, and spironolactone also impact BNP levels.

That said, BNP levels of around 900 pg/ml in individuals between the ages of 50 to 75, or over 1,200 pg/ml for those older than 75 correlate to a diagnosis of CHF 90% of the time. In most cases, patients with high BNP levels who do not have CHF have either severe lung or kidney disease.

BNP levels can not only help doctors make a diagnosis of CHF but also evaluate how far the disease has advanced, develop treatment plans, and determine how patients respond to different interventions. Generally speaking, the higher BNP levels are, the more severe the situation. As treatments take effect, backed up blood begins circulating into the rest of the body once again, and heart muscle cells begin to recover and to secrete less BNP.

A systematic review of clinical trials published in The BMJ looked at how accurate BNP measurements—both initial levels and changes in response to treatments—are for predicting risk of death, myocardial infarction (heart attack), and other cardiovascular events in heart failure patients. The authors determined that BNP has strong prognostic value for heart failure patients at all stages of the disease as well as for asymptomatic patients.

They went as far as to state that their findings raise “important questions concerning the way that heart failure is defined and diagnosed.” The majority of the recent trials and studies they analyzed used ventricular systolic function, expressed in terms of ejection fraction measurements, as the reference standard for the diagnosis of heart failure. “This is despite the fact that it is recognized that 20-50% of patients with heart failure have preserved systolic function,” they wrote. Given those statistics, they propose that BNP may be a superior method for identifying patients who would benefit from treatment for heart disease.

What Factors Impact BNP Levels, Other Than Chronic Heart Failure?

Can B-Type Natriuretic Peptide Levels Be Used to Diagnose Coronary Artery Disease?

When patients have coronary artery disease (CAD) without CHF, the muscles of their heart do not stretch in the way that spurs the release of BNP. If they have extensive coronary artery blockages, however, or active vascular inflammation, this can cause heart muscle cells to become ischemic (oxygen-deprived). Ischemic heart muscles cells also release BNP, though in smaller quantities than when they’re attempting to counterbalance the effects of CHF.

Experts are quite excited about the possible use of BNP values to diagnose CAD, particularly for patients with asymptomatic CAD. As a review published in QJM: An International Journal of Medicine put it, “It would be of great benefit if a simple blood test could identify those most likely to have CAD.” As a follow-up to that screening measure, individuals whose test results indicate they’re likely to have CAD could undergo “more definitive but more invasive tests,” like angiography and stress tests. The authors believe BNP testing “has the potential to reduce cardiac deaths” because its widespread use will let doctors “better target cardioprotective strategies to those who most need them.”

What to Expect from a BNP Test

Now that you have a sense of why experts in the field of cardiovascular health find BNP tests almost endlessly exciting, you may be wondering, what exactly occurs during a BNP test?

As you know, the test measures BNP concentrations in the blood. In clinical practices, doctors are likely to recommend a BNP test when patients have symptoms of chronic heart failure like the classic shortness of breath. This simple, inexpensive test can catch CHF in the early stages before more serious complications develop. BNP tests can also be used to evaluate whether heart disease treatments are having the desired effects.

A BNP test does not require any special preparation, such as fasting. The test involves drawing blood from a vein using a hypodermic needle, so if you feel faint at the sight of blood, you may wish to ask a family member or friend to accompany you and drive you home.

The blood sample will then be sent to a laboratory where machines measure levels of BNP as well as NT-proBNP. This process typically takes between 15 and 20 minutes if the laboratory is located in the same facility where the test was performed. If the blood sample has to be sent to a separate laboratory, it make take up to a week for the results to be ready.

Once a doctor has reviewed the BNP test results, they will let you know whether your levels are high enough to indicate a diagnosis of heart failure. If you already have a confirmed diagnosis of CHF, your doctor will update you on whether your current treatment protocol is working effectively, as evidenced by lower BNP levels.

As touched on earlier, BNP levels under the threshold of 100 pg/ml usually exclude a diagnosis of heart disease. However, normal, healthy BNP levels fluctuate depending on your age and sex.

Normal BNP levels by Age and Sex

5 Expert-Approved Methods for Lowering BNP Levels

If you improve your heart health, your BNP levels will drop. Certain risk factors for heart disease are out of your control, such as a family history of the disease and your underlying genetic makeup. However, there are a variety of steps you can take on your own to address lifestyle-related risk factors known to negatively impact heart health, including:

  1. Stop smoking cigarettes. As you almost certainly know, smoking cigarettes harms your health. Studies have shown it undermines heart health in multiple ways, including raising your blood pressure, decreasing good high-density lipoprotein (HDL) cholesterol levels, and elevating your heart rate. It can be quite challenging to stop, but the benefits are undeniably worth the effort. After just 1 year, your susceptibility to heart disease drops significantly, and 15 years after cessation, it’s equivalent to that of someone who has never smoked.
  2. Engage in regular physical activity. The Centers for Disease Control (CDC) recommend that adults get at least 2 hours and 3 minutes of moderate-intensity aerobic activity each week, along with at least two strength training sessions. If you find it difficult to fit exercise into your schedule, don’t despair: even three 10-minute sessions daily can add up to make a difference. Try taking a brisk walk or spending time outside gardening. You can also build healthy habits into your day by taking the stairs, parking in the spot furthest from the door, or commuting to work on your bike. Ideally, you should also be finding ways to enhance your fitness by increasing the intensity, frequency, and duration of your workouts.
  3. Prioritize stress management. Scientists have uncovered a clear link between uncontrolled stress and heart disease. The body responds to stress by releasing a hormone called cortisol, which can have a detrimental impact on your cardiovascular health. This is particularly true if stress becomes chronic. Be sure to find ways to manage the stress that inevitably arises as a part of life. Strong research supports the use of mediation and breathwork for this purpose.
  4. Get adequate sleep. Safeguarding your sleep is a vital part of stress management as well as the fortification of your overall health. Unfortunately, findings show that 30% of Americans experience intermittent insomnia, while many more struggle with milder forms of sleep deprivation on a regular basis. Building healthy sleep habits, such as refraining from working or eating in bed as well as using a computer or cell phone too close to your bedtime, can help you get the 7 to 8 hours experts advise for adults.
  5. Supplement with essential amino acids. As mentioned earlier, one of the physiological causes for chronic heart failure (CHF) is the weakening of the heart muscles. Researchers have found that amino acids can help counteract three of the ways that heart failure impairs muscle function: accelerated breakdown of muscle protein, poor regulation of muscle blood flow, and impaired production of cellular energy. Learn more about how to use essential amino acids to increase heart health here.

5 Ways to Lower Your BNP Levels and Enhance the Health of Your Heart

Is It Possible to Reverse Liver Cirrhosis Naturally?

How serious is liver cirrhosis, what causes it, and is it possible to reverse? Find out about how to cope with liver cirrhosis naturally.

The liver is one of the most unique organs in our bodies, with an ability to heal in a way that other vital organs cannot. Damage done to the heart, for example, is damage that cannot be undone by your body or by medical technology; it can only be worked around. Likewise with the kidneys: ground lost in kidney functioning is ground that is permanently ceded. However, some people do require liver transplants, indicating that as much as the liver can recover from damage, it can’t completely regenerate after a certain point. Where is the line between reversible damage and irreversible damage? Can you reverse liver cirrhosis naturally, without medications or a transplant? This article explores that question.

Is it possible to reverse cirrhosis naturally?

What Is Cirrhosis of the Liver?

Your liver is the largest organ inside your body (your skin itself is the largest organ overall, but it’s on the outside). The liver’s function is to help digest your food, store energy substances, and detoxify your blood of any impurities, poisons, or toxins that are eaten or otherwise ingested.

You can aid a healthy liver in its detox duties by consuming a liver flush diet. But what can you do to help an already ailing liver? First, it’s important to understand what cirrhosis is and where it falls on the liver damage continuum. What follows are the stages of liver failure.

  • Stage 1: The first stage leading to liver failure is inflammation. The liver becomes inflamed and enlarged when it is overtaxed with too many toxins and cannot filter them out at a high enough rate. Common causes of liver inflammation include viral hepatitis infection, alcohol consumption, autoimmune hepatitis, or poisoning. Sometimes this stage arises without any noticeable symptoms.
  • Stage 2: Fibrosis of the liver is the second stage of liver damage, which involves the appearance of scar tissue on the liver. A little bit of scarring can be overcome, but chronic liver fibrosis is also known as the early stages of cirrhosis. Scarring inhibits liver functioning and starts to threaten a person’s survival rate.
  • Stage 3: Cirrhosis of the liver is the third stage of liver failure, an incredibly serious and life-threatening condition that may have symptoms like jaundice (a yellowing of the eyes and skin), muscle cramps, dry mouth, peripheral edema, abdominal fluid buildup (ascites), and compromised brain function (hepatic encephalopathy).
  • Stage 4: The fourth and final stage is end-stage liver disease. This is often the cause of death in those who are not treated quickly enough or who cannot receive a liver transplant. Blood tests determine who is healthy enough to even be included on the transplant list, and not everyone is eligible.

As you can see, cirrhosis is the last stop before potential end-of-life hospitalization. When scarring of the liver becomes so extensive that it eclipses healthy liver tissue and starts to interrupt blood flow, detoxification, and digestion, medical advice and treatment is an emergency necessity, but can cirrhosis be fixed?

Cirrhosis: Symptoms, Complications, and Prognosis

The National Institute of Diabetes and Digestive and Kidney Diseases says that the most common underlying causes of liver scarring and cirrhosis are conditions like chronic hepatitis, long-term alcohol abuse, and cases of diet-induced nonalcoholic fatty liver disease. Some of those conditions can be treated or avoided entirely by getting vaccinated, making diet and lifestyle changes, practicing safe sex, and drinking alcohol in moderation, but if the damage is not stopped in time, liver failure and liver cancer may develop, which could end a person’s life.

Cirrhosis Symptoms

It’s important to recognize the symptoms of cirrhosis and liver disease as soon as possible. Those symptoms include:

  • An itching sensation of the skin
  • Swelling in the extremities (edema)
  • Unexplained fatigue or listlessness
  • Lack of appetite
  • Stomach or muscle cramping
  • A tendency to bruise or bleed easily
  • Unusually dark urine
  • Tar-colored or pale stool
  • Cognitive disorientation or confusion
  • Unexplained weight loss
  • Jaundice or yellowing of the skin or sclera of the eyes

Cirrhosis Complications

Regardless of how it comes about (hepatitis B, hepatitis C, alcohol abuse, fatty diet, or genetics), cirrhosis affects up to 10% of the population of the United States, according to the American Liver Foundation. The complications of cirrhosis quickly shorten the lifespan of those diagnosed with this disease. Complications include:

  • The creation of bile duct and gallstones
  • Portal hypertension, edema, and ascites, which can lead to the bacterial infection known as peritonitis
  • Hepatic encephalopathy, which leads to an accumulation of toxins in the brain
  • Diseases like type 2 diabetes and metabolic bone disease due to the interference in digestion and absorption of nutrients
  • Weakened immune system and spleen functioning
  • Higher risk of infection, kidney failure, and lung failure
  • Varices, which are enlarged blood vessels in the stomach or esophagus that may burst and cause deadly bleeding
  • A much higher risk of liver cancer

Cirrhosis Prognosis

Unfortunately cirrhosis isn’t curable, but it is treatable. Once you’re aware of the damage being done to the liver, the first priority is to treat and if possible cure the underlying cause, and then to stop the progression of cirrhosis and prevent deadly complications. For alcoholics that means sobriety is key. For those with hepatitis, disease management is the first priority. For those whose liver biopsy shows too much damage to overcome, a liver transplantation may be the only option, but for some, there are natural ways to help your liver cope with cirrhosis.

Is it possible to reverse cirrhosis naturally?

Can You Reverse Liver Cirrhosis Naturally?

As with scar tissue anywhere on or in your body, while you can’t reverse the damage, you may be able to minimize its impact on your life and live around it. What follows now are natural ways to cleanse your liver, support its health and functioning, and strengthen your body so you have the resources to cope with any complications that may arise.

1. Eat a Liver-Cleansing, Anti-Inflammatory Diet

Your liver detoxifies your body, so you can’t exactly detoxify it. What you can do, however, is to avoid poisoning it and provide it with the nutrients it needs to detox itself. That means avoiding alcohol intake entirely, only consuming medicine when you absolutely need to (avoid over-the-counter medications for mild aches and pains if possible), and eating a robust diet of nutrient-rich foods such as:

  • Dark, leafy greens like spinach and kale
  • Other steamed veggies like broccoli, carrots, and asparagus
  • Potassium foods like avocados, sweet potatoes, and bananas
  • Natural herbal supplements like ginger, turmeric, milk thistle, or dandelion and burdock root
  • Probiotics like Greek yogurt or sauerkraut
  • Citrus fruits and juices
  • Cold-pressed oils like coconut and extra virgin olive oil
  • Superfood supplements like wheatgrass, spirulina, and chlorella

Avoid overeating and abstain from unhealthy food substances like refined sugars and carbs, spicy and fried foods, alcohol, and caffeine. If you smoke, now is the time to quit to help preserve your liver function and quality of life.

2. Maintain a Healthy Body Weight

Obesity and fatty diet are huge contributors to liver disease in the Western world, and if those are the underlying causes of nonalcoholic fatty liver disease (NAFLD) and cirrhosis, they need to be addressed immediately.

Even if weight is not directly tied to cirrhosis (let’s say your cirrhosis is caused by a hepatitis infection), maintaining a healthy weight is still imperative. Obesity is closely linked to high blood pressure, which causes extra strain on your heart and increases your risk factors for diabetes and your cholesterol levels. By focusing on healthy, sustainable weight loss and eliminating obesity as a risk factor, you improve your liver’s health.

3. Guard Against Diseases and Toxins

The best defense is sometimes a good offense, and when it comes to liver disease and liver failure, that means reducing your exposure to toxins (household or industrial chemicals that can damage your liver cells), as well as to diseases like hepatitis (if you’re not already vaccinated, make it a top priority), and checking your medications for anything expired or unnecessary (ask your doctor about any prescriptions or take gentler alternatives to common over-the-counter drugs). By preventing toxins of any kind from reaching your liver, you preserve its remaining healthy tissue.

Managing a Cirrhosis Diagnosis

Cirrhosis cannot be reversed, as it’s the last stage of liver disease before hospitalization is required. However, the preceding stage, liver fibrosis (when scar tissue is still being accumulated), can be stopped before the damage becomes permanently debilitating. You can’t be too careful when it comes to the symptoms of liver damage: the sooner you catch it, the better diagnosis you’ll receive and the longer you’ll be able to live healthily.

Liver Failure Death: Causes, Symptoms and Stages

What are the causes and symptoms of acute and chronic liver failure? How is liver damage diagnosed? Prevented? What are the stages that lead to liver failure death? Find out here.

The human liver is one of our most vital organs, responsible for filtering our blood and detoxifying our bodies. Without a functioning liver, we first become jaundiced, and after a certain point, we can no longer stay alive without liver transplantation. Any issue with liver function is a life-threatening healthcare emergency. So come with us as we explore the leading causes of liver damage and the progressive stages of liver failure death.

What Causes Liver Failure Death?

Cirrhosis is late-stage scarring of the liver (fibrosis). According to those who study hepatology, the most common causes of cirrhosis in the United States are due to hepatitis C infections and heavy alcohol consumption. These chronic liver diseases not only affect one’s quality of life, but can also lead to the end of life.

However, there are other causes of acute liver failure that have a much faster onset, such as drug or toxin overdoses. Genetics are also among the risk factors that can contribute to liver damage and disease, as are obesity, autoimmune disorders, and various forms of cancer.

Liver failure death: causes, symptoms, and stages.

Causes and Symptoms of Acute Liver Failure

Acute liver failure is a rapid decline of liver function caused by:

  • Acetaminophen (Tylenol) overdose
  • Viral hepatitis infections (hepatitis A, B, and E)
  • Autoimmune hepatitis
  • Adverse reactions to medications for epilepsy, antibiotics, or even nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Adverse reactions to herbal supplements like kava (a nightshade plant) or ma huang (ephedra)
  • Wilson’s disease (a rare genetic disorder that causes copper buildup and poisoning)
  • Hepatic vein thrombosis (also known as Budd-Chiari syndrome)
  • Exposure to toxins like poisonous mushrooms or industrial chemicals

The symptoms of acute liver failure include:

  • General malaise or a feeling of unwellness
  • Persistent tiredness, drowsiness, or sleepiness
  • Confusion or disorientation
  • Nausea and/or vomiting
  • Abdominal pain or swelling
  • Jaundice (a yellowing of the eyes or skin)

Causes and Symptoms of Chronic Liver Failure

Chronic liver failure is characterized by long-term progressive damage from the following causes:

The symptoms of chronic liver failure and breakdown could entail:

  • Persistent fatigue
  • Loss of appetite
  • Nausea and/or vomiting
  • Abdominal pain or discomfort
  • Jaundice of the eyes or skin
  • Easy bleeding or bruising
  • Disorientation or confusion
  • Severely itchy skin
  • Darkening of the urine
  • Fluid buildup in the arms or legs (edema)
  • Fluid buildup in the abdomen (ascites)

The Symptoms of Liver Cancer

Cancer that develops in the liver (referred to as primary liver cancer) could also be the cause of liver failure. Those with cirrhosis (the third stage of liver failure) are more at risk of developing liver cancer, which could then shut down the organ or spread to the rest of the body. Liver cancer symptoms could include:

  • Loss of appetite
  • Nausea and/or vomiting
  • Jaundice
  • Itchy skin
  • Unexplained weight loss
  • Abdominal pain or swelling

The Stages of Liver Failure

Liver failure and liver disease are two different things, but one of them can cause the other. Liver disease encompasses any ongoing condition that damages the liver, including inflammation and infection. Liver failure occurs when the liver loses a portion or the entirety of its functionality.

Damage to the liver can come in stages, creating a systematic shutdown of the body and requiring end of life care from health care professionals. What follows are the details of those various stages.

1. Inflammation of the Liver

Inflammation of the liver is often the beginning of the damage that can ultimately lead to a person’s death. Not everyone will notice or feel when their liver becomes inflamed or enlarged, and if the inflammation continues unabated, permanent injury or scarring could occur, leading to the next stage of liver failure.

2. Fibrosis of the Liver

Fibrosis is liver scarring. While the liver is one of the most unique organs thanks to its ability to heal itself (unlike the heart muscle), long-term damage from repeated intoxication or uncured or incurable infections can still build up. When scar tissue begins to take the place of healthy and functional liver tissue, it diminishes the liver’s ability to function. Again, this progressive damage is not always detectable, and the longer it persists, the more it affects the individual’s survival rate.

3. Cirrhosis of the Liver

Cirrhosis is characterized by severe scarring of the liver. When the damaged tissue accumulates enough to interrupt liver functioning, it puts your health in serious jeopardy. When scarring starts to outnumber and overwhelm healthy tissue, the liver begins to fail. Sometimes this stage is the first one that presents symptoms noticeable by the individual, including jaundice, dry mouth, muscle cramps, increased ease of bleeding, buildup of fluid in the abdomen (ascites), peripheral edema, and reduced brain functioning (hepatic encephalopathy).

4. End-Stage Liver Disease

Those with end-stage or advanced liver disease require palliative care and may be placed on a waiting list for a liver transplant by their health care provider depending on their MELD score (model for end-stage liver disease). This score was established to evaluate the short-term (90-day) survival rate of people with advanced liver damage, and it is determined by a series of blood tests. The MELD score ranges from 6 to 40, with 6 being the best change of survival.

Liver failure death: causes, symptoms, and stages.

Diagnosis of Liver Failure

Doctors may use several tools and methods to diagnosis and evaluate the severity of acute liver failure, including the following.

  • Blood tests: These tests include liver blood tests for enzymes that indicate liver functionality, CBC tests (complete blood count), or other blood tests to look for issues like viral hepatitis infection or undiagnosed genetic conditions.
  • Imaging tests: An MRI, ultrasound, or CT scan may be used to visually inspect the liver.
  • Biopsy: A tissue sample may be taken from the liver to investigate for scarring or other signs of disease and infection.

Liver Failure Treatment Options

First of all, in cases of acute liver failure, the patient will need to be hospitalized, and possibly in the intensive care unit to be given round-the-clock support as medical staff attempts to stabilize and treat their condition. Depending on the cause of the liver failure, a person may either recover or require a liver transplant.

For liver failure resulting from a chronic condition, often the first step is addressing the cause. If it’s drugs or alcohol, rehab needs to be part of the protocol. If it’s due to a viral hepatitis infection, then treatment will follow accordingly. For those with autoimmune conditions, certain therapies may be suggested by the medical team depending on the effects of the condition. If liver failure is a matter of lifestyle causes (poor diet or overuse of medications), then those behaviors would have to be addressed as part of a comprehensive treatment.

The American Liver Foundation says that liver failure can actually be reversed if it’s caught at the second (fibrosis) stage. For the third or cirrhosis stage, while the damage may not be reversed, it can be slowed, stopped, or treated so that the person may continue to live healthily.

For those with end-stage liver failure, however, if a liver transplant cannot be performed, the only follow-up may be end-of-life care.

How to Prevent Liver Failure Death

Given how important liver health is to human survival, taking care of your liver and your overall health is the best way to prevent sometimes permanent and deadly liver damage. Some ways to protect your liver include:

  • Abstaining from alcohol or only drinking in moderation
  • Never mixing medications with other drugs or supplements without a doctor’s consent
  • Never mixing medications with alcohol
  • Taking over-the-counter medications only when needed
  • Taking prescribed medications only as directed and to completion
  • Maintaining a healthy weight
  • Aiding liver detox with your dietary choices
  • Getting vaccinated against hepatitis A and B

Liver Long and Prosper

If you suspect there is anything wrong with your liver, seek medical advice immediately. The sooner you intervene on behalf of your liver’s health, the better chance you have at being able to reverse the damage done and heal completely. In many cases liver failure death can be prevented, if it’s caught in time and if you follow your doctor’s advice. Eat well, detox regularly, and you may well live long and prosper.