What Is Hydrocephalus? Plus Causes, Symptoms and Prognosis

The causes of hydrocephalus, the accumulation of excess fluid around the brain, remain somewhat mysterious and the symptoms vary significantly from person to person. While it can be challenging to identify, it is treatable, though doing so requires surgery. Read on to learn more about this complex neurological condition.

Hydrocephalus, the accumulation of excess fluid around the brain, can affect infants, children, and adults. In infants and young children, the most obvious symptom tends to be a rapid increase in head circumference, or, if hydrocephalus is present from birth, an atypically large head. Older children and adults present with different symptoms, as their skulls cannot expand to make room for the buildup of fluid. While hydrocephalus causes remain somewhat mysterious, the condition can be treated, though doing so requires surgery. While prognosis after treatment varies, it’s entirely possible for individuals to recover and go on to experience a good quality of life.

What Is Hydrocephalus?

The medical term hydrocephalus, derived from Greek, is somewhat misleading. The word hydro means water in Greek while the word cephalus means head. Despite the fact that hydrocephalus was historically referred to as “water on the brain,” the accumulated liquid that’s characteristic of this condition is not water at all. It’s cerebrospinal fluid. The purpose of cerebrospinal fluid (CSF) is to surround and protect the brain as well as the spinal cord, however, a delicate balance of this fluid must be maintained.

CSF has three absolutely vital functions:

  1. Act as a cushion for brain tissue, protecting it from jostling and blows
  2. Transport nutrients and waste
  3. Offset changes to intracranial blood volume by moving between the cranium and the spine

When all is working as it should, CSF flows through the ventricular system (four spaces in the brain linked by narrow passages), spills into the cisterns located below the brainstem (which essentially act as reservoirs), travels across the exterior of the brain and spinal cord, and then enters the bloodstream where its reabsorbed.

The body continuously produces CSF, so if any element of the system malfunctions, causing the flow of CSF to be disrupted, it will begin to accumulate in the ventricles. As the ventricles widen to accommodate the buildup of fluid, excessive pressure is placed on the tissues of the brain. That pressure on the brain, in turn, causes hydrocephalus.

The Three Vital Functions of Cerebrospinal Fluid

Differentiating Between Types of Hydrocephalus

Per a fact sheet prepared by the National Institute of Neurological Disorders and Stroke (NINDS), a division of the National Institutes of Health, diagnoses of hydrocephalus fall into one or more of the following categories.

1. Congenital Hydrocephalus

When hydrocephalus is diagnosed at birth, it’s called congenital hydrocephalus. This type of hydrocephalus develops due to either genetic abnormalities or to events or environmental factors present during gestation.

2. Acquired Hydrocephalus

Any type of hydrocephalus that is not present at birth is deemed acquired hydrocephalus. This type of hydrocephalus can develop during infancy, childhood, or adulthood. It occurs as a result of diseases or injuries that affect the brain.

3. Communicating Hydrocephalus

This type of hydrocephalus describes presentations of the condition in which the normal flow of CSF stops after it leaves the ventricles. This means CSF can still move through and between the ventricles themselves.

4. Non-Communicating Hydrocephalus

Non-communicating, or obstructive, hydrocephalus (as you might be able to intuit) refers to conditions in which CSF cannot pass through one (or more than one) of the passages linking the ventricles. For example, in one type of non-communicating hydrocephalus, called aqueductal stenosis, the accumulation of CSF results from constriction of the aqueduct of Sylvius, which links the third and fourth ventricles at the center of the brain.

5. Hydrocephalus Ex-Vacuo

This form of hydrocephalus, which primarily occurs in adults, results from brain damage caused by strokes or traumatic injuries. This presentation differs somewhat from those described so far and is characterized primarily by the shrinking of brain tissue.

6. Normal Pressure Hydrocephalus

Known causes of normal pressure hydrocephalus (NPH) include head trauma, subarachnoid hemorrhages, tumors, infections, or surgical complications. However, it’s also possible for this type of hydrocephalus to transpire without the presence of a single one of the factors listed above. The highest rates of NPH are found among older adults. According to the NIH, approximately 375,000 older Americans develop NPH. The Hydrocephalus Association puts that number even higher, stating that a recent study found up to 700,000 older Americans may have NPH, with 80% of those cases going undiagnosed and untreated.

The 6 Types of Hydrocephalus

What Causes Hydrocephalus and Who Is at Risk?

In the simplest terms, hydrocephalus happens because a blockage interrupts the normal flow of CSF, the ability of your blood vessels to absorb CSF becomes compromised, or the brain begins to produce more CSF than it needs. Some common causes of hydrocephalus have already been described in the preceding section. Yet all in all, the instigating factors that result in hydrocephalus remain somewhat obscure. So far, researchers have identified the following potential triggers:

  • Genetic abnormalities
  • Developmental disorders
  • Infections during pregnancy, like rubella
  • Premature birth complications, including intraventricular hemorrhage
  • Meningitis and other central nervous system infections
  • Tumors
  • Traumatic head injuries
  • Subarachnoid hemorrhage
  • Bleeding from blood vessels within the brain
  • Complications following brain surgery

It can be challenging to determine how many people develop hydrocephalus annually or currently have this condition, especially given the potential for NPH to go undiagnosed. According to the Hydrocephalus Association, around 1 million Americans have hydrocephalus.

This condition affects people of all ethnicities, income levels, and stages of life. That said, it’s most common in infants and in adults age 60 and above. Statistics indicate that between 1 and 2 out of every 1,000 babies born have congenital hydrocephalus, making it just as prevalent as Down’s syndrome and more prevalent than both spina bifida and brain tumors. The NIH fact sheet mentions a review published in the Journal of Neurosurgery: Pediatrics in 2008 which found that hydrocephalus accounted for 1.8% of all pediatric hospital days and 3.1% of all pediatric hospital charges in the United States. It’s also the single most common reason children have to undergo brain surgery.

10 Possible Causes of Hydrocephalus

Recognizing Common Symptoms of Hydrocephalus

Because hydrocephalus can cause permanent brain damage, it’s extremely important to seek medical attention promptly. In order for that to happen, you must be able to recognize the symptoms of hydrocephalus. This can be a bit tricky, as symptoms shift depending on a person’s age at onset, how far the disease has progressed, and individual variations that impact response to fluid buildup. As an example of this, when hydrocephalus develops in an infant, their skull can adjust in response to increased CSF pressure and widening of the ventricles by expanding since the sutures (fibrous joints connecting the bones of the skull) remain open.

Here are symptoms of hydrocephalus to look for, categorized by age at onset.

Infancy

  • Protruding fontanel (the soft spot on the surface of the skull)
  • Swift increase in head circumference
  • Excessive fussiness
  • Sunsetting (tendency of eyes to deviate downward)
  • Poor feeding
  • Limited muscle tone and strength
  • Seizures
  • Vomiting

Childhood

  • Crossed eyes, double vision, or blurred vision
  • Uncontrolled eye movements
  • Sun setting
  • Craniofacial disproportion (changes to facial appearance and eye spacing)
  • Increased head size
  • Headaches
  • Difficulty concentrating
  • Balance problems
  • Muscle spasms
  • Impaired coordination
  • Delayed growth
  • Difficulty eating
  • Abnormal sleepiness
  • Low frustration tolerance
  • Decreased reasoning ability
  • Personality changes
  • Loss of bladder control
  • Nausea and vomiting
  • Seizures
  • Memory loss

Adulthood

  • Recurrent headaches
  • Difficulty walking and generalized loss of coordination
  • Bladder issues
  • Vision changes
  • Poor memory and concentration capacity
  • Slowing of movements

It’s important to note that the symptoms of normal pressure hydrocephalus, which frequently occurs in older adults, overlap with those of other disorders like Alzheimer’s disease. When a patient presents with symptoms such as urinary incontinence, difficulty walking, and increasingly worse memory, doctors are far more likely to suspect dementia than hydrocephalus. This leads to high rates of improperly diagnosed as well as undiagnosed cases of normal pressure hydrocephalus.

It should also be said that while the symptoms listed above cover the most common presentations of hydrocephalus, this condition presents differently each time it occurs.

Be Aware of These Common Symptoms of Hydrocephalus

Diagnosing Hydrocephalus

To evaluate a patient who may have hydrocephalus, a doctor will first conduct a thorough physical exam. Pediatricians in particular use this to check for a larger-than-normal head circumference, bulging fontanel, and slowed reflexes.

When evaluating an infant whose fontanel has not yet closed, a pediatrician may use ultrasound to examine the brain by bouncing high-frequency sound waves off of it to create images.

Other tests used to diagnose hydrocephalus include:

  • Neurological examination
  • Computed tomography scan (CT scan)
  • Magnetic resonance imaging (MRI)
  • Lumbar puncture, also known as a spinal tap
  • Lumbar catheter
  • Monitoring of intracranial pressure

Clinicians select the most appropriate test or tests based on a patient’s age, symptoms, and the known presence or indication of irregularities of the brain or spinal cord.

Treating Hydrocephalus

Without proper treatment, hydrocephalus can be fatal. While treatment may not allow for the reversal of brain damage that has already ensued, it can ensure that no more occurs by reestablishing a normal flow of CSF.

At this time, no medical therapy exists for the treatment of hydrocephalus—the only available options are surgical. In most cases, treatment of hydrocephalus involves conducting a surgery to insert a shunt system that allows CSF to travel out of the central nervous system and into another part of the body where reabsorbtion can occur during the normal process of circulation.

A shunt system is relatively simple in design and concept. It involves just three components: a strong, flexible tube called a shunt, a thin tube called a catheter, and a valve. During surgery, a neurosurgeon situates one end of the catheter either inside the brain itself or in the areas around the spinal cord where CSF circulates. The surgeon then places the other end of the catheter in a location where the CSF can drain and be absorbed. Typically, this is in the abdominal cavity, though the areas surrounding the lungs or heart chamber can also be viable options. The valve, located along the catheter, controls the direction and rate of CSF flow. A shunt system will typically need to remain in place throughout a person’s life and will require close monitoring.

A far less common treatment option is what’s called an endoscopic third ventriculostomy. During this surgical procedure, the surgeon uses a device called a neuroendoscope (a tiny camera) to view the surface of the ventricles. Once they have guided the scope into position, allowing them to examine this small, difficult-to-access surgical area, they use an instrument to create a very small opening in the bottom of the third ventricle. In cases where this would be a good treatment option, the hole then allows CSF to flow unobstructed into the area of reabsorption surrounding the brain’s surface.

Comparing Hydrocephalus Treatment Options

Life After Hydrocephalus

Given the number of variables involved in the development, progression, and treatment of hydrocephalus, it’s difficult to generalize about outcomes. Factors that impact a person’s prognosis include:

  • Underlying cause
  • Rapidity of diagnosis
  • Presence of related disorders
  • Degree of relief of CSF pressure

The success of shunt surgery and ventriculostomy vary quite a bit from person to person. In general, the earlier hydrocephalus is diagnosed and treated, the more complete a person’s recovery will be.

It’s important for those affected by hydrocephalus as well as their families to understand that this condition can affect cognitive as well as physical development. After surgery has been performed, treatment and management should be guided by an interdisciplinary team that includes rehabilitation specialists. When connected with the right rehabilitation therapies, individuals diagnosed with this condition can lead independent lives with few restrictions.

Unfortunately, fewer than 10 medical centers in the United States currently specialize in the treatment of this condition, according to the Hydrocephalus Association. Because it involves so many variables and unknowns, doctors who do not specialize in the condition can be reluctant to take on complicated hydrocephalus cases. This means that not everyone with hydrocephalus will be able to access appropriate care.

There has also been limited progress over the last half-century in terms of identifying more effective treatments for hydrocephalus or methods of prevention. “Research is essential,” states the Hydrocephalus Association. “At the very least, we need better treatments, with more positive long-term outcomes, and diagnostic tests that are accurate, cost-effective, and noninvasive.”

At this time, the bulk of the research that’s done is in the pediatric space. The Hydrocephalus Clinical Research Network (HCRN) is made up of seven pediatric medical centers that analyze data from all their hydrocephalus patients with the aim of more rapidly identifying treatment improvements. This collaborative research effort not only carries out concurrent studies at all seven centers, but also oversees an extensive database of patient histories and procedures.

The work of the HCRN, as well as other research efforts focused on hydrocephalus, are supported by the NINDS, along with other institutes of the NIH. While the primary goal of these endeavors is to uncover ways to treat, prevent, and cure hydrocephalus, researchers also investigate the immensely complicated mechanisms underpinning brain development with the hope of understanding more about the origins of neurological conditions.

Protein Replacement Therapy: A Promising Medical Treatment Approach

Protein replacement therapy is a method for treating diseases and disorders by replacing missing proteins in diseased cells. Clinical trials show it can help to treat rare diseases, like recessive dystrophic epidermolysis bullosa, as well as common conditions such as heart disease. Here’s what you should know about the science behind protein replacement therapy as well as its potential applications.

Most laypeople haven’t heard of protein replacement therapy, but the world of molecular medicine is abuzz with interest in this promising medical treatment. A chief aim for those working in the field of molecular medicine is to develop an efficient way to reliably replace missing proteins in diseased cells. Gene therapy is one possible method for achieving that, but according to the U.S. National Library of Medicine, a database overseen by the National Institutes of Health (NIH), this experimental approach comes with considerable risks and significant advances will need to be made before it becomes safe. Other methods of protein replacement therapy, however, do not require the transfer of genetic material into cells, which eliminates some of the most significant issues that arise with gene therapy while still allowing for the delivery of missing or deficient proteins.

Read on to learn more about protein therapy and its potential treatment applications.

The Science of Protein Replacement Therapy

So far, most of the research into protein replacement therapy has been focused on its use for the treatment of rare monogenic diseases. These conditions occur because of a single defect in a single gene found in human DNA. Though these diseases are considered rare, experts estimate there are over 10,000 of them and that they affect millions of individuals around the globe.

Supporting Research Into Treatments for Rare Diseases

Developing treatments for rare diseases can be quite challenging, in part because companies are less likely to make a profit off such treatments, and therefore less likely to fund research into potential treatments and cures. In an effort to address this, several countries have passed legislation to encourage companies to develop drugs to treat “orphan diseases,” a classification applied to “diseases with a prevalence of less than 200,000 affected individuals in the United States and less than approximately 250,000 affected individuals in the European Union (EU),” per an article titled “Protein Replacement Therapies for Rare Diseases: A Breeze for Regulatory Approval?” that was published in Science Translational Medicine in 2013.

The U.S. Orphan Drug Act, passed in 1983, extends regulatory, commercial, and tax incentives to companies investigating drugs designed to treat orphan diseases. In 2000, the EU passed a similar piece of legislation and multiple other countries have since followed suit. Currently, genetic diseases (along with rare types of cancer and drugs with pediatric indications) rank among the top three in terms of approved orphan drug treatments. And protein replacement therapies for monogenic diseases is a popular subcategory within that realm.

Justifying the Use of Monogenic Protein Replacement Therapies

Blood factors and enzyme replacement therapies for lysosomal storage disorders were two of the first monogenic protein replacement therapies (MPRTs) to receive regulatory approval with orphan drug classification in the United States and EU. When these drugs went to market, manufacturers introduced what’s known as “orphan pricing,” a system in which high premiums are charged to compensate for limited demand. According to the Science Translational Medicine article, the cost of MPRTs, a category that includes drugs like Fabrazyme, Elaprase, and Naglazyme, tops $200,000 annually while sales come in at over $100 million.

Given those numbers, it’s hardly surprising how much attention has been paid to the prices charged for orphan drugs, and, subsequently, the difficulties faced by health care systems when it comes to reimbursement. Determining which patients should be approved for these costly treatments requires complicated calculations, and not everyone agrees on which criteria should be used.

The paradigm so far has been that the use of MPRTs can be reimbursed in the United States, most member countries of the EU, and Japan. It’s also common practice for these drugs to be provided at no cost in countries with low average household income levels and underdeveloped health care systems.

The authors of the Science Translational Medicine article argue that in order to justify the high prices charged for orphan drugs and the rates at which health care systems reimburse for their use, manufacturers must demonstrate that they are, in the long-term, cost-effective treatments. While clinical trials have shown that long-term use of MPRTs can be safe, clinically effective, and lead to health-related improvements in terms of quality of life, more research is needed to conclusively prove that their use leads to net reductions in health care costs.

13 Vital Facts About Protein Replacement Therapy

Potential Applications for Protein Replacement Therapy

Clinical trials have investigated the use of protein replacement therapy for a variety of conditions, including:

Two of the most promising applications to date are for the treatment of recessive dystrophic epidermolysis bullosa and heart failure.

Protein Replacement Therapy for Recessive Dystrophic Epidermolysis Bullosa

Studies conducted on the use of protein replacement therapy to treat recessive dystrophic epidermolysis bullosa have yielded highly promising results.

This disease belongs to the epidermolysis bullosa family, a collection of genetic disorders related to structural proteins in the skin. Individuals with these disorders have atypically fragile skin and mucous membranes that are prone to splitting and blistering. To compound matters, the underlying gene defect compromises wound healing. If wounds do manage to heal, extensive scarring is typical.

Recessive dystrophic epidermolysis bullosa (RDEB), one of the most severe iterations, happens when the gene coding for type VII collagen protein either does not function properly or is absent. This protein helps the two primary layers of the skin—the epidermis and the dermis—adhere to each other. Without it, the skin often separates, leading to blisters and a higher risk of infection.

The NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases highlighted research done with mice that indicated protein replacement therapy could be the key to treating this debilitating genetic condition.

The research, published in Molecular Therapy and the Journal of Investigative Dermatology, examined two techniques for replacing absent or defective type VII collagen with the goal of improving wound healing and reversing both structural and molecular defects in the skin of individuals with RDEB.

The first technique involved topically applying human recombinant type VII collagen (rC7) to the backs of mice with normal collagen genes. After 2 weeks, the team of researchers led by David T. Woodley, M.D., and Mei Chen, Ph.D., of the University of Southern California discovered that the rC7 had been stably incorporated and sped up the skin’s healing process. It also decreased scarring compared to untreated mice. The beneficial effects lasted for 2 months.

Next, the researchers tried topical applications of rC7 on RDEB skin grafts attached to the backs of mice. When rC7 was applied to broken skin, it was successfully incorporated and improved wound healing. However, when it was applied to intact skin, it was not incorporated. The researchers concluded that this limits the use of topical rC7 as it can only help to increase the rate of healing for existing wounds and cannot prevent the formation of wounds or blisters.

The second technique was intravenous administration of rC7. The research team began by wounding the skin on the backs of mice with normal collagen genes and injecting rC7 into their tail veins. They discovered that the rC7 traveled to the wounds where it was successfully incorporated. Again, it appeared to accelerate healing. They found no evidence of rC7 in healthy, wound-free skin or internal organs.

Subsequently, the team examined the effects of administering rC7 intravenously to mice with RDEB skin grafts. The injected rC7 traveled to the skin grafts where it “created new anchoring fibril structures, which hold the epidermis together.”

According to study authors Drs. Woodley and Chen, “Intravenous delivery of rC7 opens up new prospects for more systemic treatment of the disease. Our data suggest that intravenous rC7 not only improves the healing of multiple RDEB-related wounds simultaneously, but it can also prevent new blisters from developing in RDEB skin.”

Protein Replacement Therapy for Heart Failure

While much of the excitement about protein replacement therapy has to do with its use for the treatment of rare genetic disorders, it shows promise as a treatment for more common health conditions too.

Myocardial infarction (heart attack) and heart failure are among the top causes of death in the United States and other countries. A myocardial infarction occurs when blood flow to a segment of heart muscle drops below adequate levels. The greater the length of time before treatment to restore blood flow takes effect, the greater the loss of cardiac muscle cells, or cardiomyocytes. Because the adult heart has little capacity for regeneration, the cardiomyocytes lost in the aftermath of a myocardial infarction get replaced by different types of cells, resulting in scarring and, frequently, heart failure.

To develop an efficacious means of promoting heart regeneration, researchers must find solutions to a multitude of quandaries. It appears that protein replacement therapy utilizing modified mRNA (modRNA) may avoid many common pitfalls. “Modified mRNA (modRNA) is a safe, non-immunogenic, efficient, transient, local, and controlled nucleic acid delivery system,” noted the authors of a 2019 article published in Molecular Therapy.

Increased understanding of the molecular pathways and genes involved in heart disease has led scientists to believe protein replacement therapy could be used to target signaling pathways involved in heart disease progression. Per the Molecular Therapy article cited above, delivering replacement proteins to the myocardium (the muscle tissue of the heart) can encourage the regeneration of cardiomyocytes.

Gene Therapy

Some approaches have fallen into the subcategory of gene therapy, which involves placing a defined gene into a cell to either replace a defective gene or to increase the amount of a certain gene in a specific cell or tissue in order to increase production of a needed protein. Some examples of work in that vein included using viral vectors like adeno-associated virus (AAV) to mediate the delivery of either FGF1 and p38 MAP kinase proteins or periostin.

However, the use of viral vectors comes with the risk of viral genome insertions. While preclinical studies have returned encouraging results, namely, “robust and consistent gene expression,” there has also been evidence of adverse effects, including immune responses to the viral vectors.

Direct Delivery of Proteins

As experts continue probing how best to use gene therapy to treat cardiac disease, a consensus is growing that the most practical way to change the expression of a protein of interest is to deliver the corresponding protein directly to the myocardium. This circumvents problems associated with other delivery methods, such as the potential immune responses triggered by viral vectors. It’s also been linked to benefits such as:

  • Higher levels of protein expression
  • Improved dose regulation
  • Enhanced control

Direct protein comes with some issues of its own, however, including the short half-life and overall instability of injected proteins.

Modified mRNA Therapy

Unlike gene therapy and the direct delivery of proteins, mRNA-based therapies have proven to be highly promising methods of treating heart disease as well as other disorders. One reason for that is its overall safeness, because mRNA does not integrate into the genetic code.

The first successful use of direct mRNA transfer occurred in the late 1980s in mouse models. Then, in 2008, a team of researchers from the Department of Neurosurgery and Department of Medicine at the University of Pennsylvania in Philadelphia, the Laboratory of RNA Molecular Biology at The Rockefeller University in New York, and the Department of Host Defense at the Research Institute for Microbial Diseases in Osaka discovered how mRNA therapy could be used in genetic and regenerative medicine. Essentially, by modifying mRNA with a naturally occurring modified nucleoside pseudouridine to produce modified mRNA (modRNA), researchers changed its structure so that the body was better able to utilize it to address issues related to protein defects or deficits.

According to the authors of the Molecular Therapy article, modRNA “allows rapid, transient, and efficient gene expression to a specific time window after cardiac injury.” They further state that modRNA protein replacement therapy could be “an excellent therapeutic agent to address experimental and clinical needs to induce cardiac regeneration and promote cardiac function in ischemic heart disease.”

Key Takeaways About Protein Replacement Therapy

Protein replacement therapy offers a way to treat diseases by transporting missing or deficient proteins to cells, thereby correcting the dysfunction that results in disease. Other techniques for doing this involve transferring genetic material into cells, which comes with a higher level of risk.

At this time, one of the most pertinent applications for protein replacement therapy is as a treatment for rare monogenic diseases, which fall into a category called “orphan diseases” because manufacturers are less likely to develop drugs to treat them due to the limited financial incentive for doing so. While some experts view protein replacement therapy as a much-needed option in a realm with a dearth of viable potential treatments, others feel manufacturers still need to do more work to show that using these treatments ends up being a cost-effective decision for health care systems.

It’s important to note, too, that the promise of protein replacement therapy is not limited to rare diseases. Clinical trials have shown it can also be used to overcome one of the central challenges of treating myocardial infarction and preventing heart failure.

As researchers continue to explore applications for protein replacement therapy, it seems likely that they’ll uncover an even broader swathe of diseases and conditions it can be used to treat.

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.

Amino Acids for Hearing Loss: Understanding the Vital Role Certain Amino Acids Play

Chances are, when you think about protecting your hearing health, nutrition isn’t the first thing that comes to mind. But maybe it should be. Here’s how nutrient intake, specifically of certain key amino acids, impacts hearing health.

Though nutrition may not be the first thing that comes to mind when you consider your hearing health, researchers working in the field of nutrient science have found that certain vitamins, minerals, and amino acids can be quite impactful. Before delving into what scientists have uncovered so far about amino acids for hearing loss, we’ll first review some fundamental facts about hearing loss.

Basic Facts About Hearing Loss

Hearing loss occurs when part of the ear or overall auditory system malfunctions. Possible sites where malfunctions might occur include:

  • Hair cells of the inner ear
  • Organ of corti
  • Spiral ganglion
  • Stria vascularis
  • Auditory brainstem

Hearing loss has degrees of severity ranging from mild, which limits a person’s ability to hear soft sounds, to profound, which prevents a person from hearing anything but very loud sounds.

Normal hearing is defined as hearing thresholds of 25 decibels (dB) or better in both ears. Any individual who does not meet that criteria technically has some degree of hearing loss. The colloquial phrase “hard of hearing” applies to individuals with mild, moderate, and severe hearing loss. Typically, those individuals can communicate through spoken language, though they may find hearing aids, cochlear implants, captioning, and other interventions useful.

Those who identify as deaf most likely have profound hearing loss. Because they can hear very few, or no, sounds, it’s common for deaf individuals to use sign language to communicate.

According to a fact sheet compiled by the National Institute on Deafness and Other Communication Disorders (NIDCD), more than 2 out of every 1,000 children born in the United States annually have detectable hearing loss in one or both ears. Hearing tests show that 13% of people over the age of 12 who live in the United States have hearing loss in both ears. Furthermore, 37.5 millions adults living in the United States experience some level of hearing loss.

As individuals grow older, their odds of experiencing hearing impairment increase. In fact, age is the single most significant predictor of hearing loss for adults between the ages of 20 and 69—the highest rates of hearing loss occur among those in the 60 to 69-year-old age bracket.

Sex affects your odds of experiencing hearing loss too. Men have nearly twice the risk women do of developing hearing loss. And race seems to play a role as well, with non-Hispanic white adults reporting higher rates of hearing loss than other racial and ethnic groups.

It’s common for age-related hearing loss to become increasingly severe. Approximately 2% of adults between the ages of 45 and 54 have hearing loss significant enough to be considered disabling, meaning “hearing loss of 35 decibels or more in the better ear, the level at which adults could generally benefit from hearing aids.” That rate rises to 8.5% for adults between the ages of 55 and 64. By age 65 nearly a quarter of adults could benefit from hearing aids, and by 75, more than half could.

Unfortunately, very few of the people for whom hearing aids could be helpful actually use them. Only one in three adults 70 and older with significant hearing loss have used hearing aids.

7 Quick Facts About Hearing Loss

Probing the Link Between Nutrition and Hearing Health

Though some studies on nutrition and hearing health were conducted as early as the 1930s and 40s, it took until the late 1980s for researchers to clearly state that diet plays a role in the development of certain hearing disorders. Now, scientists have conclusively determined that insufficient dietary intake of certain nutrients, including amino acids, can cause hearing loss.

These findings stem largely from population-based studies as well as trials done with animal subjects. A study done by Saudi Arabian researchers, for example, looked at whether dietary deficiencies of certain amino acids correlated to hearing impairment among 18 to 21 year olds.

The authors used a food questionnaire to determine the dietary habits of study participants—with a focus on amino acid intake—in combination with other survey questions. They also reviewed existing literature and findings on the beneficial impact amino acids can have on hearing health.

First, they looked at arginine, a conditionally essential amino acid known for its blood pressure and protein synthesis benefits. “Studies have indicated that arginine is protective against sensorineural hearing loss,” the authors note, as well as “cochlear damage caused by the toxins that are produced in Streptococcus pneumoniae infections.” Evidence supports the use of arginine as a preventative treatment in order to provide cochlea protection.

They also address the role played by methionine, an essential amino acid with powerful antioxidant properties. This amino acid has been shown to lower a person’s risk of ototoxic hearing loss, which occurs as a result of the ingestion of chemicals, including those found in some medications, that cause damage to the inner ear.

The authors mention, too, that deficiencies of methionine may produce hearing loss. They reference an epidemic of peripheral neuropathy in Cuba from 1992-1993 that affected over 50,000 people, some of whom developed high-frequency sensorineural deafness. “Obvious malnutrition was not present,” the authors wrote, “but a deficit in micronutrients including methionine appeared to be a primary determinant of the epidemic.”

They also reference the ability of glutathione, a free-radical scavenging antioxidant made up of three amino acids (L-cysteine, glycine, and L-glutamate), to reduce your risk of developing hearing loss caused by acoustic overstimulation, or noise exposure. “A depleted glutathione state increased noise-induced hearing loss, whereas replenishment of glutathione lessened the damage,” they explained. Furthermore, glutathione can protect against ototoxic hearing loss caused by gentamicin, particularly for individuals whose diets contain low levels of protein.

Last but certainly not least, they touch on the important role played by taurine, another conditionally essential amino acid. Taurine appears to make vital contributions to the development of human hearing capacities, both anatomically and functionally. “Infants with inadequate taurine in their diets had shorter auditory brain stem responses,” the authors stated. And animal studies have shown that supplementing with taurine encourages the brainstem auditory response to mature earlier.

Further Findings on Amino Acids for Hearing Loss

Taurine may hold particular promise as a means of treating tinnitus, a hearing malfunction that impacts approximately 10% of adults living in the United States. Neuroscientists at the University of California, Berkeley published findings in the journal Proceedings of the National Academy of Sciences indicating a correlation between tinnitus and decreased levels of GABA (gamma-aminobutyric acid), an inhibitory neurotransmitter. The team concluded that finding ways to change GABA functions could help to treat tinnitus, and taurine could be one possible route for doing so.

A separate study published in Hearing Research examined how daily taurine supplementation impacted chronic tinnitus in rats. Rats given a high dose of taurine—294 mg/kg—showed significantly reduced symptoms of tinnitus. “These results are consistent with the hypothesis that taurine attenuates tinnitus and improves auditory discrimination by increasing inhibitory tone and decreasing noise in the auditory pathway,” the authors concluded.

The connection between amino acids and hearing health appears to be intimately intertwined with the way amino acids influence neurotransmitter levels. A review published in Neural Regeneration Research offers perspective on this issue as it applies to glutamate and glycine. “Glutamate is well established as an excitatory neurotransmitter of auditory nerve fibers,” the authors explained, and likely other ascending auditory pathways as well. Glycine, meanwhile, acts as an inhibitory neurotransmitter in the central auditory system.

How to Use Amino Acids to Maximize Hearing Health

Your particular hearing concerns will determine which amino acids you’ll want to seek out in order to maximize your hearing health. The following overview of the links between certain amino acids and auditory functions can help you build a personalized diet and supplement plan.

Arginine

Evidence shows that arginine, a conditionally essential amino acid, helps protect against sensorineural hearing loss,  which accounts for about 90% of all cases of hearing loss. Arginine can also prevent cochlear damage resulting from illnesses caused by Streptococcus pneumoniae bacteria such as pneumonia, meningitis, and sinus and ear infections.

Foods high in arginine include:

  • Chicken
  • Dairy products
  • Lentils
  • Turkey
  • Soybeans
  • Spirulina

Carnitine

Carnitine, an amino acid already quite popular for its anti-aging impact, appears to have a positive impact on hearing loss related to brain stem auditory deficits caused by diabetes. It may also increase hearing health for older individuals.

Experts advise supplementing with acetyl-L-carnitine because the body absorbs it more readily and it facilitates the transportation of fatty acids to the mitochondria of inner ear cells, a crucial step for energy production.

Cysteine

This nonessential, sulfur-containing amino acid plays a number of important roles related to your hearing. First, it safeguards the function of inner ear cells and second, it acts as a precursor for glutathione, another amino acid relevant to hearing health.

Evidence indicates that when individuals supplement with n-acetyl-cysteine, they’re unaffected by noise levels sufficient to cause permanent hearing damage in other individuals. Plus, it can counteract the negative effects certain medications and cancer treatments have on your hearing, including cisplatin.

Glutathione

Deficiencies of glutathione (an antioxidant composed of cysteine, glycine, and glutamate) make individuals more susceptible to hearing loss following noise exposure. Those already experiencing this type of hearing loss can mitigate the damage by supplementing with glutathione. Glutathione also prevents gentamicin from harming the cochlear.

As we age, our glutathione levels decrease sharply. This can be particularly dramatic in the auditory nerve, raising the question of whether age-related hearing loss might be caused in part by dropping glutathione levels.

Histidine

Our bodies need histidine, an essential amino acid, to maintain the protective myelin sheaths that surround our nerves. Histidine deficiencies can contribute to nerve deafness as well as other types of hearing loss.

Methionine

Methionine keeps auditory hair cells as well as auditory neurons safe from ototoxicity, particularly from aminoglycosides, ionic platinum compounds, and cisplatin. However, this amino acid plays somewhat of a dual role in hearing health as it’s a precursor to homocysteine. Excess levels of homocysteine may obstruct blood flow to the inner ear.

If you increase your methionine intake, be sure to maintain optimal levels of folic acid as well as vitamins B6 and B12 to keep your homocysteine levels in check.

Taurine

As addressed in some detail previously, humans need taurine to develop brainstem auditory responses. There’s also some indication that this amino acid could be used to treat tinnitus.

Dietary taurine comes primarily from red meat, poultry, and fish, so vegetarians and vegans may need to pay particular attention to sourcing this crucial nutrient.

Use These 7 Amino Acids to Prevent and Treat Hearing Loss

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

Understanding Autophagy: Loose Skin, Chronic Disease and Cancer—Some Scientists Say It Could Be the Key to Treating and Preventing All of These 

Maximize the ability of autophagy, a cellular cleansing process, to prevent loose skin after weight loss, chronic diseases, and even cancer. Read on to learn about the science behind autophagy as well as how it can help those on weight-loss journeys.

Autophagy (pronounced ah-TAH-fuh-gee), a medical term, describes a regenerative cellular process that decreases your risk of developing a multitude of serious diseases, extends your lifespan, and improves your overall health and well-being. In some circles, there’s particularly intense interest in the impact of autophagy on loose skin following weight loss, a frustrating side effect that can require surgery to address.

Read on to learn about the science behind autophagy as well as how it can help those on weight-loss journeys.

What Is Autophagy?

In simple terms, the concept of autophagy can be defined as follows: without external nutrients, the body begins to consume itself. The term comes from the Greek words “auto” meaning self and “phage” meaning to eat.

While this may sound like the premise for a horror movie, it can be incredibly beneficial. During the process of autophagy, specialized membranes seek out cells that are dead, damaged, or diseased and use their component parts for energy or to make new cells.

“Think of it as our body’s innate recycling program,” said Dr. Colin Champ, assistant professor at the University of Pittsburgh Medical Center, in an interview. Other experts have summed it up as “cellular housekeeping” or “cellular quality control.”

Though Belgian biochemist Christian de Duve originated the term “autophagy” in 1963, much of what we now know about this vital process was not discovered until well into the 2000s. In fact, pioneering Japanese biologist Yoshinori Ohsumi won a Nobel Prize for his investigations into the mechanisms of autophagy in 2016. Scientists working in the field, however, caution that what we currently don’t know about autophagy would fill far more books than what we do.

7 Proven Benefits of Autophagy

Autophagy plays a fundamental and essential role in overall cellular function by recycling disused or dysfunctional components that, if left in place, can become problematic. By doing so, autophagy can prevent the development of several types of diseases. Here are 7 proven ways autophagy benefits your health.

1. Decrease Systemic Inflammation

A 2017 review published in Clinical and Translational Medicine states that “increasing evidence” demonstrates autophagy can help to prevent the development of inflammatory diseases.

“Autophagy plays critical roles in inflammation through influencing the development, homeostasis and survival of inflammatory cells, including macrophages, neutrophils and lymphocytes; effecting the transcription, processing and secretion of a number of cytokines, as well as being regulated by cytokines,” the authors state. Essentially, this means that autophagy helps to ensure that all the cells regulating your body’s inflammatory processes are working properly.

The authors go on to say that studies suggest autophagy’s positive influence on inflammatory cells offers promise as a therapeutic intervention for diseases linked to inflammation, including:

  • Crohn’s disease
  • Cystic fibrosis
  • Pulmonary hypertension
  • Obstructive pulmonary disease

2. Treat Neurodegenerative Diseases

Findings published in Frontiers in Neuroscience, a leading journal in its field, point to autophagy as a way to slow the progression of neurodegenerative diseases.

As we’ve established, autophagy repurposes cellular components, including misfolded proteins. The accumulation of misfolded proteins is believed to cause symptoms of many neurodegenerative diseases to worsen. So, by preventing that, autophagy can mitigate the severity of those diseases.

3. Safeguard Mental Health

Some research has shown that when autophagy does not occur with sufficient frequency, your mental health can be negatively impacted.

A study published in Molecular Psychiatry, a peer-reviewed journal, looked at the connection between autophagy and mental health. When they analyzed the brains of schizophrenia patients, the authors found clear reductions in post-mortem levels of proteins that control autophagy. They determined that the direct association between autophagy and the progression of schizophrenia could offer a pathway to new methods of treatment.

4. Increase Longevity

A review published in the Journal of Clinical Investigation claims that inducing autophagy can counteract cellular aging processes and enhance the metabolic activity of your cells, resulting in increased longevity.

This claim stems from experimental findings, and it’s not yet clear exactly how autophagy increases anti-aging activity and extends life spans, though studies with mice have shown that to be the case.

5. Suppress Tumor Growth

It’s clear that the process of autophagy is intimately linked to the development of cancer, but exactly what effect it has on tumor initiation and development remains somewhat murky.

Per a review published in the International Journal of Molecular Sciences, “Many studies have found that autophagy plays dual roles in cell survival and cell death in the context of tumor initiation and development.” The authors elaborate that while autophagy has been shown to suppress tumor formation in certain instances, it also seems to contribute to cancer progression by supplying nutrients to cancer cells in others.

More research is needed to fully understand how to harness the power of autophagy to prevent cancer. In the future, however, the authors believe it could be “a potentially effective therapeutic strategy in anticancer therapy.”

6. Support Maintenance of a Healthy Weight

Some of what we know about autophagy comes from research in what happens in its absence. For instance, a study done with mice and published in Cell Metabolism found that deleting an essential autophagy gene led to higher body weights, increased fat mass, and higher rates of glucose intolerance.

According to the authors, these findings indicate that an autophagy deficiency may play a role in the development of obesity.

7. Prevent Sagging Skin Post-Weight Loss

Though this benefit does not have rigorous scientific support, solid anecdotal evidence indicates that autophagy can help those who have lost weight—particularly, individuals who have lost a lot of weight—from needing skin removal surgeries. Dr. Jason Fung, a nephrologist who specializes in research into fasting, has developed a program designed to help people successfully lose weight and reverse conditions linked to weight gain, such as type 2 diabetes, polycystic ovarian syndrome (PCOS), and fatty liver.

“We’ve never sent a single person for skin-removal surgery,” said Dr. Fung in an interview. “We have anecdotal cases where people have lost 120, 130 pounds, and they said their skin also shrank, too.”

Fung believes this happens because the body harvests the protein contained in excess skin. “Remember, during fasting, you’re activating a pathway within your body that says, ‘Okay, we need to buckle down because we’re in a time of famine, so to speak, and we don’t need all that extra skin, so let’s burn it. And if you need it, we’ll build it again.’”

How to Increase the Efficacy of Autophagy for Loose Skin

Is It Possible to Trigger Autophagy?

Though it has not yet been definitively proved that it’s possible to trigger autophagy in humans, studies done with animals indicate that fasting and calorie restriction may be means of inducing autophagy.

A literature review published in Ageing Research Reviews in 2018 found that “the evidence overwhelmingly suggests that autophagy is induced in a wide variety of tissues and organs in response to food deprivation.” In other words, there’s a very high likelihood that if you fast, autophagy will occur.

Studies done with mice have historically delineated 24 hours as the marker for when autophagy sets in, but it’s not clear whether the same would hold true for humans. Dr. Fung believes that autophagy most likely sets in during the later stages of an extended fast, “somewhere around 20 to 24 hours is my guess, and it probably maxes out somewhere around 32 hours, again, my best guess.”

While scientists have yet to agree upon a surefire way to trigger autophagy, this process does occur naturally, though it’s unclear how frequently or extensively it takes place without outside stimulus. Fasting, exercise, and other forms of physiological stress seems to cause the process to accelerate.

However, it’s quite challenging to measure autophagy (technically, what would be measured would be termed autophagic flux) in humans, as it requires tracking the levels of minuscule proteins, including protein 1A and LC3.

Does Autophagy Have Any Negative Effects?

While autophagy clearly has a host of remarkable benefits, it can cause problems too. An article published in PLOS Biology termed it a “double-edged sword.”

Author Andrew Thorburn of the Department of Pharmacology at the University of Colorado School of Medicine explained that “autophagy’s effects may work for both the good and the bad of an organism.” When it comes to conditions like treating bacterial infections, autophagy sometimes leads to improvement and sometimes causes conditions to worsen. According to Thorburn, using autophagy effectively will require a better understanding of which cells it degrades and under what circumstances.

It’s important to note as well that using fasting as a method for inducing autophagy comes with its own risks. There are no universal medical recommendations at this time, but most experts agree that extended fasts—going without food for 36-, 48-, or even a full 72 hour-fast—should only be undertaken by those in good health. Extended fasting should not be done too frequently either. As a general rule, it should only be undertaken 2 or 3 times annually. Confer with a trusted doctor before embarking on a fast to make sure it’s safe for you.

If you have previously engaged in unhealthy food restrictions behaviors or have been diagnosed with an eating disorder like anorexia, it’s likely best to avoid fasting.

Expert Advice on Triggering Autophagy

Because autophagy is a stress response, to intentionally trigger it, you will have to endure some discomfort. “It’s our ancestral and evolutionary response to dealing with feast and famine in times of stress,” said Dr. Champ.

If you’d like to try triggering autophagy, one of these three methods is a good place to start.

1. Enter a State of Ketosis

If the idea of fasting feels daunting or there are reasons you should avoid it, evidence shows you can also activate autophagy by entering ketosis. By restricting your carbohydrate intake and increasing your fat intake, you can shift your body into a state in which it uses fat rather than carbs as its primary source of fuel. This is the scientific basis for the immensely popular high-fat, low-carb ketogenic diet, commonly abbreviated as the keto diet.

In order to adhere to the keto diet, you’ll need to keep your carbohydrate intake at no more than 5% of your total calories, your protein intake between 20% and 30%, and your fat percentage at between 60% and 70%.

Studies have shown that entering ketosis can bring about significant fat loss while maintaining muscle mass. Other proven medical uses for the keto diet include improving the treatment of epilepsy and other brain conditions (in fact, it was developed to treat epilepsy in children), lowering your risk of diabetes, and assisting your body in defeating cancerous tumors.

According to Champ, “Ketosis is like an autophagy hack. You get a lot of the same metabolic changes and benefits of fasting without actually fasting.”

2. Experiment with Intermittent Fasting

Extended fasts can be grueling, but that may not be necessary in order to spur autophagy.

A Brazilian research team published a research review indicating that intermittent fasting can help increase autophagy, which makes cancer treatments more effective and reduces side effects. They note, however: “Additional studies are required to better understand the molecular mechanisms evoked by fasting, aiming to identify the context in which fasting may be beneficial as an adjunct to cancer treatment.”

In the meantime, it certainly seems worthwhile to give intermittent fasting a try, if for no other reason than the wealth of benefits they mention that have been associated with intermittent fasting, such as an extended lifespan and a lower risk of diseases including:

  • Diabetes
  • Heart disease
  • Neurodegenerative conditions

As with extended fasting, there are limitations on who should try intermittent fasting. It’s typically not advisable for children, pregnant women, or individuals with diabetes or other blood sugar issues to follow this fasting protocol.

3. Engage in Regular Exercise

As you may know, exercising creates microscopic tears in your muscles. When your body repairs those tears, that process leads to bigger, stronger muscles. It appears that exercise also increases the rate at which your body carries out autophagy.

A study published in Nature, an international journal of science, found: “Acute exercise induces autophagy in skeletal and cardiac muscle of fed mice.” The authors discovered that after 30 minutes of running on a treadmill, the rate at which mice recycled their own cells via autophagy increased significantly and continued to do so until the 80-minute marker at which point rates leveled out.

Scientists have not yet pinpointed the threshold require for humans to kickstart autophagy. Dr. Daniel Kilonsky, a cellular biologist specializing in autophagy, says that at the moment, it’s proving quite difficult to answer that question.  However, he reminds us that exercise, like intermittent fasting, has many other benefits.

3 Possible Methods for Triggering Autophagy

Additional Advice on Naturally Addressing Loose Skin

If your primary interest in autophagy has to do with its potential role in addressing loose skin following weight loss, you may want to incorporate these other natural methods for resolving loose skin without plastic surgery.

A key aspect of doing so is improving skin elasticity. Without proper elasticity, your skin cannot adapt to physical changes such as weight loss. To maintain or enhance skin elasticity, you’ll need to sustain an adequate supply of collagen.

All the collagen in your body begins as procollagen. To make procollagen, your body uses two amino acids: glycine and proline. Certain nutrients have been shown to increase the rate at which your body produces those amino acids, such as vitamin C, copper, selenium, and zinc.

Citrus fruits, strawberries, bell peppers, and raw liver all contain high concentrations of vitamin C. Organ meats are generally high in copper, as are cashews, sesame seeds, lentils, and cocoa powder. You can get plenty of selenium from seafood (salmon in particular) and Brazil nuts, while oysters and red meat are rich in zinc.

Consuming foods high in glycine and proline themselves also boosts procollagen production. Good sources of glycine include gelatin as well as pork and chicken skin, while egg whites, dairy products, wheat germ, mushrooms, asparagus, and cabbage provide lots of proline.

Because your body needs a balanced supply of all the amino acids in order to effectively utilize them, you’ll also want to eat foods with overall high levels of amino acids, like:

  • Red meat
  • Poultry
  • Seafood
  • Legumes
  • Tofu

Interestingly, eating foods high in collagen, such as bone broth, is not necessarily the best way to raise levels in the body. That’s because when you consume protein, your body breaks it down into its component amino acids.

3 Possible Methods for Triggering Autophagy

How to Avoid Loose Skin After Weight Loss

Significant weight loss can result in loose, sagging skin. Studies show these 6 methods can help you avoid loose skin or minimize its appearance.

We tend to treat weight loss, particularly major weight loss, as the triumphant endpoint of a difficult journey. We divide weight-loss journeys into “Before” and “After,” often with a single photo representing the start and finish of that journey. However, this story only captures one aspect of what it’s like to lose weight. What often gets left out of weight-loss stories is that when you move from a higher body weight to a significantly lower one, you may experience other unwanted physical changes, such as loose skin. There is absolutely nothing wrong with embracing loose skin—as individuals like Kenzie Brenna, an actress, writer, and body-positivity activist, have publicly done—in fact, it’s an admirable goal and an indication of deep self-acceptance. That said, there’s also nothing wrong with wanting to learn how to avoid loose skin after weight loss.

For some people, loose skin can be damaging to their mental health and self-esteem. It can also be physically uncomfortable, particularly during physical exercise. Once you develop loose skin, it can be quite challenging to reverse without plastic surgery.

Less invasive options do exist, however, many of which are most effective when put in place preemptively. Before sharing eight ways you can avoid loose skin after weight loss, we’ll first cover some basic facts about the skin as well as risk factors that impact how likely you are to develop loose skin.

How Does Skin Function?

One of the pitfalls of the rapid loss of a lot of weight is the development of excess skin. A New York Times article covering a pioneering study that followed contestants from season eight of the popular TV show “The Biggest Loser” for 6 years after the series finale addressed this issue. Per the article, prior to the finale weigh-in during the show’s finale to determine the winner, contestants “dressed carefully to hide the rolls of loose skin that remained, to their surprise and horror, after they had lost weight. They wore compression undergarments to hold it in.”

In order to understand why rapid, significant weight loss so often results in loose skin, you must have a basic grasp of how skin functions.

The skin—which is the largest human organ—acts as a barrier to keep your body safe from viruses, fungi, bacteria, and other potentially harmful contaminants. Collagen and elastin, two proteins found in the second layer of the skin, (the dermis), allow it to stretch and contract as we move and grow.

As an individual gains weight, those proteins must continually stretch to allow the skin to adapt to that change. This can cause the fibers of those proteins to become weak and damaged. Thus, when significant weight-loss occurs, the elastin and collagen in the skin may not be readily able to contract.

“Skin stretches to form the shape of your body since it’s an ‘elastic’ organ,” Certified Exercise Physiologist Lizbeth Simancas summarized. “Your skin may not contract back to its smaller shape if weight is lost too quickly.” This can be seen most clearly for individuals who undergo bariatric surgery, but those who quickly lose a lot of weight through intense diet and exercise practices, like competitors on “Biggest Loser,” can experience this too.

The more weight is lost, the greater the demand on the skin’s previously overtaxed capacity for elasticity. And, therefore, the greater the likelihood of saggy skin post-weight loss.

What Factors Contribute to the Development of Loose Skin After Weight Loss?

Dr. Christine Choi Kim, medical and cosmetic dermatologist, underlines that fact that the skin is a living organ, and while it responds to weight gain by stretching and expanding, its ability to contract in response to weight loss is inherently more limited. Dr. Kim notes, too, that this ability to tighten depends on a number of factors, such as:

  • Age: The aging process often causes the skin to become less elastic, impairing its ability to tighten after weight loss.
  • Genetics: Some individuals are more prone to sagging skin as they grow older, regardless of weight loss.
  • Baseline strength of elastin and collagen proteins: As is the case when it comes to your genes and your age, you can’t control the impact your baseline skin elasticity will have on its ability to bounce back after you lose weight.
  • Degree of weight gain and loss: As touched on previously, the more weight you lose, and the shorter the period of time in which you lose it, the harder it will be for your skin to adapt.
  • Nutrient intake: To keep your skin healthy, you’ll need to provide it with a balanced intake of nutrients, particularly vitamins C and E and the substances that act as precursors for the development of collagen and elastin.
  • Sun exposure: While some degree of sun exposure is a healthy way to meet your body’s vitamin D needs, excess exposure can lead to skin damage.
  • Smoking history: Yet another reason to kick the habit, or avoid  cigarettes in the first place. A plethora of studies show that smoking speeds the normal aging process of your skin.

Understanding the factors that influence skin elasticity can help you avoid loose skin after weight loss. If possible, it’s best to address this issue preventatively as it’s far more difficult to tighten skin that has already begun to sag than it is to forestall the sagging.

According to Kim, “Excess skin can lead to embarrassment and a lack of satisfaction with your body image—even after significant weight loss.” Equip yourself with the knowledge you need to keep the triumph of achieving a major weight-loss goal from being marred by unexpected changes to your skin.

7 Factors That Contribute to the Development of Loose Skin

How to Avoid Loose Skin After Weight Loss

First, it’s important to be clear that there is no guaranteed way to avoid loose skin after weight loss. Depending on the amount of weight you lose, when you gained the weight and how long you carried it, as well as your skin’s baseline elasticity, some extra skin may be unavoidable. However, the experts say that the following 6 practices can help you avoid loose skin after weight loss, or minimize the appearance of existing excess skin.

1. Lose Weight Gradually

Perhaps the single most effective way to avoid loose skin after weight loss is to progress gradually toward your weight-loss goal. Slower weight loss makes it less arduous for skin to snap back into place.

The Centers for Disease Control and Prevention (CDC) recommends aiming to lose between 1 and 2 pounds per week. Not only will this make it easier for your skin to keep pace, but it also makes it less likely that you’ll regain the weight.

Furthermore, a study published in the International Journal of Endocrinology and Metabolism found that losing weight slowly results in more favorable changes to body composition. Study participants were randomly divided into two groups—a rapid weight-loss group that followed a diet plan designed to produce a daily 1,000- to 1,500-calorie deficit and a slow weight-loss group whose diet produced an energy deficit of 500 to 750 calories daily.

While both protocols led to reductions in waist circumference, hip circumference, body fat mass, and more, individuals in the slow weight-loss group experienced more significant reductions to waist circumference, hip circumference, fat mass, and percentage of body fat, all of which are linked to improved health.

2. Engage in Regular Cardio and Strength Training Exercise

Adding exercise to your gradual weight-loss plan also increases the odds that your skin will be able to tighten up as your weight decreases.

Both strength training and cardio make important contributions. Cardio, or aerobic exercise, can be a highly effective way to burn calories, which will help you move toward your weight-loss goal. However, if you exclusively engage in cardio training, you may lose lean muscle mass also with fat, which can increase the appearance of saggy skin as well as adversely impact your metabolism.

Strength training, however, can help you build muscle, which in turn raises your metabolic rate. One of the factors that determines your basal metabolic rate (BMR), which accounts for the vast majority of the calories you burn each day, is the amount of lean muscle you have. Muscle tissue has higher energy (calorie) demands than fat while at rest, meaning that even when you’re not working out, having more muscles translates to a greater caloric expenditure. No matter what you weigh, the more muscle and the less fat you have, the higher your BMR.

“If you have more muscle, it burns fuel more rapidly,” stated Columbia University professor Michael Rosenbaum, who specializes in weight loss and metabolism. Rosenbaum cautions, though, that if you do succeed in speeding up your metabolism, “you have to fight the natural tendency to [want to] eat more as a result of your higher metabolism.”

Still, when taking the long view of your overall health, there are clearly more benefits to physical activity than drawbacks, including the fact that weight lifting and resistance training can minimize the appearance of existing loose skin by building muscles that will fill it out. If your goal is to look lean and toned rather than built and bulky, don’t worry, you won’t accidentally develop the physique of a bodybuilder—that requires a high level of intention and commitment.

3. Optimize Your Diet

In order to lose weight and ensure you don’t subsequently gain weight, it’s important to build a diet based on whole, minimally processed foods.

A 2017 clinical trial called the DIETFITS study (the acronym stands for “Diet intervention examining the factors interacting with treatment success) set out to identify factors that predispose individuals to experience greater success when following certain weight-loss diets so that experts can more effectively match patients with dietary interventions.

Interestingly, participants in both the low-fat and low-carbohydrate groups lost comparable amounts of weight. This drew attention among health practitioners reviewing the results to the elements that remained consistent between the two diets.

Both groups were encouraged to:

  • Focus on unprocessed, high-quality foods
  • Eat as many vegetables as possible
  • Prepare meals at home
  • Restrict or eliminate trans fats, added sugars, and refined carbohydrates, including flour

Participants also had regular sessions with dietitians and access to counseling to help them break emotional eating patterns.

The findings are quite encouraging. You don’t need to follow a complicated or overly restrictive diet in order to lose weight. Instead, you can use the principles described above, which leave plenty of room for shaping a diet that accounts for your personal preferences and lifestyle.

4. Stop Smoking

Research unequivocally shows that skin damage is among the many adverse effects of cigarette smoking. In fact, even secondhand smoke exposure has been shown to decrease collagen levels, increase inflammation, and fuel oxidative damage.

A study published in Biochemical and Biophysical Research Communications found that when rats were exposed to cigarette smoke, collagen levels in their skin decreased significantly compared to control rats. The authors concluded that long-term secondhand smoke exposure would likely “affect the appearance of the skin [and] accelerate the skin aging process.”

If you’re serious about maximizing the elasticity of your skin, which you will need to do in order to prevent it from becoming loose or saggy, the decision is clear: stop smoking.

5. Try Firming Creams

If you have room in your budget and are looking for a way to immediately tighten loose skin, you may want to try firming creams.

The results of these products tend to be rather subtle, and most impactful when skin is also in need of hydration. These products often use retinoids or collagen as their active ingredient.

One of the ways retinoids work is by preventing free radical damage that negatively impacts skin tone. They can also speed up collagen production, which can boost the elasticity of the skin.

As you know, collagen is one of the key proteins that keeps your skin tight and firm. There’s some evidence that the topical application of collagen can temporarily improve the appearance of the skin, but collagen molecules are too large to be absorbed through the skin so the results will not be lasting.

A popular natural treatment, grapeseed oil, does have some scientific backing. A study published in Pharmacognosy Magazine looked at a number of herbal ingredients touted for their ability to increase skin’s elasticity and found that grapeseed did produce measurable changes to moisture levels, softness, and tightness.

6. Supplement Strategically

As wonderful as it would be if scientists could formulate a magic pill, or combination of supplements, that completely prevents or treats loose skin, that’s yet to be announced. In the meantime, an optimal supply of the following nutrients will ensure your skin has all the raw materials it needs to be maximally healthy.

While you might assume that collagen supplements would be on this list, it tends to be more effective to consume supplements that increase collagen production, such as vitamin C and certain amino acids.

Vitamin C

Scientists have confirmed that vitamin C has impressive abilities when it comes to stimulating collagen production.

A 2018 systematic review examined the efficacy of vitamin C supplementation as a means of promoting collagen synthesis, and found that not only did vitamin C increase collagen synthesis, but it also reduced oxidative stress. The authors also found no evidence of adverse side effects.

Furthermore, an article published in Nutrients in 2017 specifically touched on the impact of dietary vitamin C intake on skin sagging related to weight loss. According to the article, a higher intake of vitamin C can be linked to improved skin tightness.

Glycine

Collagen, one of the most abundant proteins not only in the skin, but also throughout the entire human body, contains between 2 and 10 amino acids. Glycine might be the most impactful of those. This simple, naturally occurring amino acid elevates collagen production, facilitates skin regeneration, and increases moisture retention.

Though your body produces its own glycine from other amino acids, it can be beneficial to increase your glycine intake, either by eating glycine-rich foods like red meat, poultry, fish, dairy products, and legumes or by taking a high-quality amino acid supplement.

Lysine

This essential amino acid plays a vital role in the function of your skin, ensuring that its supportive structures remain strong and intact. Our bodies also need lysine for collagen development, tissue repair, and other important physiological processes.

Good food sources of lysine include:

  • Meat
  • Poultry
  • Fish (especially cod and sardines)
  • Cheese (especially Parmesan)
  • Soy products
  • Spirulina
  • Fenugreek
  • Legumes
  • Nuts

6 Science-Backed Methods for Avoiding Loose Skin After Weight Loss

Losing a significant amount of weight, particularly if you do so after weight-loss surgery, or using another method to lose a lot of weight in a short period of time often causes loose skin to develop. Embracing this physical change is a viable and commendable option, but it’s equally valid to seek out ways to avoid loose skin after weight loss or to encourage skin to tighten.

There’s no one single skin tightening technique that can fully restore skin elasticity for each and every person; however, scientific findings indicate that using one or more of the methods described above will likely prevent or reduce the appearance of loose skin.

When to Take BCAAs: Pre- or Post- Workout? Morning, Noon or Night?

When is the best time to take BCAA supplements: pre-, during, or post-workout? Is it safe to consume them before bed? What about in between meals? We have the science and the answers.

There are many reasons to take protein supplements, and not all of them have to do with working out. Vegetarians and vegans often take them to make sure they’re getting enough plant-based protein. Those recovering from surgery are often on doctor’s orders to consume more protein to help heal faster. Those working to lose weight also find that consuming more protein helps fuel their energy and their weight-loss efforts by curbing hunger and increasing muscle growth. All of the above is even more true for those who consume protein like whey, creatine, or BCAAs (branched-chain amino acids) to boost their workout or to build muscle: you need enough protein to function, you need even more protein for recovery, and you need to control your calorie consumption as you aim to bulk up. If you’re new to trying BCAAs, the first question you have after what they are and how do they work is likely to be: when to take BCAAs? We have the best practical advice here.

Muscles, Amino Acids, and BCAAs

Muscles are made out of protein, and protein is made out of amino acids. Specifically, the human body needs all nine essential amino acids (EAAs) to synthesize any new muscle protein. Of those nine essentials (as opposed to the nonessential amino acids that your body can make on its own, meaning it’s not essential to consume them in food), three are branched-chain amino acids, so called because of their molecular structure.

So what are the three BCAAs and why are they singled out for workout supplements? Let’s start with their names.

  • Leucine: This is the amino acid thought to make the biggest difference when it comes to building new muscle proteins.
  • Isoleucine: An isolated form of leucine (hence its name), isoleucine helps regulate blood sugar levels and energy production.
  • Valine: This BCAA is important not only for maintaining muscles but also for supporting immune function.

Together these three aminos make up about 40% of the EAAs in the body, and about 18% of the EAA content of muscle. They are broken down in the skeletal muscles directly instead of in the liver with the majority of the other EAAs, which leads researchers to theorize that they play a more direct part in energy production during exercise. Not only are BCAAs essential building blocks for protein synthesis and muscle growth, but they also positively impact your blood sugar levels and help ward off exercise fatigue.

All of the essential amino acids depreciate more rapidly during exercise due to a protein breakdown process known as catabolism (more on this later). If you are fit, active, and looking to build more muscle, you’ll want to increase protein-rich foods in your diet, which is why taking targeted amino acids like BCAAs is so popular among fitness aficionados.

Muscles, Amino Acids and BCAAs

The Scientifically Proven Benefits of BCAA Supplementation

Here’s a quick rundown on the science behind BCAAs, and why so many professional bodybuilders use them.

1. Increased Muscle Growth

Leucine particularly has been shown time and time again to stimulate new muscle protein synthesis. This 2017 study showed that those taking 5.6 grams of BCAAs post-workout enjoyed an increase in muscle protein synthesis 22% higher than the control group.

2. Decreased Exercise Fatigue and Muscle Soreness

Some fatigue will always be a part of a proper workout: if you’re not at all tired after a workout, you’re probably not doing it right! But exercise fatigue that sets in too soon or when your workout is hardly begun? You may be suffering from a low energy source, and that is where BCAAs can come in swinging.

Studies show that when your BCAA levels decrease, your tryptophan levels increase in the brain. Tryptophan is the amino acid that famously makes a turkey dinner so sleep-inducing. Tryptophan is converted to serotonin, and serotonin leads to feelings of fatigue and lethargy.

Because BCAAs are burned up in the muscles during a vigorous workout, making sure your body has more than enough to burn through helps delay exercise fatigue, providing time for a few more reps or a few more steps.

BCAAs can also help mitigate delayed onset muscle soreness (DOMS), so that you can go strong with more workouts per week because you aren’t still achingly sore from the last one. BCAAs have not only been shown to decrease muscle damage and protein breakdown during workouts, but they also lead to fewer reported instances of delayed onset muscle soreness when tested against a control group.

3. Prevention of Muscle Wasting

While muscle protein is forever in a cycle of build-up and breakdown, actual muscle wasting occurs when protein breaks down at a far faster pace than it can be rebuilt. It happens to those who are malnourished or fasting excessively, as well as to the sick and the elderly. But it can also happen to those who overexert themselves in workouts.

During times of muscle wasting, it’s important to resupply the body with the building blocks of protein that are the amino acids, which includes BCAAs. Studies reveal that one of the effects of BCAA supplementation is to inhibit muscle protein breakdown, not only in those seeking to gain muscle with resistance training or reach new heights with endurance exercise, but also in those with cancer and other wasting diseases.

Counterbalancing Catabolism

Muscle breakdown is known as “destructive metabolism” or catabolism, and while it’s a process that bodybuilders do their best to ward off, it’s also part of the natural cycle between catabolism and anabolism.

Muscle protein turnover is not unlike the regenerative properties of a forest fire. Balance is the key. Catabolism of protein molecules that are old or damaged is great; it clears the dead wood and repurposes those nutrients for healthy new growth. However, when your body doesn’t have enough amino acids to build with, unlike a forest it will start chopping down healthy molecules to meet the production demand of new lean muscle mass. This is why the timing of protein supplements like BCAAs is important.

That being said, it should be noted that an abundance of BCAAs without the rest of the nine essential amino acids will not effectively prevent unnecessary catabolism. Think of building new muscle like building furniture (perhaps with wood from the above-mentioned forest metaphor): the BCAAs are the different cuts of wood for the frame, but without cushions, fabric, springs, wood glue, nails, and screws, would you have a new couch, or just an overabundance of wood?

For this reason, we suggest taking BCAAs as part of a balanced formula of all the EAAs, because if the body lacks any one ingredient, it will burn down your hard-earned muscle tissue to take it.

Still don’t believe us? While studies on BCAA supplementation confirm that they boost muscle protein synthesis much better than a placebo, that boost is still 50% lower than the boost seen in studies with whey protein, which contains some measure of all nine essential amino acids. Taking anything less than all the EAAs is scientifically considered suboptimal, an important aspect to keep in mind when selecting the most robust and effective protein powder for your muscle-building workout.

Counterbalancing Catabolism

When to Take BCAAs

If you’ve decided BCAAs are what’s missing from your workout routine, the question still remains: when is the best time to take protein for optimal exercise performance, body fat loss, and muscle growth? The quick answers are:

  • Pre-workout: Always, for everything. To make sure you have the supplies on-hand for the vigors of your workout, take between 5 and 10 grams (depending on your body weight) of amino acids within half an hour before your workout. This helps boost your energy, endurance, and muscle recovery speed.
  • During workout: For resistance exercise and longer workouts, another dose of BCAAs can help see you through to the end and keep your muscles in A+ anabolic territory.
  • Post-workout: Across the board, yes again. While timing may vary, consuming more protein in the form of amino acids after any workout contributes to the rebuilding efforts of your muscles.
  • Before bed: This one is for bodybuilders in particular. Consuming complex proteins your body can digest while sleeping helps prevent catabolism while you rest.

The more fat burning and bodybuilding you do, the more nutrients you will need from both whole food sources and amino acid supplements. This could mean supplementing with meals or between meals multiple times a day depending on your body, your body goals, and your workout regimen. When it comes to sports nutrition, fitness professionals, athletes, or those undergoing rigorous training periods may need to consume anywhere between 15 and 20 grams of BCAAs along with other proteins each day, far more than those who are working out a handful of times or fewer per week to stay in shape throughout their daily lives.

When to take BCAAs for muscle building?

Boosting with BCAAs

The amino acids leucine, isoleucine, and valine are the core components of BCAA supplements, and while their effectiveness is proven in the areas of fitness and muscle building, it’s also known that BCAA powders or supplements alone underperform when compared to more comprehensive EAA supplements and proteins. Take your BCAAs, but take them alongside the rest of their essential team for optimal results.

What Do Astronauts Eat? Which Essential Nutrients Make It to Outer Space?

What does it take to get food into space? What do astronauts eat in space? What has spaceflight taught us about human health, and how can you use those findings to improve your health? We have (some of) the answers.

What do astronauts eat? Is it some sort of nutritional toothpaste or protein cube? Are there traditional kitchens in space modules? How far away are we from a Star Trek-style food replicator?

While it’s not yet reached the level of science fiction, space food has come a long way from where it started, not just for the sake of the crew members’ taste buds, but for their health and the necessity of maintaining earthly levels of muscle and bone mass in zero gravity conditions. Our own Dr. Robert Wolfe, who developed an amino acid supplement for civilian consumer use, has contributed to this very NASA research in the sphere of muscle preservation and amino acid supplementation in space. We have the details below on what astronauts eat, why certain nutrients are so essential, and what that tells us about the health of all humankind.

What’s on the Menu for NASA Astronauts?

When the U.S. space program first began, astronaut food was not so great. The same way that food packages for our soldiers have evolved into more nutritious fare (and now come in self-heating food containers), NASA space food has come a long way, and the same is true for the European Space Agency.

Astronauts who first braved the final frontier ate freeze-dried powder, concentrated food cubes, and aluminum tubes full of liquid gels. There was no real variety of flavor choice either, though one of the first evolutions of space food was to provide taste options like applesauce, butterscotch pudding, and shrimp cocktail as soon as the packaging improved enough for freeze-dried preservation.

Hot water was available on space missions by the 1960s with the Gemini and Apollo programs. This advancement enabled astronauts to rehydrate their food and enjoy easier access to hot meals. By the 1970s, the food pouches included up to 72 different flavors, and today the technology is even more advanced, allowing astronauts to better enjoy their food during long periods in zero gravity.

Taste isn’t the only factor to consider, of course: priority one is to make sure astronauts are as healthy as possible. Here are a few of the factors at play when it comes to feeding men and women who aren’t Earth-bound.

1. Nutrient Needs

There can be no cutting-corners in space: astronauts need 100% of their daily required nutrients and minerals from the food they eat. That means that not only do scientists and nutritionists have to figure out a way to transport and preserve the various foods we enjoy so casually on Earth, but they also have to take into account which nutrients astronauts need different levels of, like vitamin D (which we get from spending time in sunlight), sodium, and iron. Astronauts need low-iron foods because they’re working with fewer red blood cells while in space, but vitamin D and sodium are needed in higher levels to support bone density. There are no sunny days on a space station, and a lack vitamin D can lead to dangerous bone loss or spaceflight osteopenia.

Food selection also takes into account storage requirements, packaging necessities, and sensory impact (smelly food on a space station, where you absolutely cannot open a window to the vacuum of space, is not good for astronaut morale).

2. Astronaut Feedback

While the mission at hand is the priority of the astronauts sent into space, the main mission of so many other minds on the ground is astronaut health, well-being, and stamina. That means that not only can astronauts provide feedback on preferences they have for the packaged meals, but they are also allowed “bonus foods” they can bring along independently, a choice that garnered a lot of public interest and attention in 2013 when Canadian astronaut Chris Hadfield crowd-sourced ideas for what foods he could bring along for a 6-month stay on the International Space Station (ISS) with fellow astronauts, American Thomas Marshburn and Russian Roman Romanenko.

The requirements for bonus foods include having a long shelf life and being appropriate for space travel: nothing that can explode, nothing too wet or messy, and, of course, nothing too smelly for the sake of international (and interstellar) cooperation.

Hadfield ended up taking along foods like dried apple pieces, chocolate, orange zest cookies, jerky, and maple syrup in a tube, all sourced from his Canadian homeland. Those were treats on top of the menu selection each astronaut gets to choose before departing: they can have the same thing every day, or plan for a 7-day meal cycle so no one food gets too dull.

3. Future Hydroponics

NASA researchers are still looking for ways to grow fresh food in space. With an 18-month mission to Mars in the works, the Advance Food System division of NASA has already chosen 10 crops that would provide the nutrition needs for those in space. Those foods are:

  • Bell peppers
  • Cabbages
  • Carrots
  • Fresh herbs
  • Green onions
  • Lettuce
  • Radishes
  • Spinach
  • Strawberries
  • Tomatoes

Their hopes are to one day get rice, peanuts, beans, wheat, and potatoes growing in space too (you may have seen Matt Damon on the big screen farming potatoes in The Martian, but as of yet that is science fiction still just beyond our reach).

What do astronauts eat in space?

What Do Astronauts Eat? A Space Menu

According to NASA’s own website, astronauts have choices for three meals a day: breakfast, lunch, and dinner, with the calories provided adjusted to the needs and size of each astronaut. The types of food range from fresh fruits (for the first few days before they spoil), nuts (including peanut butter), meats like seafood, chicken, and beef, desserts like brownies and candy, plus beverages like lemonade, fruit punch, orange juice, coffee, and tea. While they can’t yet grow rice in space, they can be sent up with it and other foods like cereals, mushrooms, flour tortillas, bread rolls, granola bars, scrambled eggs, and mac and cheese.

Long-term storage of food in space means that a lot of the food items are rehydratable: dried until the astronauts add water generated by the station’s fuel cells. Many items are thermostabilized or heat-treated to destroy any enzymes or microorganisms that might cause the food to spoil. Packaged fish, fruit, and irradiated meat can be transported into space this way, along with more complex packaged meals like casseroles. Beverages all come in powdered form until they are mixed with water at the time of consumption. Condiments like mustard, mayo, ketchup, and hot sauce (strangely enough) stay exactly the same, and can be sent to space in their commercially available packets.

1. Ham Salad Sandwich

This is actually the first meal that American astronauts had on the moon. Not unlike the chicken, egg, or tuna salad sandwiches we enjoy on Earth, Neil Armstrong and Buzz Aldrin ate these sandwiches along with “fortified fruit strips” and rehydratable drinks on the very first lunar excursion. Time magazine states that the Apollo 11 mission ate four meals in total on the moon’s surface, and that their resulting waste is still left behind today in the lunar module.

2. Tubes of Applesauce

Another first here: the first food eaten in space by an American (John Glenn), and this one confirms a lot of what people assume about food during space travel: it’s in a tube, thick enough so it won’t float away from you in a microgravity environment. Just like squeezing out toothpaste, the first American in space squeezed applesauce out of an aluminum tube during the Mercury space mission of 1962.

3. Rehydratable Mac and Cheese

The instant macaroni and cheese you pour hot water over isn’t wholly unlike the kind they eat in space. The same goes for other dishes besides this standard American comfort food, like chicken and rice, dried soups, and instant mashed potatoes. Astronauts can even eat breakfast cereals this way, which come fortified with essential nutrients and packaged with dry milk and sugar for that familiar taste of home.

4. Irradiated Lunch Meat

“Irradiated” sounds like this food just came out of Chernobyl, but in fact most of what astronauts eat is irradiated (not radioactive) to eliminate any traces of insect activity or microorganisms that might otherwise spoil or damage the food before the astronauts can partake. It happens to food on Earth too, especially seafoods and other animal products that have a high potential to spoil when preserved for a long period of time, but it’s also done to fresh fruits and seasoning herbs too. It’s all FDA- and NASA-approved for safety.

5. Cubed Foods (Like Bacon)

Here’s another menu item in line with what the imagination expects: cubed food was part of a space diet from the very beginning, and that still remains true in some instances. In the early days, these bite-sized cubes were rather unappetizing. Let’s just say that along with the hassle of squeezing tubes and dealing with the crumbs from freeze-dried foods, which might interrupt instrument functioning on the vessel, the cubes were not a crowd favorite. (To reduce crumbs, sandwiches and food cubes like cookies used to be coated in gelatin, which makes spaceflight sound less glamorous than ever.)

One of those cubed foods was bacon squares. That’s right: compressed bacon that was enjoyed regularly by the Apollo 7 astronauts according to Popular Science—they were much the favorite over bacon bars, most of which returned to Earth when the mission was complete. Now the nearest approximation to bacon cubes on the International Space Station are some freeze-dried sausage patties, not unlike the kind many people keep in their home freezers.

The variety of food has since expanded to over 200 menu items, but some of them (like chicken dishes) are still cut up into bite-sized chunks: no one has time to carve a turkey in space.

6. Shrimp Cocktail and Hot Sauce

The most popular dish on the International Space Station across the nations is shrimp cocktail. With a powdered sauce infused with horseradish, for whatever reason, among the hundreds of dishes from Russia, the United States, and Japan, shrimp cocktail is the most highly preferred.

Maybe it has something to do with that spicy sauce, because another people-pleaser in space is hot sauce. Even for those star-walkers who don’t like hot sauce back home, hot sauce in space not only livens up otherwise bland dishes, but some astronauts say that taste doesn’t work the same way in space, and that all of the food tastes bland to them, including their usual favorites.

Likewise hot sauce also works practically to help clear the nasal passages: if you get a stuffed up head in space, there’s no fresh air to be found. That “stuffiness” may be what accounts for an inability to taste most flavors and why hot sauce has become a favorite for many.

7. Liquid Spices

Without gravity’s assistance, you can just pepper or salt your food in space like you would on the ground. That leads to items like liquid salt and pepper, so that the spices are actually applied directly to the food instead of floating off to get grit in the space station’s sensitive machines or to end up in a fellow astronaut’s nose or eyes. Salt is applied in the form of salt water, while pepper is suspended in an oil.

8. Powdered Liquids

All the drinks in space start as powders, including orange juice, apple cider, coffee, and tea. The powder is pre-loaded in a foil laminate package. So the dusty particles cannot escape, astronauts must secure the water source to a connector on the packet to add liquid. After that, they drink it from a straw (sort of like a Capri-Sun, but with way more at stake).

Not all foods work in powdered forms however. Ground control used to send people to space with freeze-dried astronaut ice cream, but it’s no longer included on the International Space Station. The astronauts disliked it too much due to its crumbly, chalky texture, which felt uncomfortable against their teeth and left an unpleasant film on the tongue.

9. Tortilla Wraps

Instead of bread (another crumby entity) or lettuce (which wilts), NASA now uses tortillas to make sandwich wraps for space travel. They’re partially dehydrated, and can last up to 18 months on the ISS. It was only thanks to Mexican payload specialist Rodolfo Neri Vela that tortillas were introduced to the space food system, where they are now invaluable.

The ability to last for long periods of time is essential due to the inherent delays in space travel. Fresh fruit and veggies sent to space have to be kept in a special fresh food locker that is resupplied a little more frequently by a space shuttle, but when the supply comes in they have to be eaten quickly before they spoil and rot.

10. Thermostabilized Fish

Remember the irradiated lunch meat from before? Thermostabilization is another type of heat treatment applied to food that may have destructive microorganisms. It’s the same tech used on Earth before canning our seafood, be it tuna, salmon, or sardines. While fish is one of the smellier items allowed on the ISS, it’s nevertheless too important a source of protein and nutrients like omega-3 fatty acids to do without.

What the NASA Diet Tells Us About Human Nutrition

It is imperative that the food sent up with our astronauts helps them keep muscle mass in space, and the same goes for bone density. The more scientists learn about what space does to the human body and how to protect astronauts from damage, the more the world learns about overall human health.

For example, studies on astronaut Scott Kelly and his twin brother reveal how leaving the bonds of Earth impacts the human body, and suggests how long we as a species can withstand the weight loss of zero gravity. Space travel biology provides data on human biology we may never have known otherwise, and here’s how it can positively impact you.

New muscle growth cannot happen without the proper balance of all nine essential amino acids. Discovering that ideal ratio was the first step, and developing the formula was the next. Now there is a supplement appropriate for people under extreme conditions to preserve the muscle they have and replace the muscle that is lost with new growth, reversing space- or age-related muscle loss. In that sense, space exploration and experimentation today is a lot like Star Trek: in many ways exploring space involves finding out what it means to be human.

The Space Between

As humans we should all be proud of the advances we’ve made in space travel, and just how far we’ve gone as a species. Likewise we here at the Amino Co. are proud to be associated with the important work Dr. Wolfe has done, and the findings he’s brought back from NASA that are now accessible to anyone looking to preserve or build muscle, even under circumstances that are literally out of this world. Explore the available formulas, and help your body become space-strong.