We all shed tears. Our eyes produce tears continually, and when we blink, those tears spread across the front surface of our eyes to lubricate them. Tears also clear our eyes of debris and protect them from infection. But in some people, tears don’t work the way they’re supposed to and dry eye disease is the result.

If you’re one of those people, you’re not alone.

In the United States, more than 16 million people suffer from dry eyes.  That’s nearly seven percent of the population. And that figure is likely much higher because not all people with dry eye symptoms see a doctor for treatment. But about 33 percent of patients who visit eye doctors complain of dry eye symptoms.

Symptoms of dry eye can be very uncomfortable and include decreased vision or occasional blurry vision, dryness, redness, itching, burning, eye fatigue and the feeling there’s something in your eye. And believe it or not, some people with dry eye experience excessive tearing.

There are two types of dry eye disease. There’s the aqueous-deficient type, which is when your eyes don’t make enough tears. Then there’s the evaporative type, which is when your tears don’t stay on your eyeball long enough to keep it properly lubricated.  Evaporative dry eye disease is the more common of the two.

Most of the time, evaporative dry eye occurs when the eye’s oil glands, the Meibomian glands, become clogged and can’t release the oils necessary for healthy tears. The oil component of tears helps keep them from evaporating off the surface of your eyes.

When the Meibomian glands are clogged, inflammation and an overgrowth of bacteria on the eyelids can also occur, which makes dry eye symptoms even worse. These conditions make it difficult for the Meibomian glands to work properly, which is referred to as Meibomian gland dysfunction, or MGD.

Treatment for MGD typically begins with artificial tears, warm compresses and eyelid cleansing. When these steps fall to improve MGD, and subsequently your dry eye symptoms, there’s a newer treatment available called intense pulsed light, or IPL.

IPL was originally designed for use in dermatology to treat conditions such as rosacea and acne but was introduced into ophthalmology a few years ago. IPL is the use of short bursts of powerful light in various wavelengths to treat MGD. The wavelengths chosen for your treatment depends on your skin color and tone.

The IPL light generates heat below the skin of the eyelids, warming and thinning the thickened oil, or meibum, blocking the glands. Once the meibum is thinned, it can more easily be removed through Meibomian gland expression or MGX. During MGX, the doctor uses a cotton-tipped applicator and manual pressure to squeeze out the meibum from the glands.

In addition to thinning the meibum, IPL also closes the small blood vessels on the surface of the skin that contributes to inflammation. The heat IPL generates also kills the problematic bacteria flourishing on the eyelids. All of these functions have beneficial effects on MGD and, as a result, dry eye symptoms.

During an IPL treatment, the doctor will first place shields on your eyes to protect them from the light. The doctor will also place a thin layer of cooling gel on the areas of skin to be treated. The pulses of light are delivered from the outer area of the right eye, across the cheeks and nose to the outer area of the left eye.

You may feel a warm sensation during treatment, but that’s all. IPL treatment is not painful. A typical treatment consists of about 30 pulses and takes 15 to 20 minutes to complete. Afterward, you may be instructed to use low-dose anti-inflammatory eye drops for a few days.

Many people experience improvement in their symptoms after one IPL treatment, but for best results, a series of four treatments over four months is typically recommended. Maintenance treatments are also recommended every six months to a year.

A number of studies confirmed that IPL reduces both signs and symptoms of MGD and dry eye. In one study, more than 90 percent of patients improved in the three areas used to assess MGD. Results are validated subjectively through your report of symptom improvement and objectively when your doctor examines the surface of your eyes under a light.

The image many people form when thinking of medical researchers at work is one of serious men and women using sophisticated technology to investigate treatments and cures for diseases. But in some cases, these professionals use simple, everyday devices to combat people’s disorders and manage their symptoms.

A recent study, published in Nature Biomedical Engineering on August 5, reported on a new wireless device that regulates neural circuits in the brain using a tiny implant controlled by a simple smartphone. The researchers say this device speeds up efforts to uncover various brain disorders including Parkinson’s disease, Alzheimer’s disease, addiction, depression and pain.

The wireless device enables consistent chemical and optical nerve stimulation, which targets specific brain cells. Previous methods to achieve this effect involved the use of rigid metal tubes and optical fibers to deliver the drugs and light. This method limited the subject’s movement due to the physical connections to bulky equipment. It also often led to lesions in the brain’s soft tissue over time, making that method unsuitable for long-term use.

But this new approach uses large, Lego-like replaceable drug cartridges and powerful Bluetooth-enabled low-energy. This method allows for the targeting of specific nerve cells in the brain for prolonged periods without the limits of a physical connection to equipment or the risk of brain lesions.

Controlled by a simple user interface on a smartphone, researchers using this device can easily trigger any specific combination or the precise sequence of light and drug delivery without being inside a laboratory. And because it can be used for long periods, the device may contribute to uncovering the basis of many neuropsychiatric diseases.

Last year, scientists from the Ulsan National Institute of Science and Technology in South Korea reported on advances in technology using wireless communication and portable devices for diabetes monitoring. Their study results were published in the January 2018 issue of Scientific Advances.

The researchers studied a new technology involving a smart soft contact lens capable of monitoring blood glucose levels in tear fluid, as well as other relevant physiological data in real-time. This data can then be used to facilitate disease management.

Previous attempts at using contact lenses for this purpose came under criticism because the material used was too opaque and rigid, and could potentially damage the eyes. The research team in South Korea addressed these concerns by placing the operational components around the edge of the lens away from the pupil.

The new contact lens that was developed is equipped with sensors that can detect blood glucose changes in the tears, as well as other biomarkers typically found in the blood. These biomarkers include cholesterol, sodium ion and potassium ion levels, offering additional disease monitoring possibilities.

The study researchers note that the contact lens collects tears for measuring glucose changes from those created by normal activities such as blinking. As a result, invasive collection methods, such as finger sticks to collect blood for testing, are avoided. The goal of the new technology is to increase patient compliance with regular blood glucose monitoring.

Other noninvasive methods for measuring blood glucose levels in people with diabetes are also being studied. One study is looking at a technology that measures blood glucose by placing a device near the eye. This technique uses a novel biochemical sensor embedded on a small hydrogel disk. The disk is inserted below the patient’s conjunctiva during a simple, painless procedure performed by an ophthalmologist.

The chemical in the disk reacts with blood glucose in the interstitial fluid below the conjunctiva and emits fluorescent light that is quantified by a special photometer device. This device is placed in front of the person’s eve. It can record blood glucose results in less than 20 seconds.

Another noninvasive device uses occlusion spectroscopy measurements to determine blood glucose measurements. It involves placing a ring-shaped probe around the person’s finger and applying gentle pressure. This pressure temporarily stops blood flow, and optical elements in the device’s sensor perform a sensitive measurement of the light transmitted through the finger.

In one study, measurements taken using this device were compared with measurements taken using invasive methods, and this device proved comparable. Tests showed this device to be a painless and accurate alternative to invasive methods such as finger sticks for continuous glucose monitoring in patients with diabetes.

Married couples aren’t the only ones who sometimes wish their honeymoons would last a little longer. People being treated for Parkinson’s disease often express the same wish regarding their treatment. Before long, their wish may be granted.

A clinical trial that began in July at the University of Arizona is aimed at finding out if ketamine, a drug used to treat depression, can extend what physicians refer to as “the honeymoon period’’ for Parkinson’s patients being treated with levodopa.

Levodopa, an amino acid created naturally in the human body, has long been used to treat some of the symptoms associated with Parkinson’s disease, particularly the stiffness and slow movement that comes with it.

The problem is that levodopa typically works great for a few years. That’s what doctors call the honeymoon period. After that, severe side effects such as uncontrollable and involuntary movement of the arms, legs and head develop.

Research has shown that 40-percent of all Parkinson’s patients being treated with levodopa experience these side effects, known clinically as dyskinesia and that the only way to stop them is to halt the levodopa treatments.

The intentions of the three-year, $750,000 clinical trial is to determine if ketamine, which has also been used to treat chronic pain, can help reduce the rash of involuntary movements brought on by the use of levodopa.

The belief that it can is shared by two University of Arizona doctors who first discovered ketamine’s added potential in the treatment of Parkinson’s disease several years ago when they began using it as a pain reliever for Parkinson’s patients.

Parkinson’s disease is a chronic progressive neurological disease that is marked by the tremor of resting muscles, rigidity, slowness of movement, impaired balance, and a shuffling gait.

In addition to learning that ketamine helped ease pain in patients with Parkinson’s disease, the doctors discovered that the patients who were given ketamine treatments also experienced a noticeable reduction in dyskinesia.

The doctors later discovered that similar results were found when lab rodents with Parkinson’s disease were treated with ketamine, which can bring about some side effects of its own.

An increase in blood pressure and a feeling of disassociation with the body has sometimes been experience by people being treated with ketamine, which has also been used recreationally.

During the trial, however, the doctors intend to closely monitor blood pressure levels and they are confident the dosage needed to relieve the dyskinesia falls well below the dosage at which the disassociation effect is realized.

The trial is currently monitoring the effects of ketamine in 10 patients with Parkinson’s disease and is being conducted in conjunction with a separate study using rodents to determine how ketamine affects the brain.

If you read the recent posting, you learned the basics of breast cancer. You know it’s a nasty disease. In fact, death rates from breast cancer are higher than those of any other cancer except lung cancer for American women. Knowing that may help you appreciate these remarkable breakthroughs recently announced by breast cancer researchers.

The results of one study were released in February and published in the journal Nature. The investigators in the study reported their findings that a certain protein found in many foods may reduce a dangerous type of breast cancer’s tendency to spread. This suggests that your diet may be a factor in treating this form of breast cancer.

The type of cancer is called triple-negative breast cancer because its cells lack receptors   for estrogen and progesterone and don’t make very much of a protein known as HER2. It is often deadly because it tends to travel to distant sites in the body.

In this multicenter study, which used laboratory mice, investigators found that by limiting an amino acid called asparagine, they could dramatically reduce the cancer’s ability to spread to the farther reaches of the body. That’s great news!

One of the drawbacks of this good news is that many foods contain a lot of asparagine. These include beef, poultry, fish, seafood, dairy products, eggs, potatoes, nuts, seeds, soy, whole grains and, surprise, surprise, asparagus. Most fruits and vegetables are low in the amino acid.

Unless you’re vegan, your diet will change dramatically. But it’s worth it if it stops the spread of this deadly cancer. The next step for researchers is to begin an early phase clinical trial using healthy subjects. The subjects would eat a low-asparagine diet, and the investigators would test for drops in asparagine levels.

After that, investigators will move on the next phase clinical trial and test their diet treatment on cancer patients. In that case, diet changes would be made in combination with the patients’ chemotherapy or other traditional treatments.

The results of another study were made public in September but are not due to be officially presented until the 2018 American Society of Clinical Oncology Annual Meeting in June. This study was a federally funded phase III clinical trial of women with an early-stage breast cancer that had certain characteristics.

The early stage breast cancer studied must be hormone receptor-positive, HER2-negative and axillary node-negative. It must also score in the mid-range on a specialized test called a 21-tunor gene expression assay. The study investigators have some welcome news for women with this type of cancer.

Here’s something you’ll want to hear. The clinical trial showed that women with this breast cancer do not need to have chemotherapy after surgery. That’s awesome because you avoid all those horrible side effects. Apparently, there wasn’t any improvement in disease-free survival when chemotherapy was added to other treatments after surgery.

This is especially good news when you consider that half of all breast cancers are hormone receptor-positive, HER2-negative and axillary node-negative. That means a lot of women are affected by this study’s outcome. Read what the study’s lead author, Joseph A. Sparano, MD, has to say about it:

“Our study shows that chemotherapy may be avoided in about seventy percent of these women when its use is guided by the test (21-tumor gene expression assay), thus limiting chemotherapy to the thirty percent who we can predict will benefit from it.”

These are the results of just two recently completed studies on breast cancer. These are many more that have been completed or are in progress. Because breast cancer is so deadly, research on it is ongoing. If you want to get involved in a clinical trial of a new drug or treatment, ask your doctor about one close to you or visit clinicaltrials.gov.

Between the last posting and this one, we’ve increased our awareness of breast cancer two-fold. Don’t keep your knowledge to yourself. Share a fact about breast cancer with someone else. Keep the awareness alive in others.

There’s good news and bad news about Parkinson’s disease, the neurodegenerative disorder that affects movement. The bad news is that an estimated seven to ten million people worldwide have it, and that number is growing with the aging population. The good news is there might be a new, noninvasive way to treat it.

Treatment for Parkinson’s, as well as other movement disorders such as essential tremor, rigidity, stiffness and walking problems, are generally initially treated with medications. These medications target cells in the brain that make the chemicals that help cells pass along messages telling the body to move. Many people respond to this therapy.

For years, when people were at the point their disorder did not respond to medicines, or it began interfering with daily activities, they had few good options. Then in 2002, the FDA approved a procedure called deep brain stimulation (DBS) as a therapy for advanced Parkinson’s disease. After that, its use in thousands of patients in the US and Europe prompted studies of the treatment in earlier stages of the disease as well.

DBS is a surgical procedure that blocks nerve signals in targeted areas of the brain, which are generally identified using MRI or CT imaging. During DBS, a battery-operated medical device, similar to a pacemaker, is implanted to deliver electrical stimulation to the specific brain areas to control movement and other Parkinson’s symptoms.

The DBS system has three components, including the lead, which is a thin, insulated wire that is inserted through a small opening in the skull and implanted in the brain. The extension is another insulated wire that is passed under the skin of the head, neck and shoulder and connects the lead to the third component, the neurostimulator. That is the battery pack, and it is usually implanted under the skin near the collarbone or in the abdomen.

DBS has proven very effective in helping to reduce symptoms and medication use, as well as increase patients’ quality of life. However, DBS surgery has risks, including infection, stroke, cranial bleeding and other complications. Then in June, researchers at MIT announced they developed a new, noninvasive method for deep brain stimulation.

The MIT researchers, in collaboration with investigators at Beth Israel Deaconess Medical Center and the IT’IS Foundation, have developed a method to stimulate regions deep in the brain using electrodes placed on the scalp. This approach could make DBS less risky, less expensive and more accessible to patients.

The approach involves generating two high-frequency electrical currents using the electrodes on the scalp. These currents are too fast for the brain cells, or neurons, to respond to. However, the two currents interfere with one another, and when they intersect, deep in the brain, they essentially cancel out all but a small, low-frequency current. This current can influence the neurons’ response, while the high-frequency current has no effect on surrounding tissue.

Using the electrodes this way, researchers can target the areas they want deep inside the brain, without affecting any other brain structures. Also, without having to move the electrodes, they can direct the location of the stimulation by altering the currents. They can stimulate the brain for treatment or research.

The new method has shown promise in mice, and researchers have started testing the strategy on people without disorders to see if it works on human brains. A clinician at Boston Children’s Hospital and Harvard Medical School said if those testing results are promising, he would collaborate with the MIT team to evaluate the technique for treatment of another disorder, epilepsy.

The pulses of electricity delivered by DBS can improve the quality of life for people with Parkinson’s disease. They can also be used to treat those with obsessive-compulsive disorder, depression and other psychiatric disorders that fail to respond to medication. This noninvasive approach to DBS could help more people enjoy that improvement.

The world has a drug problem! It’s getting so bad that the United Nations held a special meeting last September to discuss it. It was only the fourth time ever the UN called a high-level meeting on a global health issue. This time, the delegates discussed antibiotic-resistant infections – superbugs impervious to our current arsenal of germ-fighting drugs.

Drug-resistant bacteria, as well as drug-resistant parasites, viruses and fungi, have been lurking for a while. One superbug has been popping up, even here in the US, that is resistant to our last-ditch antibiotic. Without medications that can fight these germs, there will be untreatable infections that will have devastating consequences across the globe.

Already, it’s estimated that more than 700,000 people worldwide die each year from drug-resistant infections. And that’s a lowball figure because tens of thousands of deaths from these infections are not reported or are attributed to other causes. One review on antimicrobial resistance suggests that by 2050, 10 million people around the world will die each year from these infections!

Drug resistance happens naturally over time, usually through genetic changes. However, the overuse and misuse of antibiotics and other drugs developed to treat microbial infections accelerated this process. Using antibiotics for every little illness, especially for viral infections such as colds and flu, and to promote growth in livestock, are examples of this misuse. After years of doing this, we now have a resistance problem.

One superbug that’s got everybody scrambling is a bacterium that can’t be killed by the drug of last resort, Colistin. Infections with this bacteria had been seen in animals and humans in China and Europe, but have been discovered in the US as well. Fortunately in those cases, the infections responded to other antibiotics, but the bacteria’s resistance to Colistin is significant.

Why? Without getting too technical, the genetic change that makes this bacteria resistant to Colistin can be spread to other strains of bacteria. That includes strains that are already resistant to all other antibiotics. That would create bacteria that are totally untreatable with any drug we currently have available.

With superbugs like these, routine medical procedures such as C-sections, hip replacements and chemotherapy become extremely high risk. Without effective antibiotics to treat them, minor infections could become life-threatening crises. Little, if anything, could be done to treat common conditions such as gonorrhea and pneumonia.

What can be done? At the UN meeting in September, World Health Organization director general Margaret Chan stressed that it is imperative for consumers and medical providers to rely less on antibiotics for disease treatment. She also appealed for more progress in antibiotic development. After all, only two new classes of antibiotics have reached the market in the past half-century.

As they brought the meeting to a close, the UN delegates signed a declaration committing to encouraging innovation in antibiotic development and increasing public awareness of the growing threat of drug-resistant infections. They also agreed to develop surveillance and regulatory systems on the sales and use of antimicrobial medicines for humans and animals.

Facing a new kind of drug problem, the world is poised to take on the challenge.

Are you tempted to use one of those at-home DNA kits like 23andMe, Ancestry DNA and Family Tree DNA to find out more about your ancestry? Before you buy, learn a little more about what they can do and what they can’t.

When you get one of these kits, you’ll be instructed to either use a sterile swab to gently scrape the inside of your cheek or spit a prepared solution after swishing it thoroughly in your mouth. These are both decent methods for collecting cells for DNA testing.

After your sample is collected, you send it back to the company, who’ll either mail your results to you or post them on a secure, password-protected website. It generally takes a few weeks to get the results.

Most of us have seen shows like CSI on which they gather and analyze DNA evidence. They always claim their results are something like 99.9 percent accurate and reliable. Don’t think you’ll get that kind of accuracy from an at-home, spit or swab test. These kits can tell you a lot about your background, but you still have to fill in the blanks.

For example, an at-home DNA test can tell you which regions of the world have people who share your DNA imprint, but not necessarily the country and not a specific city or town. That’s because most of our ancestors and their children for generations didn’t stay in the same geographic area.

Instead, most people moved around, spreading their DNA imprints in other areas. This makes it difficult for researchers to distinguish one area’s genetic population from another, limiting degree of specificity on testing.

With the at-home DNA tests, companies compare the individual’s DNA to a reference database of DNA samples from people living in various regions today. Their DNA is actually different from that of the people who lived in those regions years ago, including your ancestors. Also, just because you share DNA with the people living in those areas now doesn’t necessarily mean your genetic genealogy is exactly the same.

During a recent investigation by Inside Edition, identical triplets were used to test the accuracy of at-home DNA kits. The results for one set of triplets revealed a discrepancy as far as countries of origin. The trio shares the same DNA, but the tests showed different percentages for each from a certain region. Program producers did some follow-up with the companies to get answers.

Family Tree DNA said they have since improved the algorithm they use to determine results and have already begun to implement the updated method. 23and Me explained that their results are based on a sliding confidence scale, ranging from 50 percent to 90 percent. The higher the confidence level chosen, the less specific the results can be as to the region or country of the individual’s ancestry. One interesting test used triplets to illustrate how well the kits worked.

Do you really want to know your full story? That’s where traditional genealogy research comes in. By mixing the modern science of DNA with old-fashioned searching methods, you can make a lot of progress in learning about your ancestors and discovering the amazing story of you.

Anyone who remembers the emergence of AIDS in the early 1980s might be astonished at how much has changed in 35 years.

In the beginning, doctors didn’t know much about a strange disease that seemed to affect gay men. One of the first alerts appeared to be an outbreak of a rare cancer. Scientists eventually discovered the virus called HIV, the cause of AIDS, and how AIDS attacks the immune system.

At one time, an HIV infection was a virtual death sentence. There were no effective treatments to stop progression to full-blown AIDS. A timeline of the epidemic shows that by 1992, AIDS was the leading cause of death for men ages 25-44 in the US.

Today, it’s a much different story.

A new British medical study shows that a young adult with HIV in North America and Europe, who is being treated with antiretroviral drugs, can expect to live a near-normal lifespan.

Specifically, the study indicates that a 20-year-old with HIV who began antiretroviral treatment between 2008 and 2010, and had a low viral load after a year of treatment, has a life expectancy of around 78 years old. That’s lower than the general population, but far higher than for people who lived with HIV before antiretroviral drugs were available. It’s a decade more than the life expectancy of people treated with early antiretroviral medications.

Antiretroviral drugs to fight HIV were introduced in mid-1990s. They were game-changing at the time, and have since improved. Today’s versions work better, are less toxic and require fewer pills. The improvements in care are why people with HIV are living longer, according to researchers.

So where are we now? US health guidelines recommend routine HIV screening tests for teens and adults between 13 and 64. Even if you aren’t in a high-risk category, the Centers for Disease Control and Prevention says that you should get an HIV test at least once to know your status.

And, of course, people who fall into higher risk categories should be tested more often. Sexually active gay and bisexual men might consider testing every three to six months, in fact, says the CDC. Heterosexuals with multiple sex partners also should seek routine HIV screening. (The CDC offers an online HIV risk reduction tool that can be customized for information specific to gender, sexual orientation and more).

Remarkably, a large percentage of people with HIV don’t know they have the virus. In 2015, the CDC estimated that one in eight Americans with HIV were unaware they had it. They accounted for about one-third of HIV transmissions in the US.

In the US, Southern states have become the epicenter of HIV and AIDS. By 2014, they accounted for 50 percent of new HIV cases in the entire country. According to news reports, poor rural areas and ethnic minorities have been disproportionately affected. These are places with fewer resources to treat HIV and where many with the virus don’t know they have it.

Yet, if all people with HIV infections were diagnosed and treated promptly, 90 percent of new cases could be prevented, according to the CDC.

Tremendous strides against HIV and AIDS have been made since those first reports of a strange sickness appeared in the early 1980s. Hopefully, the progress can continue until HIV is controlled – or gone entirely – in the US and around the world.

Post Traumatic Stress Disorder (PTSD) can often be accompanied by a high level of misunderstanding of the condition. In fact, several myths appear to contribute to the stigma that surrounds those with PTSD.

PTSD is an anxiety disorder. It develops in response to traumatic or life-threatening experiences such as active duty combat, sexual assault, car accidents, natural disasters and even bullying in school or the workplace.

Emotional symptoms include anxiety, anger, depression, irritability and sadness. Physical symptoms of PTSD can include increased fatigue, headaches, trouble digesting food and high or low blood pressure. The risks for developing PTSD vary depending upon the trauma experienced.

The latest research shows that PTSD actually causes a part of the brain called the amygdala to shrink. The amygdala is the part of the brain that processes emotions and fear. Researchers believe that when the amygdala is smaller, it makes it more difficult for people to process their anxiety resulting from trauma.

I write this post with the hope of educating others on how to recognize the symptoms, how to help someone who has it and most importantly to create an understanding that PTSD does not define the person.

The myths surrounding PTSD create further misunderstanding of the disorder and those who suffer from it. Some of those myths include:

1. PTSD is a sign of mental weakness: Developing PTSD is not a sign of weakness, be it mental weakness or weakness of character. It is an understandable human response to uncommon experiences. There are several factors that may influence whether an individual will develop PTSD, including: severity of the trauma and type of trauma.
2. You only get PTSD immediately after an experience: In order for these stress reactions to merit a diagnosis of PTSD, the symptoms must last at least a month. Within the first month, these stress reactions are considered “acute stress,” which is very similar to PTSD, but traditionally has a slightly greater emphasis on dissociative symptoms (e.g., altered sense of reality, inability to remember important aspects of the traumatic event), and can be diagnosed within the first month of the trauma. Only if the symptoms last longer than a month, can the diagnosis of PTSD be considered.
3. People with PTSD are crazy: PTSD is not characterized by psychosis or violence. Rather, symptoms of PTSD surround coping with the memory and implications of a traumatic experience. “Crazy” is a damaging stigma.
4. People with PTSD cannot function normally: People can have PTSD and still effectively do their job, even a military job. It is a manageable and treatable diagnosis, and being diagnosed with PTSD does not mean one’s career is over.
5. People with PTSD should just “get over it”: PTSD symptoms do not just magically go away after a certain period of time has passed. While many people are able to find ways of coping on their own, many others benefit from working with a professional for guidance.
6. Veterans with PTSD are not “wounded”: The fact is, veterans went to war and made sacrifices for this country. It may help reduce stigma to think of psychological injuries as similar to physical injuries — inevitable, collateral damage of war that is not indicative of personal weakness.
7. Nothing can be done to help PTSD sufferers: There are several different types of treatments, developed for different types of people, which have all been found to be effective, including medications and therapy. New interventions continue to be developed.

Women are twice as likely to develop PTSD as men. Treatment for PTSD can include SSRI medication (selective serotonin reuptake inhibitors), also known as antidepressants, psychotherapy, cognitive behavioral therapy, exposure therapy and stress therapy.

Please speak with your medical professional if you or someone you love is experiencing the symptoms of PTSD and may need help coping. There are also resources available to help with PTSD.