Princeton Engineering researchers report they have isolated a compound that kills bacteria that can cause incurable infections. The compound, called cloacaenodin, is a short, slip-knotted chain of amino acids known as a lasso peptide, encoded by gut-dwelling bacteria as a defense mechanism. The peptide works by attacking rival bacteria.
“Using genome mining and heterologous expression, we report the discovery and production of a new antimicrobial lasso peptide from species related to the Enterobacter cloacae complex,” wrote the researchers. “Using NMR and mass spectrometric analysis, we show that this lasso peptide, named cloacaenodin, employs a threaded lasso fold which imparts proteolytic resistance that its unthreaded counterpart lacks.”
The peptide hooks into a target cell’s RNA-producing enzymes and shuts down basic cell functions.
“Not only does [this peptide] kill off-the-shelf, historical Enterobacter strains, it also kills Enterobacter strains that actually have come from patients in the hospital and that are drug-resistant,” explained Link.
Link’s research group has discovered several peptides in this same class. He said cloacaenodin is unique because it can kill clinically relevant drug-resistant strains, making it a promising subject for antibiotic development.
“If it’s made by one Enterobacter species, it’s likely going to kill other species of Enterobacter. So it’s this sort of guilt-by-association approach,” Link said. This gives researchers a way to prioritize peptide-mining hits, since peptides that are encoded in strains related to pathogens are more likely to have interesting bioactivity, he said.
The researchers plan to start testing the compound in animal infection models to confirm that it can clear the infection and that it is safe for animal cells.
Their findings suggest if the compound is harnessed by science, it could be redirected to fight infections that are not treatable by today’s medicines.
In July 2022, the World Health Organization (WHO) announced that monkeypox was a public health emergency of international concern. And, as of early December 2022, more than 82,000 human monkeypox cases have been confirmed in 110 countries worldwide. New preventative and therapeutic measures against the virus are needed.
Monkeypox is caused by monkeypox virus, an enveloped double-stranded DNA virus that belongs to the Orthopoxvirus genus of the Poxviridae family. The monkeypox virus has its own DNA polymerase F8 which, when together with the processive cofactors A22 and E4, constitutes the polymerase holoenzyme for genome replication.
Now, researchers present a high-resolution structure of the monkeypox virus DNA polymerase holoenzyme—a complex that plays a key role in the genome replication process of the virus. The findings reveal the mechanism that underlies monkeypox virus genome replication and could be used to guide the development of antiviral drugs.
Qi Peng, PhD, and colleagues at the CAS Key Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology at the Chinese Academy of Sciences in Beijing, used cryo-electron microscopy to determine a high-resolution structure of the monkeypox virus DNA polymerase holoenzyme.
They determined the holoenzyme structure in complex with DNA using cryo-electron microscopy at the global resolution of ~2.8 Å. According to the findings, the holoenzyme possesses an architecture that indicates a “forward sliding clamp” mechanism for DNA replication. Monkeypox virus polymerase has a similar DNA binding mode to other B-family DNA polymerases from different species. These findings reveal the mechanism of the monkeypox virus genome replication and may guide the development of anti-poxvirus drugs.
Scientists at Scripps Research and Massachusetts Institute of Technology (MIT) have found a clue to the molecular cause of Alzheimer’s disease (AD), which may also explain why women are at greater risk for the disease than men.
The team found that a particularly harmful, chemically modified form of an inflammatory immune protein called complement C3 was present at much higher levels in the brains of women who had died with AD, compared with the brains of men who had died with the disease. The results also showed that estrogen—levels of which drop during menopause—normally protects against the production of this form of complement C3.
“Our new findings suggest that chemical modification of a component of the complement system helps drive Alzheimer’s, and may explain, at least in part, why the disease predominantly affects women,” said research lead Stuart Lipton, MD, PhD, professor and Step Family Foundation endowed chair in the department of molecular medicine at Scripps Research and a clinical neurologist in La Jolla, CA. Lipton is senior author of the team’s published paper in Science Advances, which is titled, “Mechanistic insight into female predominance in Alzheimer’s disease based on aberrant protein S-nitrosylation of C3.” In their paper the researchers concluded, “Collectively, we demonstrate robust alterations in the S-nitrosoproteome that contribute to AD pathogenesis in a sex-dependent manner.” The study was a collaboration with a team led by Steven Tannenbaum, PhD, post-tenure Underwood-Prescott professor of biological engineering, chemistry, and toxicology at MIT.
AD, the most common form of dementia that occurs with aging, currently afflicts about six million people in the U.S. alone. “AD—characterized by the accumulation of misfolded amyloid-β (Aβ) peptide and neurofibrillary hyperphosphorylated tau tangles in the brain—is arguably the most common neurodegenerative disorder leading to dementia,” the team wrote.
Alzheimer’s disease is always ultimately fatal, usually within a decade of onset, and there is no approved treatment that can halt the disease process, let alone reverse it. The shortcomings of treatments reflect the fact that scientists have never fully understood how Alzheimer’s develops. “The etiology and pathogenesis of AD are incompletely understood, and effective, disease-modifying drug treatments are lacking,” they continued. Scientists also don’t know fully why women account for nearly two-thirds of cases. “Although tremendous strides have been made in AD research over the past decade, additional consideration of sex differences will be important to explain the increased incidence of disease in females.”
Lipton’s lab studies biochemical and molecular events that may underlie neurodegenerative diseases, including the chemical reaction that forms a modified type of complement C3—a process called protein S-nitrosylation (SNO). Lipton and his colleagues previously discovered this chemical reaction, which happens when a nitric oxide (NO)-related molecule binds tightly to a sulfur atom (S) on a particular amino acid building-block of proteins to form a modified SNO-protein.
Protein modifications by small clusters of atoms such as NO are common in cells and typically activate or deactivate a target protein’s functions. For technical reasons, S-nitrosylation has been more difficult to study than other protein modifications, but Lipton suspects that “SNO-storms” of these proteins could be a key contributor to Alzheimer’s and other neurodegenerative disorders. “SNO can influence protein activity, localization, conformation, or interactions with other proteins; aberrant protein SNO may play a key role in the pathogenesis of various neurodegenerative diseases,” the investigators commented in their paper. “Prior work has linked SNO proteins in neurons and glial cells to neurodegenerative diseases, including AD.”
For their newly reported study, the researchers used novel methods for detecting S-nitrosylation to quantify proteins modified in 40 postmortem human brains. Half of the brains were from people who had died of Alzheimer’s, and half were from people who hadn’t—and each group was divided equally between males and females.
In these brains, the scientists found 1,449 different proteins that had been S-nitrosylated. Among the proteins most often modified in this way, there were several that have already been tied to Alzheimer’s, including complement C3. Strikingly, the levels of S-nitrosylated C3 (SNO-C3) were more than six-fold higher in female Alzheimer’s brains compared to male Alzheimer’s brains. “Notably, SNO proteins associated with complement pathways are enriched in both male and female AD brains,” they stated. “However, SNO of C3, representing the point of convergence of the various complement cascades, was detected predominantly in female AD brains … In our SNO protein datasets, we observed a significant increase in SNO-C3 in female AD brains, exhibiting a 34.2-fold increase over female non-AD control brain.”
In postmenopausal women, depletion of estrogen causes excessive elevation of nitric oxide (NO) in the brain and thus generates S-nitrosylated complement factor C3 (SNO-C3). SNO-C3 triggers activated microglial cells, the innate immune cells in the brain, to phagocytose (or “eat”) neuronal synapses—the connections that mediate signaling between nerve cells in the brain. This aberrant chemical biology process results in synapse loss, leading to cognitive decline in Alzheimer’s disease. [Chang-ki Oh and Stuart Lipton, Scripps Research]
The complement system is an evolutionarily older part of the human immune system. It consists of a family of proteins, including C3, that can activate one another to drive inflammation in what is called the “complement cascade.” Scientists have known for more than 30 years that Alzheimer’s brains have higher levels of complement proteins and other markers of inflammation, compared to neurologically normal brains. More recent research has shown specifically that complement proteins can trigger brain-resident immune cells called microglia to destroy synapses—the connection points through which neurons send signals to one another. Many researchers now suspect that this synapse-destroying mechanism at least partly underlies the Alzheimer’s disease process, and loss of synapses has been demonstrated to be a significant correlate of cognitive decline in Alzheimer’s brains.
Why would SNO-C3 be more common in female brains with Alzheimer’s? There has long been evidence that the female hormone estrogen can have brain-protective effects under some conditions; thus, the researchers hypothesized that estrogen specifically protects women’s brains from C3 S-nitrosylation—and this protection is lost when estrogen levels fall sharply with menopause.
“We hypothesized that menopause-associated up-regulation of inflammation in the brain could be causally linked to the aberrant increase in SNO-C3 that we observed,” the authors noted. “Experiments with cultured human brain cells supported this hypothesis, revealing that SNO-C3 increases as estrogen (β-estradiol) levels fall, due to the activation of an enzyme that makes NO in brain cells. This increase in SNO-C3 activates microglial destruction of synapses. “Mechanistically, we show that formation of SNO-C3 is dependent on falling β-estradiol levels, leading to increased synaptic phagocytosis and thus synapse loss and consequent cognitive decline,” they stated. “Thus, dysregulation of the complement system may play a role in the pathogenesis of AD and explain, at least in part, the female predominance of the disease.”
“Why women are more likely to get Alzheimer’s has long been a mystery, but I think our results represent an important piece of the puzzle that mechanistically explains the increased vulnerability of women as they age,” Lipton said. “To our knowledge, this is the first investigation comparing changes in NO-modified protein levels in the brains of male and female humans with AD,” the team stated. “ … our data suggest a unique mechanism by which protein SNO modulates complement (C3) activity in a sex-dependent manner, thereby providing a molecular link between NO signaling and the complement cascade in AD pathogenesis.”
The researchers now hope to conduct further experiments with de-nitrosylating compounds—which remove the SNO modification—to see if they can reduce pathology in animal models of Alzheimer’s and eventually in humans.
Healthcare isn’t immune from the influence of America’s litigious culture
Over the Thanksgiving holiday, The Washington Postpublished an articleopens in a new tab or window about a South Floridian woman who filed a lawsuit against the Kraft Heinz Co. for false advertising. The lawsuit alleges that the company’s Velveeta mac and cheese cups take longer than 3.5 minutes to prepare. The instructions on the back of the box, the plaintiffs say, call for 3.5 minutes of microwave time alone. The time it takes to tear open the lid and stir the ingredients together are not taken into account, and therefore the product’s packaging is deceptive.
The class action suit, led by plaintiff Amanda Ramirez, is asking Kraft to pay $5 million in damages for deceptive and unfair trade practices. The lawyers say there are probably more than “100 victims” spread across multiple states where the product is sold.
The reason why the story is so compelling, and has been amplified by many social media platforms, is that it possesses shock appeal — it grabs our attention and elicits a visceral reaction. Perhaps it even offends our moral instincts. We say to ourselves, “That’s absurd,” or “That’s ridiculous,” or “I can’t believe it.” Deep within our collective guts, we have a sense that the complaint lacks merit, and so it gnaws at our sense of right and wrong.
So, you’re probably asking yourself, how does this mac and cheese complaint pertain to the subject of medicine? How does it relate to the glut of malpractice lawsuits in the U.S.?
In my opinion, cases like these that garner national attention trickle into our collective subconsciousness. They influence our attitude toward litigiousness. When a person suffers an apparent medical insult or injury, whether or not they decide to take legal action is partly determined by the cultural milieu in which they live.
Now, let me be clear, I’m all for defending individual consumers against unchecked corporate power. The country and the world are a better place as a result of our protections under state and federal law. However, there is a tipping point where the law can be co-opted and misused as an instrument for personal reward rather than as a protective mechanism. Perhaps this case represents such an inflection point.
One of the attorneys representing the case, Spencer Sheehan, who is based in Great Neck, New York, has filed over 400 similar food and beverage product cases in recent years. According to NPRopens in a new tab or window, he has “almost single-handedly caused a historic spike in the number of class action lawsuits against food and beverage companies.”
He told the outlet, “I guess I’ve always been the type who would become annoyed [and] never liked it when companies cheated people for small amounts it would be difficult to recoup.”
While some of the lawsuits he has filed must have met the legal standard to proceed, in my opinion the pattern of lawsuits suggests that he’s using our legal system’s protection of individual consumer rights to his advantage — filing a large number of class action lawsuits (which are often taken on a contingency basis) and seeing if any of them stick.
There are very few consequences for law firms that operate in this manner. If a complaint is truly frivolous, the plaintiff’s lawyer can be sanctioned by the court, amongst other things. However, “frivolous” is a very difficult legal standard to meet, even if the plaintiff’s case is weak.
Now imagine, for example, how a person who believes they suffered a minor, medical injury might process this story. Their logic could run something like this: “If a multinational company such as Kraft Heinz Co. is forced to payout $5 million for miscalculating the time it takes to make instant mac and cheese, then I am certainly well within my rights to sue my physician. Even though I like my doctor, and I’m not sure whether or not they made a mistake during my procedure, he or she has insurance, so nobody really gets hurt if I sue.”
Even if this precise reasoning does not occur in the mind of a potential litigant, the mac and cheese story — and others like it — can influence our societal attitude. It adds gasoline to the contentious flames we see burning all around us every day: on personal injury billboards, on television commercials, and on public transportation advertisements.
I’m not hopeful that the American attitude toward litigiousness will change anytime soon. In the meantime, perhaps all we can do is point out that even if a complaint may possess enough legal merit to be heard in a court of law, bringing it forward may have a detrimental, cumulative effect on the culture in which we live.
With that being said, I think it’s time for me to prepare myself a piping hot bowl of mac and cheese, which always seems to brighten up my dour outlook.
“I’ve been dealing with problems with my health for a long time, and it’s been really difficult for me to face these challenges and to talk about everything that I’ve been going through,” said Dion. “It hurts me to tell you that I won’t be ready to restart my tour in Europe in February.”
“Recently, I’ve been diagnosed with a very rare neurological condition called stiff-person syndrome, which affects something like one in a million people,” she continued. “While we’re still learning about this rare condition, we now know that this is what has been causing all of the spasms that I’ve been having.”
“Unfortunately, these spasms affect every aspect of my daily life, sometimes causing difficulties when I walk and not allowing me to use my vocal cords to sing the way I’m used to,” Dion added. “I’m working hard with my sports medicine therapist every day to build back my strength and my ability to perform again. But I have to admit, it’s been a struggle.”
What Is Stiff-Person Syndrome?
According to the National Institute of Neurological Disorders and Strokeopens in a new tab or window, “stiff-person syndrome (SPS) is a rare, progressive neurological disorder. Symptoms may include stiff muscles in the trunk, arms, and legs; and greater sensitivity to noise, touch, and emotional distress, which can set off muscle spasms.”
It was first described in 1956opens in a new tab or window by Frederick Moersch, MD, and Henry Woltman, MD, based on a case series of 14 patients with progressive fluctuating tightness of the spinal, abdominal, and thigh muscles.
SPS affects one to two people per millionopens in a new tab or window. It is two to three times more common in women than men and typically occurs between the ages of 20 and 50 years old. Because of its rarity, it is not often recognized by medical providers. It can take, on average, 5 to 7 years to diagnose.
SPS is often misdiagnosed as Parkinson’s disease, multiple sclerosis, fibromyalgia, psychosomatic illness, or anxiety and phobia.
SPS is considered an autoimmune disease associated with high titers of autoantibodies to a variety of components of inhibitory synapses. The autoantibodies cause impaired function due to low levels of gamma-aminobutyric acid on pre- or post-synaptic neuronal junctions. This leads to hyperexcitability of the motor cortex and impairment of muscle relaxation.
Symptoms
Symptoms are dependent on the type of SPS, of which there are several forms.
Classic SPS
Classic SPSopens in a new tab or window is the most common form, occurring in 70% to 80% of patients. Symptoms include muscle rigidity, stiffness, and spasms in muscles of the trunk, especially the back, and limbs. Muscle spasms vary in intensity and duration and typically become worse over time (months to years).
Patients may complain of difficulty bending or turning and may describe their walking as like a “tin-man.” Stiffness and rigidity may eventually lead to chronic orthopedic problems such as lumbar lordosis, joint deformities, and abnormal posturing. Gait is often affected and can result in multiple falls.
Painful muscle spasms and exaggerated startle responses are also prominent symptoms and may be precipitated or exacerbated by unexpected tactile, visual, or acoustic stimuli, as well as strong emotions. The frequency and duration of muscle spasms can vary widely, and in some cases can last for hours (“status spasticus”).
Involvement of the distal extremities and face are later developments. In rare cases, the respiratory muscles may be involved.
Psychological comorbidities are not uncommon and include depression, task-specific phobias, fear of open spaces, and anticipatory anxiety.
Partial (or Focal) SPS Variants
SPS can present with isolated limb involvement, mostly in one leg. Muscle stiffness, spasm, and jerking may be present. Walking becomes increasingly difficult. Abnormal posturing may resemble dystonia. Later, truncal muscles may become involved. Stiff trunk syndrome involves spasms in the axial musculature only, sparing the extremities.
Progressive Encephalomyelitis with Rigidity and Myoclonus (PERM)
This is a more severe form of SPS and is usually associated with rapid deterioration. The brain and spinal cord are also involved. This form of SPS may include jerky muscle contractions (myoclonus), abnormal eye and eyelid movements, seizures, cognitive and behavioral changes, and difficulty swallowing, along with problems regulating blood pressure, heart rate, and body temperature.
Paraneoplastic Stiff-Person Syndrome
This is a very rare disorder in which the autoimmune antibodies are associated with tumors that may or may not be cancerous. The most common tumors associated with this form of SPS include those of the thymus, colon, lung, breast, and ovary.
Diagnosis
The diagnosis of SPS depends on multiple factors including history, physical examination, bloodwork, and other possible tests.
One particularly useful test looks for antibodies to glutamic acid decarboxylase (GAD), of which approximately 80% of people with SPS have, although their absence does not rule SPS out. Extremely high levels of GAD antibodies (>10,000 IU/mL) support a diagnosis of SPS.
Although nerve conduction studies in SPS are usually normal, needle electromyography shows continuous involuntary motor activity, even at rest. This continuous motor activity, as well as co-activation of agonist-antagonist muscles, are key diagnostic features, especially when seen in trunk muscles.
Treatment
There is currently no curative treatment for SPS. Treatment instead focuses on relief of symptoms with the use of muscle relaxants, anti-seizure medications, physical therapy, myofascial release, massage therapy, acupuncture, acupressure, yoga, meditation, and aqua therapy.
As anxiety and depression often accompany SPS, mental health treatment is also important for these patients, including cognitive behavioral therapy and selective serotonin reuptake inhibitors. Serotonin and norepinephrine reuptake inhibitors should be avoided as they can exacerbate symptoms.
Immunotherapy in SPS
Immunotherapy can be used to reduce or remove autoantibodies. First-line immunotherapies include intravenous immunoglobulins, subcutaneous immunoglobulin typically delivered with a pump system, and intravenous methylprednisolone. Second-line immunotherapies target B or T cells and include rituximab (Rituxan), cyclophosphamide, mycophenolate mofetil (Cellcept), and azathioprine (Imuran).
Described in a paper in Science Advances, these nanoparticles can fight harmful molecules, called reactive oxygen species (ROS), that can worsen IBD in excessive amounts. They are made from poly(propylene sulfide) – a polymer that can neutralize ROS – and hyaluronic acid, a compatible compound commonly used in medicine.
The nanoparticles – the researchers call them “backpacks” – can be attached to probiotics, which deliver them to the gut.
“Due to the colonizing property of probiotics in colon tissues, the nanoparticles could be delivered to colon tissues by probiotics and released slowly,” says study author Quanyin Hu, PhD, a biomedical engineer and assistant professor at the University of Wisconsin-Madison School of Pharmacy.
This helps give the nanoparticles time to bring the ROS level back down to normal. But that’s only part of the IBD treatment the researchers envision.
Signs Your IBD Is Getting Worse
With mild IBD, most people feel better with medication, but there are severe cases and symptoms to look out for.
The technology builds on a previous development from Hu and his team – a protective probiotic shell coating. The coating, which is about 330 nanometers thick, helps probiotics survive long enough to establish and multiply in the gut.
“The harsh environment of gastric acid and bile salt would kill most probiotics,” Hu says. “Moreover, antibiotics usually used in inflammatory bowel disease treatment also harm probiotic growth.”
Early results are promising, he says. Mice with IBD that received the full treatment – combining the ROS-targeting nanoparticles with the coated probiotics – had fewer IBD symptoms, like less weight loss and colon shortening, than those treated with the encapsulated probiotics alone.
By attacking the disease on multiple fronts – reducing the ROS and improving the balance of gut microbiota – a healthy gut environment could be restored, Hu says. In other words: “[It] might be possible to finally cure inflammatory bowel disease.”
Nanotechnology offers all kinds of unique advantages over traditional IBD treatments, he says. Nanoparticles can be designed to target specific tissues, like colon tissues. And compared to small molecules, they can circulate throughout the body longer, so they have more time to build up and do their job.
The next steps will be to test the treatment in large animals and “to develop a stable formulation that can be stored for a long time and produced in a scalable and economical manner,” Hu says.
Current IBD treatments “can only relieve symptoms,” not cure the disease, he says.
“This study is our first try to fundamentally treat inflammatory bowel disease by recovering a healthy microenvironment in the intestines, and our preliminary data demonstrated that this strategy is delivering promises to pave a new treatment strategy for IBD,” Hu says.
Most people with diabetes can enjoy some alcohol. Rules are the same as for everyone else: one drink per day for women; two for men. But you need to know how alcohol affects your blood sugar. A sugary drink might spike your blood sugar. But if you drink on an empty stomach or take certain meds, your levels could swing too low.
Beer
2/9
A 12-ounce beer has about 15 grams of carbohydrates, compared to 3 to 6 grams in light beer. Also, “light” and “low carb” are pretty much the same thing — and also your best bet. Be careful with craft beers. Most have twice the alcohol and calories as regular beer.
Wine
3/9
Some research says wine (red or white) may help your body use insulin better and may even make you less likely to get type 2 diabetes in the first place. It may also have heart benefits, to boot! Moderation is the key as too much alcohol can cause hypoglycemia. A standard 5-ounce serving has about 120 calories, nearly all of which come from alcohol, not carbs.
Sangria
4/9
Recipes vary, but depending on the fruit and juices involved, this drink may have as much sugar as a regular soda. Instead of sangria, go with one glass of dry red or white wine. Those only have about 4 grams of carbs. Avoid sweeter varieties, like flavored wines and dessert wines.
Liquor
5/9
One ounce of liquor, depending on the proof, has about the same amount of alcohol as 5 ounces of wine. While liquor is often carb-free, mixers like soda and juice can send blood sugar levels through the roof. To prevent a spike, mix your liquor with a calorie-free drink like water or seltzer.
Cupcake Cocktails
6/9
Sweet drinks like margaritas and mojitos don’t have to be off-limits. Use sugar-free mixers for margaritas and fresh fruit for daiquiris. And instead of pouring simple syrup into mojitos and martinis, try a natural sweetener like stevia or a sugar substitute.
Bloody Mary
7/9
This brunch classic can be a diabetes diet disaster. Take out the alcohol to make it “virgin.” Add a celery spear, and use low-sodium tomato juice. A virgin bloody Mary contains about one serving of carbohydrates (around 15 g).
Drinking Dos
8/9
Stay hydrated — it helps keep you sober.
Wear ID that says you have diabetes — a buzz and low blood sugar can look the same.
Be careful if you take insulin or another diabetes medication — alcohol can make your blood sugar drop.
Drinking Don’ts
9/9
Don’t drink on an empty stomach. Food helps you process alcohol.
Don’t drink your meals. Booze lowers blood sugar.
Don’t forget to test. Alcohol can affect your blood sugar for up to 24 hours. Especially test blood sugar before bed to see if it’s under 100. If it is, have a small snack.
It’s a type of depression that returns at the same time every year, usually in late fall or early winter, when there is less sunlight as the days get shorter. Some people get it in spring or early summer, but that’s not as common.
What Are the Symptoms?
2/12
You could feel tired, sluggish, and in low spirits for much of the day. It can sometimes last for weeks at a time. You might find it hard to sleep, concentrate, or enjoy your favorite activities. It’s possible you’ll overeat and gain weight as well.
What Causes SAD?
3/12
Doctors think less sunlight at certain times of year can trigger your body to change the way it makes and uses certain key brain chemicals. It may be that fewer daylight hours raises levels of melatonin and lowers levels of serotonin, two substances that help keep your sleep regular and your mood even.
Who Gets SAD?
4/12
The farther you are from the equator, the more likely you are to have SAD. For example, you’re about seven times more likely to get it if you live in New Hampshire than in Florida. Anyone can have the condition, but people with a family or personal history of depression get it more and their symptoms are often worse. And women get it four times more than men.
How Do You Know if You Have It?
5/12
Tell your doctor about your symptoms. They’ll ask about your family history and check to see if you have other conditions that could cause similar problems. For example, low energy could be a sign of a virus, thyroid problems, or low blood sugar. Lack of sleep, weight gain, and feeling moody might be symptoms of hormone issues and other things not related to seasonal changes.
Treatment: Medication
6/12
Your doctor might suggest an antidepressant drug called a selective serotonin reuptake inhibitor (SSRI.) These pills help keep more serotonin in your brain, which can help mood and sleep. Ask about the risks and side effects, which might include dry mouth, nausea, sleep problems, dizziness, headache, and sexual problems. You may need to try different SSRIs or other antidepressants to find one that works best for you.
Treatment: Light Therapy
7/12
You can use special lamps to help replace the sun that you miss during the winter months. These light boxes provide about 20 times more light than regular indoor lighting and screen out the UV rays that can damage your skin. Just 20 to 60 minutes each morning in front of one of these lamps during the winter could help ease your symptoms.
Treatment: Talk Therapy
8/12
A therapist can help you identify patterns of negative thinking that make you feel down. One approach, cognitive behavioral therapy, tries to replace those thoughts with happier ones as well as with activities that engage you and give you pleasure. This might help distract you from the gloom of the winter months.
Treatment: Vitamin D
9/12
Research shows mixed results on whether taking this vitamin can help with SAD. People typically have less vitamin D in their blood in the winter, but doctors don’t yet know if that’s a cause of SAD. There have been some studies that show vitamin D supplements help people feel better, but others seem to show there is no effect at all.
Keep SAD Blues at Bay
10/12
There are things you can do on your own to manage your symptoms. Connect and spend time with loved ones who understand your condition. Exercise! It can really lift your mood. Do it outside in the sunshine for even more benefit. Eat a balanced diet of veggies, whole grains, and fruits, and avoid sugar and “simple carbs” like white bread. Keep your sleep on a regular schedule to keep your mood even and to maximize your time in daylight.
SAD in the Spring or Summer
11/12
If you get seasonal affective disorder in the sunnier seasons, the symptoms are different from the winter version. You may get agitated and anxious as well as depressed. Instead of craving certain foods, you may lose your appetite. This could lead to weight loss, rather than adding a few pounds like you sometimes do with winter SAD.
When to See a Doctor
12/12
Most people feel down once in a while. But if you get the blues for days or weeks, for no clear reason, it may be time for an appointment. Your doctor can help you and your loved ones understand your condition so that you can start to treat and manage it. Be sure to tell your doctor right away if your depression leads you to thoughts of self-harm.
It’s a clump of cells and protein in your blood. A clot helps slow bleeding when you’re injured. It usually dissolves as you heal. But if it doesn’t, or if it forms when it’s not needed, it can clog up or completely block a blood vessel.
What Problems Can It Cause?
2/14
An unexpected clot can lead to serious problems and even death. In an artery, it can give you a heart attack or a stroke. If it happens in a vein, you can feel pain and swelling. A clot deep inside your body is called a deep vein thrombosis (DVT). One in your lungs is a pulmonary embolism (PE). They’re both medical emergencies.
Know Your Chances
3/14
You can get a blood clot if you break a bone or pull a muscle badly. But sometimes you may not know why it happened or even realize you have one. There are clues though. Your odds of a clot are higher if you:
Are recovering from surgery or had to sit for many hours on a flight or in a wheelchair
Are overweight or obese
Have diabetes or high cholesterol
Are over 60
Clue: Swelling
4/14
When a clot slows or stops the flow of blood, it can build up in the vessel and make it swell. If it happens in your lower leg or calf, it’s often a sign of DVT. But you also can have a clot in your arms or belly. Even after it goes away, one in three people still have swelling and sometimes pain and sores from damage to the blood vessel.
Clue: Skin Color
5/14
If a clot plugs up veins in your arms or legs, they may look bluish or reddish. Your skin also might stay discolored from the damage to blood vessels afterward. A PE in your lung could make your skin pale, bluish, and clammy.
Clue: Pain
6/14
Sudden, intense chest pain could mean the clot has broken off and caused a PE. Or it could be a sign that a clot in your artery gave you a heart attack. If so, you also might feel pain in your arm, especially on the left. A clot often hurts where it’s located, like in your lower leg, stomach, or under your throat.
Clue: Trouble Breathing
7/14
This is a serious symptom. It could be a sign that you have a clot in your lung or your heart. Your heart might also race, or you may feel sweaty or faint.
Location: Lung
8/14
A clot can give you different symptoms based on where it is. A PE can give you a fast pulse, chest pain, bloody cough, and shortness of breath. Get to the hospital right away. You also might have no signs.
Location: Heart
9/14
This can feel similar to a clot in the lung. But if it’s a heart attack, you also might feel nausea and lightheadedness along with the chest pain. Either way, call 911 or get to a hospital right away.
Location: Brain
10/14
Pressure builds when blood can’t flow normally. A severe blockage sometimes can lead to a stroke. Without oxygen from the blood, your brain cells start to die in minutes. A clot in your brain can cause headaches, confusion, seizures, speech problems, and weakness, sometimes on just one side of the body.
Location: Belly
11/14
Often, you have no symptoms at all. Blocked veins in the stomach or esophagus, a tube that connects it to your throat, can rip and leak blood. That can hurt a lot. You may poop or vomit blood, and your stool might look black and smell unusually bad.
Location: Kidneys
12/14
Also called renal vein thrombosis, these clots usually grow slowly and mostly in adults. You probably won’t have symptoms unless a piece breaks off and lodges in your lung. Rarely, especially in children, it can happen fast and cause nausea, fever, and vomiting. You also might have blood in your pee and go less often.
If You Suspect a Blood Clot
13/14
See your doctor or go to the emergency room right away. A clot can be deadly, and you won’t know for sure you have it until you get checked. Your doctor may give you a clot-busting drug or surgically thread a thin tube to the site of the clot to dissolve it.
Prevention Tips
14/14
You can act to lower your odds of a clot. First, keep a healthy weight, eat right, and exercise. Also:
Don’t sit or stay still for long, especially after a long trip or surgery.
If you’re a desk jockey, get up and move at least every couple of hours. Flex your legs, feet, and toes in your chair.
Check if tight-fitting compression socks or garments can help your blood flow.
Ask your doctor if you might need to take clot-fighting drugs called anticoagulants.
Every puff of tobacco is packed with 250 harmful chemicals. Nearly 70 of them cause cancer. And it’s more than just lung cancer. Cigarettes are linked to 12 other kinds, including stomach, bladder, kidney, mouth, and throat. The sooner you stop, the better. Ask your doctor for advice on quit-smoking methods.
Eat More Broccoli
2/14
Fruits and veggies pack an anti-cancer punch because they’re high in nutrients and fiber, and low in fat. Try broccoli, Brussels sprouts, cabbage, kale, watercress, or other cruciferous vegetables. They protect against DNA damage that can turn cells cancerous. Or eat colorful berries. Studies show they have cancer-fighting chemicals that ward off damage to cells.
Trim a Few Pounds
3/14
Extra weight around your middle could add up to a greater chance of having cancer, especially of the breast, colon, uterus, pancreas, esophagus, and gallbladder. Researchers say one reason may be that fat cells release substances that encourage cancer cells to grow.
Go Easy on Alcohol
4/14
Tip back too many martinis each day, and your odds of cancer go up. Alcohol is linked to cancers of the mouth, breast, liver, esophagus, and others. The more you drink, the higher your risk. If you drink, do it in moderation. Women should stick to one drink a day, men up to two.
Cut Back on Hot Dogs
5/14
Think twice before you throw some on the grill. Studies show that processed meats, like hot dogs, bacon, and sausage, have chemicals called nitrites and nitrates that may be linked to cancer. And research suggests too much red meat like steak and burgers could be a long-term risk for colorectal cancer. Choose safer alternatives for your backyard cookout, like chicken breast or fish.
Get Off the Couch
6/14
Do you spend too much time lounging around? Cancer prevention is one more reason to get moving. Exercise fights obesity and lowers levels of hormones like estrogen and insulin, which have been linked to cancer. Aim for 30 minutes of aerobic exercise — the kind that gets your heart pumping — on most days of the week.
Put on Sunscreen
7/14
Baking in the sun might give you a healthy-looking glow, but under the surface, UV rays cause skin damage that could lead to cancer. Because you can burn in just 15 minutes, rub on sunscreen before you go outside. Pick a broad-spectrum product with an SPF of 30 or higher. Reapply whenever you sweat or swim. And when you’re out in the sun, wear a wide-brimmed hat and wraparound sunglasses.
Practice Safer Sex
8/14
Sexually transmitted diseases (STDs) aren’t your only worry during unprotected sex. Some of these infections also increase your odds of having cancer. About 70% of cervical cancers start with human papillomavirus (HPV) types 16 and 18. Some types of hepatitis can cause liver cancer. To stay safe, use a latex condom every time you have sex.
Get Vaccinated
9/14
When it comes to vaccines, think beyond your annual flu shot. Some can protect against cancer, too. Certain HPV vaccines prevent cancers of the cervix, vulva, vagina, and anus. The time to get vaccinated is between ages 9 and 26. The hepatitis B vaccine wards off the virus that causes liver cancer. It’s part of the childhood vaccination schedule.
Avoid Toxic Chemicals
10/14
Chemicals called carcinogens damage DNA in your cells and raise your chance of having cancer if you touch, eat, or breathe them in. Asbestos, radon, and benzene are a few that some people come into contact with at work or home. Chemicals in weedkillers, plastics, and some home products may also be risky. You can’t avoid every chemical, but know which ones are in products you use and switch to safer options if you can.
Know Your Family History
11/14
You inherited more than your mother’s eyes or your father’s grin. They may also have shared their chances for having diseases like cancer. Some genes that parents pass down to their kids have flaws. They don’t repair damaged DNA the way they should, which lets cells turn into cancer. Learn about your family’s medical history and ask your doctor if a genetic test is a good idea for you.
Stay Up to Date With Screenings
12/14
Screening tests catch cancer early — sometimes even before it starts. A colonoscopy often finds polyps in the colon and rectum before they turn into cancer. The Pap test locates pre–cancerous and cancerous cells in a woman’s cervix. Mammograms and low-dose computed tomography (LDCT) look for early breast and lung cancers. Ask your doctor when to start getting these tests, and how often you need them.
Take Meds if You Need Them
13/14
Some drugs lower your odds of getting certain cancers. Tamoxifen (Nolvadex, Soltamox) and raloxifene (Evista) can reduce breast cancer risk but may have serious side effects. Aspirin may protect against colorectal and prostate cancers. Be wary, though, of supplements that promise to keep you cancer-free. Many haven’t been proven, and some have side effects.
Be Cautious About Hormone Therapy
14/14
It can ease menopause symptoms like hot flashes and fatigue, and protect your bones. But hormone therapy may raise your chances of breast cancer and make cancer harder to detect. Ask your doctor about your risks before you try this treatment.
ARYAN'S BLOG 