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YOGA VS PILATES. WHICH PRACTICE IS RIGHT FOR YOU?

Eating And Lifestyle For Better Hormone Health In Peri-Menopause

While women’s hormone health is always foundational to overall wellness, a time called perimenopause—the years before menopause, when the ovaries begin to make less oestrogen—is characterized by significant hormonal shifts, in addition to negative symptoms including anxiety, depression, night sweats, and more. .By consuming larger amounts of cruciferous vegetables, which “promote estrogen metabolism and detoxification in the liver,” the article mentions incorporating flaxseed into routines, focusing on foods that support bone health, eating plenty of omega-3-rich foods, and replacing simple & processed sugars with more high-fiber complex carbohydrates. Overall, the research supports a strong focus on foods that “decrease inflammation, support a healthy mood, and balance hormones and insulin levels.”

Here at Compounding Lab , we’re all about women’s hormone health. We strongly believe that our hormones benefit from a healthy lifestyle and that every green smoothie, yoga , pilates class, and minute of meditation matters. But there’s a time in every woman’s hormonal life—called perimenopause—that’s long been overlooked. This era is marked by big hormonal shifts that can greatly affect quality of life, causing a lot of anxiety and discomfort. So this week, lets get down and dirty and uncover our hormones so that we’re all more informed and empowered.

So perimenopause refers to the years that precede menopause, when women can experience unwelcome symptoms of hormones changing like night sweats, mood swings, irritability, depression, missed or heavy periods, and vaginal dryness. These symptoms are no walk in the park! Most women start experiencing perimenopause n their mid-40s, but for some women it will begin as early as their 30s.

So what’s happening to your hormones during this time? During perimenopause, oestrogen and progesterone hormones start to decrease. Progesterone tends to drop first, and oestrogen can fluctuate up and down until it settles. You can’t avoid these hormonal changes altogether, but you can do a lot to empower yourself with specific dietary and lifestyle choices that help you feel more like yourself. Here are some important foods I tell women to focus on during this time in your life:

1. Load Up On Cuciferous Vegetables.

In the early stages of perimenopause, progesterone drops faster than oestrogen. This can lead to oestrogen dominance, or a higher oestrogen level compared to progesterone. During this phase, it’s important to support the body’s ability to metabolize oestrogen properly, and vegetables from the cruciferous family are best at that. “Rich in indole 3-carbinol and chlorophyll, these veggies promote oestrogen metabolism and detoxification in the liver, shifting ‘dirty’ oestrogens to ‘clean’ oestrogens,” I recommend eating cruciferous vegetables on a daily basis during perimenopause. If you’re not used to consuming this type of vegetable and need some inspiration, try sautéing and incorporating broccoli, Brussels sprouts, and bok choy into omelets and stir-fries. You can also mix raw shredded broccoli, cabbage, or Brussels sprouts into your salads. One of my favorite substitutes is to make cauliflower rice instead of mashed potatoes or white rice for more fiber and fewer carbs. Or, simply snack on cruciferous veggies alone or dipped in guacamole or hummus. If they cause gas or bloating, start slowly and stick with cooked forms, as cooking these cruciferous veggies makes them easier for your digestive system to tolerate. If you can’t tolerate them FIX your GUT girls.

2. Eat Protein-Rich Foods At Every Single Meal , Especially Breakfast At Around 10am

Blood sugar issues during perimenopause will worsen your mood swings, increase irritability, and stress your adrenals. Eating protein at every meal will stabilize blood sugar and reduce the spikes and crashes, which will also help you lose weight, prevent weight gain, and reduce your risk for insulin resistance, diabetes, and metabolic syndrome. Protein also helps you stay full and burn more calories without feeling deprived or constantly hungry. Your muscle mass and bone density take a hit as you enter menopause, and getting enough protein in your day, along with resistance training or weights will preserve them and reduce their decline. The best high-protein foods to incorporate into your diet are pastured eggs, wild-caught fish, lean poultry, grass-fed meats, and legumes (if you can tolerate them). Aim for 21 to 28 grams of protein at each meal, including breakfast. Skip the morning pastry and have a savory breakfast like a vegetable omelet or organic, preservative-free turkey or chicken sausage with some broccoli or cauliflower. If you like oatmeal, add high-protein nuts and seeds like almond butter, hemp, or pumpkin seeds for a delicious and high-protein treat.

3. Incorporate Flaxseed Into Your Routine.

Flaxseed can be one of the most supportive superfoods throughout perimenopause. Carper frequently recommends it in the later perimenopause stages as it contains lignans, which are phytoestrogens, weaker plant-based oestrogens that provide gentle oestrogen support when estrogen is waning. Conversely, she adds, “it can act adaptively and block oestrogen when oestrogen dominance is present in the earlier stages.” That said, if adding flaxseed worsens your periods, mood swings, breast tenderness, or other symptoms you’re experiencing, it may be amplifying your oestrogen dominance, and you should discontinue use. Expert tip: Always grind flaxseeds to reap the benefits, as we don’t have the digestive enzymes needed to break down the outer shell. If possible, buy them whole, grind them in small batches every few days, and store in the fridge to maximize freshness. Flaxseeds can be enjoyed in smoothies, as an egg replacement in vegan or egg-free recipes, or simply added to casseroles or Greek yogurt. If you’re into healthy baked goods, you can also use ground flaxseed to replace white or processed flours in muffins and other baked goods to increase fiber and protein.

4. Focus On Foods That Support Bone Health.

OEstrogen protects against bone loss, so when it starts to drop, women are at an increased risk for osteoporosis. This means that perimenopause is a very important time to support your bone health to prevent osteoporosis and its complications. You can do this in a few ways, but this first is by eating calcium-rich foods. If you choose and tolerate dairy, eat two servings per day and choose organic or grass-fed varieties. Plain or Greek yogurt are great options as they also contain live bacteria that support the gut. Skip sweetened and fruit-flavored yogurts and mix in chopped cucumber and fresh herbs instead of fruit as a savory snack. Plain cottage cheese and aged cheeses without additives or colorings are good sources of calcium and protein as well. If you don’t tolerate dairy, there are many nondairy calcium-rich foods to choose from. Try broccoli, bok choy, collard greens, kale, almonds, and canned salmon and sardines with bones. Many of these foods contain vitamin D, which helps your body absorb the calcium, but I find that most of my patients are who are defiecnet in Vit D need to supplement for optimal bone health—especially during perimenopause. To continue to support your bone health during perimenopause, ask your doctor to test your vitamin D levels and take a dose that’s right for you. Aim for 120 level. Two other often overlooked nutrients critical for bone health are magnesium and vitamin K2. Magnesium, found in nuts, legumes, leafy greens, and dark chocolate, is another mineral that makes up your bones. Vitamin K2, found in natto (fermented soy), egg yolks, cheese, and butter, tells your body to deposit the calcium in your bones, not your arteries or other organs. Just like vitamin D, food doesn’t typically provide an adequate amount of vitamin K2. Because of the emerging research on its role in bone health—as well as heart disease and diabetes—I recommend that women during and after perimenopause add a high-quality vitamin K2 supplement to their daily routine.

5. Don’t Forget Omega-3-Rich Foods.

During the transition to menopause, try to eat 4 ounces of omega-3-rich fish like salmon, sardines, tuna, mackerel, cod, and trout twice a week. Research shows that EPA and DHA, the two omega-3 fatty acids found in fish, reduce inflammation, improve mood, and reduce depression. They also reduce the risk for heart disease, another condition that women become at higher risk for after perimenopause. But what about plant-based omega-3s like walnuts and flaxseed? These foods contain the plant-based omega-3 ALA, which needs to be converted to EPA and DHA in order for you to receive the benefits. This means that nut-based omega-3s don’t replace fish-based ones, but they are still a great source of healthy fats and fiber. If you’re at an increased risk of heart disease or don’t like eating fish, ask your doctor about starting a high-quality fish oil supplement.

6. Eat More High-Fiber Complex Carbohydrates (Because Not All Carbs Are Bad).

Cutting out simple and processed sugars and replacing them with high-fiber complex carbohydrates will help balance your blood sugar during perimenopause. Healthy carbohydrates can also reduce mood swings, irritability, and depression and HOT Flushes. They increase the production of serotonin, one of the happy, feed-good hormones. I find that the best types and amounts of carbohydrates will vary from one person to another, as several things must be factored in like your medical history, activity level, and digestive health. If tolerated, beans, lentils, oats, quinoa, buckwheat, and other whole grains a few times a week are good options. Starchy vegetables like sweet potatoes, pumpkin , carrots, beets, winter squashes, and other root vegetables are great choices because they are rich in nutrients and fiber. By focusing on these foods—which can help decrease inflammation, support a healthy mood, and balance hormones and insulin levels—perimenopause doesn’t have to be something we dread. In fact, entering perimenopause is a great excuse to prioritize cooking at home, learning to love healthy foods and exercise, and generally taking a little extra care of yourself. That doesn’t sound like anything we should be afraid of!

cleannutritionals.com.au

Age-Related Cognitive Decline

Lets talk about an issue that all of us have to face after a certain point in our lives: COGNITIVE DECLINE.

 As we grow and develop from children to young adults, there is a palpable upward trend in our mental development and ability, and there is a sense that we are always growing to some greater height. Unfortunately, this trend can’t go on forever, and it is all too clear as the decades progress, that our minds are never going to be quite what they were. 

SOME OF THE QUESTIONS WE FACE:

  • What is the process behind this gradual cognitive decline? 
  • What are the factors involved? Are there any in our control? 
  • Can we slow or stop this process in order to preserve our quality of life? 

Let’s break it down.

WHAT IS COGNITIVE DECLINE?

Cognitive decline is something that is generally known to happen as people age, but there are degrees of decline that can be considered excessive and unhealthy. 
There is no universally accepted definition of successful cognitive health in elderly individuals, but cognitive health is generally defined as “the development and preservation of the multidimensional cognitive structure that enables ongoing social connectedness, sense of purpose, and the ability to function independently” (1). That, broadly speaking, is the definition of the standard of cognitive ability that we all should be able to enjoy for our entire lives. 
Cognition encompasses a broad range of mental processes, which are often taken for granted until they are lost. There are two essential forms of cognition: 

  1. There is “fluid” cognition, which relies on short-term memory to process information when solving new problems, using spatial reasoning and when identifying patterns.
  2. There is also “crystallized” cognition, where knowledge and life experience accumulate, and this relies more on long-term memory (2)

Fluid cognitive abilities are thought to peak in the mid-twenties, and then very gradually decline over a period of years until about age 60, when the decline tends to become more rapid. But this is only for fluid cognition, while crystallized cognition continues to increase over the life span through education and life experiences.

Pathological cognitive decline is something that tends to be seen earlier than expected, or it hits the individual harder than expected, resulting in disruption of social connectedness, and individual autonomy. 

Mild Cognitive Impairment (MCI) is a condition presenting with memory deficits that are below what is considered normal. This condition can often foreshadow the onset of frank dementia, and early detection is very important, so that preventative measures may be taken to stem the progression of the condition.

Signs & Symptoms of MCI (Mild Cognitive Impairment)

Symptoms are often vague and can include the following:

  • Memory loss
  • Language disturbance (eg, difficulty in finding words)
  • Attention deficit (eg, difficulty in following or focusing on conversations)
  • Deterioration in visual-spatial skills (eg, disorientation in familiar surroundings in the absence of motor and sensory conditions that would account for the complaint) 

Cerebrovascular Conditions
Cerebrovascular disease (CVD) is defined as brain lesions caused by vascular disorders. This can be something as dramatic and severe as a stroke, where there is cessation of blood flow to a particular part of the brain, usually caused by a blood clot. But then there is also vascular dementia. 
Vascular dementia is a chronic progressive loss of cognitive function, due to multiple small infarcts (4). These can be thought of as very small mini-strokes that only affect minor sections of brain tissue at a time. By themselves, each one of these little infarcts doesn’t have a huge impact on cognitive function, as the brain is able to re-route to other neural pathways that bypass the section affected by the mini-stroke. 
However, over a period of years, as these mini-strokes accumulate, the available pathways the brain is left with become ever more restrictive, and so because of this you see a progressive decline in cognitive function.  

Prevalence of Dementia
In 2005, the global population suffering dementia was estimated to be 24.3 million people, and there are around 4.6 million new cases diagnosed every year (3). It is expected that this population will double every 20 years, with an alarming 81.1 million dementia patients in 2040 (3). A major consequence of this is an increased burden on the healthcare system, with higher rates of hospitalizations, surgeries and visits to the doctor, leading to spiraling healthcare costs.

DEMENTIA and CHRONIC INFLAMMATION

Chronic systemic inflammation is the underlying culprit of many such chronic conditions, including heart disease, diabetes, cancer, and this very form of progressive damage to the brain. 

Increased chronic inflammation means greater chances of clotting factors activating, and causing the aforementioned “mini-strokes” that promote cognitive decline. Therefore, eating an anti-inflammatory Mediterranean type diet, avoiding simple sugar and carbs, avoiding fried foods and ensuring adequate intake of Omega 3 fatty acids, are some of the basic means of helping to preserve cognitive function as we mature.

In other words, less chronic inflammation, less clotting factors floating around in the system, less potential for oxidative damage, all equals less chance of a mini-clot causing these kinds of tiny infarcts in the brain.

There is a growing body of research demonstrating that adherence to a Mediterranean type diet significantly reduces risk of developing Mild Cognitive Decline, and risk of progression to Alzheimer’s Disease. (5)

MEDITERRANEAN DIET
In general, the Mediterranean diet, which is low calories and rich in fruits and vegetables, has the greatest benefit for reducing inflammation. Data show that high dietary fiber, which is typically a sign of a low glycemic load diet, was associated with lower levels of various inflammatory markers (6).
The dietary pattern most consistently associated with a reduction of CVD is predominantly plant-based, emphasizing fruits, vegetables, whole grains, nuts, fiber, and sources of Omega 3 fatty acids.

EXERCISE!

Cognitive Exercise
Another way to keep the brain functioning well, is just to make sure you are using it well. The brain tissue is very plastic, meaning that it always hast the ability to form new connections, and keep existing connections strong, as long as you challenge it with tasks to do. 
Evidence is not conclusive, but it is generally believed that exercising the brain by reading, doing crossword puzzles, and brain teasers can help to prevent, delay, or reduce cognitive decline. These should always be fun, stimulating activities that you enjoy doing, so that you will want to do them a lot.

Moderate Physical Exercise
Not only is moderate exercise a well established, and yet all too often overlooked, means of reducing chronic inflammation in the body (7), there is a growing body of evidence indicating that it can help prevent mild cognitive impairment as we age. 

SPECIFIC NUTRIENTS
Vitamin D
has been shown to be deficient or insufficient on pandemic levels, and lower levels are associated with several chronic diseases. It serves as a significant factor in a number of physiologic functions, specifically as a biological inhibitor of inflammatory hyperactivity (8, 9, 10). Vitamin D produces dose dependant reductions of several inflammatory markers, and supplemental benefit has been shown for osteoarthritis, multiple sclerosis, type 1 diabetes, Graves Disease, ankylosing spondylitis, SLE, and rheumatoid arthritis (8, 9, 10).
Data from the National Health and Nutrition Examination Survey (NHANES) from 2001-2004, involving more than 8000 human subjects, showed that those with vitamin D levels below 30 ng/ml were more likely to be at high risk of cardiovascular disease.

Fish Oil
A good quality fish oil supplement will be standardized to have large quantities of EPA and DHA, in a 3:1 or 3:2 ratio for adults. These omega 3 fatty acids promote the formation of anti-inflammatory eicosenoids that become incorporated into our cell membranes, helping them to remain fluid and pliable (11). This can help prevent heart disease and any associated cerebrovascular disease in the brain. 

Natural Antioxidants and Anti-inflammatories
Although a diet rich in fruits and vegetables is generally anti-inflammatory, some foods seem to exert some specific benefit along these lines. These include Blueberries (Vaccinium myrtillus), chocolate (dark), cranberries (Vaccinium macrocarpon), garlic (Alliu sativum), ginger (Zingiber officinalis), grape (Vitis vinifera), green tea (Camellia sinsensis), and turmeric (Curcuma longa).

Oxytocin Intranasal Treatment for socialization, obesity, pain, and substance abuse

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Oxytocin is a hormone secreted by the posterior lobe of the pituitary gland, a pea-sized structure at the base of the brain. Sometimes known as the “cuddle hormone” or the “love hormone,” oxytocin promotes feelings of devotion, trust, and bonding and is released through physical touches, such as hugs, and also linked to the intensity of orgasms during sexual activity.

2013 review noted all of oxytocin’s possible relationship-enhancing effects, which were said to include:

  • Fostering pro-relationship mindsets and behaviors
  • Enhancing the processing of bonding cues
  • Facilitating improved communication
  • Empathy
  • Trust
  • Fidelity

For females, it is the neuropeptide responsible for inducing labor contractions in pregnant women and also the “let down reflex,” which stimulates the production of milk during breastfeeding. Oxytocin is synthesized in the hypothalamus and stored in the posterior pituitary where it can be released when needed.

Chapter 16 Nutritional Aspects of Pregnancy and Breastfeeding Vicky Pehling

 Figure 1: Chapter 16- Nutritional Aspects of Pregnancy and Breastfeeding. Vicky Pehling

  1. suckling stimulates nerves in the nipple and areola that travel to the hypothalamus
  2. In response, the hypothalamus stimulates the posterior pituitary to release oxytocin and anterior pituitary to release prolactin
  3. Oxytocin stimulates lobules in the breast to let down (release) milk from storage. Prolactin stimulates additional milk production

Oxytocin Uses In Childbirth

In general, oxytocin should not be used to start labor unless there are specific medical reasons. However, the FDA approves the use of oxytocin for pregnant women who have complications of childbirth, such as:

  • Cardiovascular-Renal Disease
  • Eclampsia
  • Preeclampsia
  • Premature Rupture of Membranes (PROM)

It can also be used to reduce and control postpartum uterine bleeding with minimal side effects, namely nausea, vomiting, and headaches.  

Alternative Uses of Oxytocin

In recent years, it has been suggested that oxytocin may prove beneficial for a number of clinical conditions beyond those approved by the FDA.

Oxytocin uses studied outside of FDA indication include: 

Chronic / Acute Pain – Numerous randomized studies have shown promising results of oxytocin use for chronic and acute pain. In addition to activating its own receptors and decreasing pain signals, oxytocin binds to opioid receptors and stimulates endogenous opioid release in the brain. In addition to relieving pain, oxytocin lowers serum cortisol and can produce a calming effect and improve mood.(1)

Oxytocin can also modulate pain by counteracting with psychological features such as calming the emotion of pain or removing the cognitive attention to pain.

Autism Spectrum Disorder (ASD) – Oxytocin has been implicated in the regulation of repetitive and affiliative behaviors and stress reactivity. Therefore, it is expected to be a potential therapeutic resource for the social core symptoms of ASD, since this neuropeptide can modulate human social behavior and cognition. (2)

Hypoactive Sexual Desire Disorder (HSDD) – HSDD is attributed to an imbalance in central sexual excitatory (dopamine, norepinephrine, melanocortin, and oxytocin) and sexual inhibitory (serotonin, opioid, endocannabinoid, and prolactin) pathways. For some, treatment with oxytocin nasal spray has shown to improve the sexual quality of life significantly.

Post-Traumatic Stress Disorder (PTSD) – Research findings indicate that repeated intranasal oxytocin offers promising early preventive intervention for PTSD for individuals at increased risk for PTSD due to high acute symptom severity.(3)

Obesity / Weight Loss – Scientists suspect that one element of the obesity epidemic is that the brains of obese people respond differently to images of delicious, calorically dense foods. Studies have shown that oxytocin reduces activation in the hypothalamus, an area of the brain that controls hunger, and increases activation in areas of the brain associated with impulse control. Thus, some believe that the hormone creates less of a need to eat, reduces the compulsion to eat for fun, and improves impulse control when it comes to actually reaching for that second slice of cake.(4

Addiction & Withdrawal – Oxytocin has also been used as a potential mediator and regulator of drug addiction. Several studies have shown good outcomes in cocaine, opioid, and cannabis addiction. In a placebo-controlled trial the administration of oxytocin demonstrated efficacy in reducing withdrawal symptoms, anxiety and need for lorazepam in subjects with alcohol dependence undergoing detoxification.(5)

The ‘Cuddle Hormone’ Might Help America Take On the Obesity Epidemic

A man and a woman cuddle on a rock.

Scientists suspect that one element of the obesity epidemic is that the brains of obese people respond differently to images of delicious, calorically dense foods. Obese individuals’ brains seem to light up at the sight of donuts, pizza, and other calorie bombs, even when they’re no longer hungry.

Some studies have suggested that this heightened activity might predispose people to overeating. Today, nearly 40 percent of American adults are obese, and obesity is predicted to become the leading cause of cancer among Americans, replacing smoking, within five or 10 years. (It’s still not clear yet which comes first—the obesity or the overactive brain activity.) “Part of the reason for the obesity epidemic is that people eat when they’re not hungry,” says Elizabeth Lawson, an associate professor of medicine at Harvard Medical School and a neuroendocrinologist at Massachusetts General Hospital.

A remedy for this over-activation in the brain might come from an unexpected source: oxytocin, the brain chemical often associated with love and social relationships. Oxytocin is sometimes called the “cuddle hormone” because it’s released during sex, childbirth, and breastfeeding. People who are in the early stages of falling in love have higher levels of oxytocin than normal. The drug ecstasy also increases concentrations of the hormone in the blood.

Oxytocin has a variety of other surprising functions. A form of the chemical, Pitocin, induces labor, and another form might help treat stomach pain. Early studies have suggested that the hormone might boost social skills among kids with autism. Now Lawson and other researchers are investigating whether oxytocin might also prevent overeating.

Lawson and her colleagues recently showed images of high-calorie foods to 10 overweight and obese men. She found that the regions of the brain involved in eating for pleasure lit up when the men viewed the images. A dose of oxytocin, compared with a placebo, weakened the activity in those regions, and it also reduced the activity between them. Meanwhile, oxytocin didn’t have that effect when the men viewed images of low-calorie foods or household items. Lawson’s colleagues presented the research, which has not yet been published in a peer-reviewed journal, last month at Endo 2019, the Endocrine Society’s annual meeting.

“One of the key ways oxytocin works in limiting the amount of food that we eat is that it speeds up the satiety process, or reaching fullness,” says Pawel Olszewski, an associate professor of physiology at the University of Waikato, in New Zealand, who was not involved with Lawson’s study. “Then, oxytocin works through brain areas that are associated with the pleasure of eating, and it decreases our eating for pleasure.

That’s just one of the ways oxytocin shows potential as an obesity treatment. Previously, Lawson and her colleagues found that the hormone improves insulin sensitivity and encourages the body to use fat as fuel. Lawson’s other studies have shown that oxytocin reduces activation in the hypothalamus, an area of the brain that controls hunger, and increases activation in areas of the brain associated with impulse control. To Lawson, the results together suggest that the hormone creates less of a need to eat, reduces the compulsion to eat for fun, and improves impulse control when it comes to actually reaching for that second slice of cake. Oxytocin, in other words, appears to make food seem less rewarding.

Other researchers have found that oxytocin might weaken alcoholics’ dependence on alcohol, drawing parallels to the hormone’s effects on how some obese people’s brains perceive food. A study published in the journal PLOS this month showed that oxytocin cut the desire to drink among alcohol-dependent rats. It’s not clear what this anti-drinking element of oxytocin has to do with its love-hormone properties, if anything.

So why can’t we just pick up bottles of oxytocin at CVS? For one thing, most of these studies have been very small; 10 is a minuscule sample size. They’ve been largely conducted on men, so future research would need to be expanded to women. The mechanism behind oxytocin’s effects on eating behavior and metabolism needs to be clarified, and the safety of using the hormone long term needs to be established.

The way that Lawson’s and many other studies have been conducted is by putting oxytocin in a nasal spray and attempting to shoot it directly toward the brain. But it’s not clear how much of the drug the person is actually getting through this kind of application, and researchers are still working on making it more precise. To answer some of these questions, Lawson is currently conducting an NIH-funded randomized controlled trial that will administer oxytocin to obese men and women for eight weeks.

Finally, even if all these studies are successful, it’s important to remember that there are myriad reasons—social, economic, biological, cultural—that people become obese, addicted to food, or addicted to other substances. An oxytocin treatment might only work for some of them, and even if it did, not all obese people desire to lose weight. “Its effectiveness may depend on the reason for why the obese individual is obese,” Olszewski says.

Still, a drug that helped even a fraction of America’s 93 million obese people would be a major breakthrough. If all this research bears results, many years from now, there may be another reason to love the love hormone.

Oxytocin may treat abdominal pain

Australian researchers have found a key to treating chronic abdominal pain may lie in a hormone that induces labour and encourages social bonding.

The researchers, led by The University of Queensland’s Professor Paul Alewood from and the University of Adelaide’s Dr Stuart Brierley, have developed a version of the hormone oxytocin to treat chronic abdominal pain associated with conditions such as irritable bowel syndrome.

Oxytocin is known as ‘the love drug’ for its ability to enhance social interactions including maternal behaviour, partnership and bonding.

Professor Alewood, from UQ’s Institute for Molecular Bioscience, said the molecule they had developed – a version of oxytocin with improved stability – showed significant potential in alleviating abdominal pain.

“It can potentially survive in the digestive tract until it reaches the gut,” he said.

“This molecule acts on oxytocin nerve receptors in the bowel, which display increased sensitivity in conditions such as irritable bowel syndrome.”

Professor Alewood said it had no effect on healthy gut tissue, which was an important advantage in drug development where minimising side effects is crucial.

Chronic abdominal pain is a major health problem, with irritable bowel syndrome alone affecting around 11 per cent of the Western population.

Despite the high number of sufferers, there are currently no drugs that directly treat abdominal pain.

Oxytocin spray boosts social skills in children with autism

Treatment with the hormone oxytocin improves social skills in some children with autism, suggest results from a small clinical trial. The results appeared today in the Proceedings of the National Academy of Sciences1.

Oxytocin, dubbed the ‘love hormone,’ enhances social behavior in animals. This effect makes it attractive as a potential autism treatment. But studies in people have been inconsistent: Some small trials have shown that the hormone improves social skills in people with autism, and others have shown no benefit. This may be because only a subset of people with autism respond to the treatment.

In the new study, researchers tried to identify this subset. The same team showed in 2014 that children with relatively high blood levels of oxytocin have better social skills than do those with low levels2.

In their new work, the researchers examined whether oxytocin levels in children with autism alter the children’s response to treatment with the hormone. They found that low levels of the hormone prior to treatment are associated with the most improvement in social skills.

“We need to be thinking about a precision-medicine approach for autism,” says Karen Parker, associate professor of psychiatry at Stanford University in California, who co-led the study. “There’s been a reasonable number of failed [oxytocin] trials, and the question is: Could they have failed because all of the kids, by blind, dumb luck, had really high baseline oxytocin levels?”

The study marks the first successful attempt to find a biological marker that predicts response to the t

herapy.

“This study is suggestive of a hormonal-based biomarker for oxytocin treatment, which makes sense and is a promising step forward,” says Adam Guastella, professor of psychology at the Brain and Mind Centre at the University of Sydney in Australia, who was not involved in the study.

Hormone help:

The researchers enrolled 34 children with autism, aged 6 to 12 years. Parents gave their children a nasal spray twice a day for four weeks; 16 children got a spray containing oxytocin, and 18 got a spray with placebo. (Two of the children in the oxytocin group later dropped out of the study.)

The researchers measured oxytocin levels in the children’s blood at the start and end of the trial. They assessed the children’s social skills using a parent questionnaire called the Social Responsiveness Scale (SRS) and used other tests to assess the drug’s effects on repetitive behaviors and anxiety levels.

Based on SRS scores alone, oxytocin treatment did not lead to a statistically significant improvement in social skills. But when the researchers built a statistical model that accounted for the children’s oxytocin levels at the trial’s start, they found that the children who received oxytocin improved more on the SRS than did those on the placebo. The children with the lowest initial blood levels of oxytocin generally showed the most improvement.

Some children who received the placebo also showed an improvement in their social skills. These children also showed a rise in oxytocin levels over the course of the study. This indicates that simply participating in the study boosted their oxytocin levels, and may underlie their improvement, Parker says. Boosting oxytocin levels in other ways — say, through a behavioral intervention — could also be beneficial, she says.

The treated children showed no decrease in repetitive behaviors or anxiety, suggesting that the findings are specific to social skills. The therapy had no serious side effects.

Looking ahead:

Oxytocin levels vary naturally among people, and may even change throughout the day. The researchers tried to mitigate some of this variability by drawing each child’s blood at roughly the same time each day.

Still, the change in oxytocin levels in the placebo group could be a result of natural variation and might not be meaningful, says Linmarie Sikich, associate director of the Duke Center for Autism and Brain Development in Durham, North Carolina, who was not involved in the study.

Researchers also note that the trial did not assess oxytocin’s long-term effects. “Should oxytocin be found effective, no one is going to use it for four weeks and stop. We have to make sure that long-term administration is safe,” says co-lead researcher Antonio Hardan, professor of psychiatry and behavioral sciences at Stanford University.

Confirming oxytocin’s effectiveness as an autism treatment requires larger, longer-term studies. With that goal in mind, Sikich and her colleagues have enrolled nearly 300 people with autism in a placebo-controlled 24-week trial of the hormone. The placebo and treatment groups will then receive treatment for another six months.

The team is measuring the participants’ blood levels of oxytocin before, during and after treatment. They are also monitoring factors that alter the expression of the oxytocin gene, and of other genes involved in the same pathway.

Oxytocin reduces caloric intake in men.

OBJECTIVE:

Preclinical studies indicate that oxytocin is anorexigenic and has beneficial metabolic effects. Oxytocin effects on nutrition and metabolism in humans are not well defined. It was hypothesized that oxytocin would reduce caloric intake and appetite and alter levels of appetite-regulating hormones. Metabolic effects of oxytocin were also explored.

METHODS:

A randomized, placebo-controlled crossover study of single-dose intranasal oxytocin (24 IU) in 25 fasting healthy men was performed. After oxytocin/placebo, subjects selected breakfast from a menu and were given double portions. Caloric content of food consumed was measured. Visual analog scales were used to assess appetite, and blood was drawn for appetite-regulating hormones, insulin, and glucose before and after oxytocin/placebo. Indirect calorimetry assessed resting energy expenditure (REE) and substrate utilization.

RESULTS:

Oxytocin reduced caloric intake with a preferential effect on fat intake and increased levels of the anorexigenic hormone cholecystokinin without affecting appetite or other appetite-regulating hormones. There was no effect of oxytocin on REE. Oxytocin resulted in a shift from carbohydrate to fat utilization and improved insulin sensitivity.

CONCLUSIONS:

Intranasal oxytocin reduces caloric intake and has beneficial metabolic effects in men without concerning side effects. The efficacy and safety of sustained oxytocin administration in the treatment of obesity warrants investigation.

Oxytocin Study for Alcohol Withdrawal

Background: We recently showed in a placebo-controlled trial (n=11) that oxytocin (OXY) (24 IU insufflation bid) demonstrated efficacy in reducing withdrawal symptoms, anxiety and need for lorazepam in subjects with alcohol dependence undergoing detoxification (Pedersen et al, ACER 37:484, 2013).

Methods: The current pilot study tested for safety and efficacy of OXY compared to placebo (PBO) in subjects admitted to a residential community detoxification center. Effects on withdrawal and on subsequent drinking behavior, craving and anxiety were examined. Subjects with alcohol dependence and a history of withdrawal were enrolled within 48 hours of admission and received 4 insufflations of OXY (24 IU per dose) or PBO on Day 1, 3 doses on subsequent inpatient days and then bid dosing on outpatient days. Subjects were also recruited post-detox for the drinking trial and received similar dosing except no qid dosing on Day 1. Subjects were followed for 12 weeks as outpatients and received Medical Management.

Results: 115 subjects were prescreened to give 30 subjects fully screened to yield 19 randomized subjects. 8 subjects (4 OXY) form the detox inpatient group with the outpatient group consisting of 9 subjects (6 OXY) who completed at least 4 weeks of medication. Subjects receiving OXY during detox had a mean reduction in CIWA of 2.8 in the 48 hrs post-randomization vs an increase of 1.0 on PBO (p=.025) and used a mean of 2.25 mg lorazepam vs 5.25 mg lorazepam with PBO (p=.076). During the outpatient phase both the OXY and PBO groups had large reductions in heavy drinking days and large increases in abstinent days with decreased craving and anxiety but no significant OXY/PBO differences were found. No serious adverse events were seen, 2 OXY subjects complained of nose irritation and 2 subjects stopped meds (1 PBO for hives and 1 OXY for burning in the nose).

Conclusions: The finding of a significant reduction in alcohol withdrawal symptoms with less lorazepam use in the OXY vs PBO condition is compatible with our initial trial and is of therapeutic interest given that OXY does not have the deleterious profile of sedation and addiction liability associated with the benzodiazepines. The failure to find an OXY vs PBO effect on drinking behavior, anxiety or craving post-detox is difficult to interpret given the limited power of the trial. Tolerability of OXY was reasonable. Additional OXY trials in alcohol dependence are warranted.

In the future, there will be a pill for falling in love

Oxytocin could help treat alcohol use disorder

Oxytocin could help treat alcohol use disorder

by Public Library of Science

Oxytocin
Spacefilling model of oxytocin. Created using ACD/ChemSketch 8.0, ACD/3D Viewer and The GIMP. Credit: Wikipedia.

The neuropeptide oxytocin blocks enhanced drinking in alcohol-dependent rats, according to a study published April 16 in the open-access journal PLOS Biology led by Drs. Tunstall, Koob and Vendruscolo of the National Institutes of Health, and Drs. Kirson and Roberto of The Scripps Research Institute. Targeting the oxytocin system, the authors note, may provide novel pharmaceutical interventions for the treatment of alcohol-use disorder.

Administering oxytocin can decrease consumption, withdrawal symptoms, and drug-seeking behavior associated with several drugs of abuse, and shows promise as a pharmacological approach to treat drug addiction. But first, researchers need to understand how oxytocin mediates these effects in animal models.

To address this question, Tunstall and colleagues tested the hypothesis that oxytocin administration could normalize the maladaptive brain changes that occur in alcohol dependence and thereby reduce alcohol drinking in an established rat model of alcohol dependence.

The authors investigated oxytocin’s effects on dependence-induced alcohol consumption and altered signaling of the inhibitory neurotransmitter GABA in the central nucleus of the amygdala (CeA)—a key brain region in the network affected by alcohol dependence.

The experiments demonstrated that oxytocin administered systemically, intranasally or into the brain blocked excess drinking in alcohol-dependent but not in normal rats. Moreover, oxytocin blocked GABA signaling in the CeA. Taken together, these results provide evidence that oxytocin likely blocks enhanced drinking by altering CeA GABA transmission.

These results provide evidence that aberrations in the oxytocin system may underlie alcohol use disorder and that targeting this system, possibly by intranasal administration, could prove a promising therapy in people who misuse alcohol.

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Depression Therapy With Party-Drug Roots Faces FDA Panel Review

Depression Therapy With Party-Drug Roots Faces FDA Panel Review



Depression Therapy With Party-Drug Roots Faces FDA Panel Review

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Potential for abuse and strategies for containing any risks from an experimental depression treatment from Johnson & Johnson will be in focus at an Food and Drug Administration panel next week.

J&J’s nasal spray, esketamine, a close cousin of the party drug ketamine, will be considered by an FDA advisory panel on Feb. 12. While agency staff seemed satisfied that the likelihood of abuse is low, they raised questions about safety issues connected to a dreamlike sensation the medication can create in some users.

“Ketamine abuse is relatively uncommon in the general population,” agency staff said in a report ahead of next week’s meeting. Just 1.3 percent of people over age 12 abuse the drug, lower than abuse rates for other hallucinogens like ecstasy and LSD.

At the same time, reviewers worried that patients could get into accidents or otherwise be harmed if they leave a doctor’s office while still experiencing disassociation, a known side effect of ketamine — and a sought-after experience for casual users who have dubbed the spacey feeling the “K-hole.”

It takes roughly 90 minutes for disassociation symptoms from esketamine to resolve, according to the report. FDA staff also cited elevated blood pressure as a safety concern.

Esketamine is a key part of J&J’s pharmaceutical pipeline, as the company faces flagging sales this year weighed down by drug pricing scrutiny and looming generic competition. Its shares, which rose 2.3 percent this year through Thursday’s close, were were little changed in early trading on Friday.

In addition to weighing in on the drug’s safety and a proposed risk-evaluation and mitigation strategy, FDA staff will ask advisers to vote on whether esketamine effectively treated the depression of patients who weren’t helped by other therapies. They’ll also discuss whether additional studies are needed before or after the drug is potentially approved.

The staff report noted there were six deaths among patients taking the J&J drug, of which three were suicide in the esketamine depression program, but they didn’t see a clear link to the drug itself.

“Given the small number of cases, the severity of the patients’ underlying illness, and the lack of a consistent pattern among these cases, it is difficult to consider these deaths as drug related,” staff reviewers noted.

A decision on whether to allow the drug on the market is expected by March 4. Esketamine has the FDA’s breakthrough-therapy designation in treatment-resistant depression as well as for depressed people at risk of suicide. Results from a study in suicidal patients are expected this year. Allergan is also testing a fast-acting antidepressant, rapastinel, which is about a year behind esketamine in testing.



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Ketamine Is Showing Early Success With Treating OCD

Tonic Video

By the time she signed up for an experimental ketamine study, one young mother’s obsessive compulsive disorder had forced her to give up her daughter for adoption. “When the baby was just a couple of days old it hit her like an injection of anxiety,” Carolyn Rodriguez, assistant professor of psychiatry and behavioral sciences at Stanford University, tells me about her participant. “She was having difficulties even with changing the baby’s diapers.”

Another participant suffering from contamination obsessions would brush his teeth compulsively, despite painful and bleeding gums. “Eventually he avoided brushing and dental hygiene altogether, and then ended up losing a fair amount of his teeth,” Rodriguez says.

Rather than being a “personality quirk,” she emphasizes, OCD can be debilitating and even life threatening—one in seven adults with the condition will attempt suicide in their lifetime. Existing treatments—which include serotonin reuptake inhibitors (the group of medications that SSRIs belong to), cognitive behavioral therapy (CBT) and exposure and response prevention (ERP)—help in around 50 percent of cases.

Rodriguez is two years into a five-year study of the effects of ketamine on OCD symptoms. So far, she has seen promising results. In 2013, she conducted the first randomized controlled study of intravenous ketamine infusions for OCD sufferers. Each patient got a 40-minute infusion at a dose of 0.5 mg per kg. Half of those given ketamine, rather than saline, still reported at least a 35 percent reduction in obsessive and compulsive symptoms (such as cleaning or checking rituals or uncontrollable taboo thoughts) after one week.

“Patients said it was as if the weight of OCD had been lifted,” she recalls. “People were really as surprised as I was.”

Ketamine acts far more rapidly than existing treatments, which can take months to have an effect and, in the case of talking therapy, require a lot of determination. One patient, a high school teacher, told Rodriguez the treatment was like a “vacation” from her condition.

While SSRIs work on serotonin in the brain, ketamine acts on another neurotransmitter called glutamate. Though scientists don’t know what type of imbalance in neurotransmitters cause OCD for sure, glutamate abnormalities have been linked with the condition.

GLUTAMATE ABNORMALITIES IN OBSESSIVE COMPULSIVE DISORDER NEUROBIOLOGY, PATHOPHYSIOLOGY, AND TREATMENT

Rodriguez’s research is pioneering in the scientific world but ketamine clinics across the US are already offering infusions as a treatment for OCD. These clinics primarily treat depression, PTSD and chronic pain, with OCD as a relatively recent addition which is taken up by a small proportion of patients. Ketamine isn’t FDA-approved for these uses but, as it is legal as an anaesthetic, it can be administered off-label.

Rodriguez is in two minds about the use of ketamine for OCD in the absence of the same body of research that backs ketamine as a treatment for depression.

“I’ve seen it work and some patients really benefit from it,” she says. “I think it’s important for patients who are in dire straits—so, individuals who are suicidal, have tried every possible medication and just continue to suffer.”

But Rodriguez has concerns about the infusions’ side effects, which can include nausea, vomiting and disassociation. She compares this floating feeling to getting “nitrous oxide at the dentist.” The sensation does not match the intensity of a K-hole (or ketamine high), but participants aren’t allowed to drive for 24 hours after having the treatment.

Treatment center Ketamine Clinics of Los Angeles began administering the drug for OCD after patients who experienced obsessions and compulsions alongside other conditions found it worked on these symptoms too. Apart from Antarctica, the clinic has received visitors from every continent.

“We were very gratified with the results,” Steven L. Mandel, the center’s president, tells me. “They can shake hands again, they can go to a public toilet without it being an hour’s worth of rituals.”

K for OCD

euris “Jerry” Rivas, a native of New York, was diagnosed with severe obsessive-compulsive disorder when he was 15. Obsessions with organizing and reorganizing the belongings in his bedroom — posters, comic books, videos — took over most of his life.

Extra

volumehigh audio interview

Forced by germ obsessions to compulsively wash and rewash his hands, he started wearing gloves all day to both protect him from the germs and stop him from washing his hands raw. Now, at 36, OCD symptoms continue to cost him jobs and relationships. He’s managed to turn his organizational skills into a profession — he’s a home organizer and house cleaner — but still he struggles daily with his obsessions.

“It’s caused me a great deal of suffering,” Rivas says. “I’ve tried many, many medications. I’ve wasted so much of my life.”

In 2012, running out of answers, Rivas took part in the first clinical trial to test ketamine as a treatment for OCD. While ketamine is approved by the U.S. Food and Drug Administration as an anesthetic, it is also an illicit party drug known as “Special K,” with hallucinogenic effects and the potential for abuse. Over the past 10 years, dozens of small studies of ketamine’s ability to treat a variety of mood and anxiety disorders have reported remarkable results — including the sudden alleviation of treatment-resistant depression, bipolar disorder and post-traumatic stress disorder. And these effects lasted days, sometimes weeks, after the hallucinogenic effects of the drug wore off.

With a single infusion of the drug, Rivas experienced for two weeks what it was like to live without the compulsions and obsessions that had for years controlled his life.

“I felt like, for the first time, I was able to function like a regular person,” he says.

Illustration of a giant K being painted by a man in a white coat
Kotryna Zukauskaite

Pros and cons

Ketamine has brought hope to a psychiatric field desperate to find new treatments for severe OCD, a chronic condition marked by debilitating obsessions and repetitive behaviors. Current treatments, which include antidepressants such as Prozac, can take months to have any effect on the disease, if they work at all.

“Severe OCD takes such a toll on patients,” says Carolyn Rodriguez, MD, PhD, who as a researcher at Columbia University ran the OCD trial. Now an assistant professor of psychiatry and behavioral sciences at Stanford, she has continued to explore the pros and cons of using ketamine to treat OCD. “The constant, intrusive thoughts that something is contaminated, the checking and rechecking, the repetitive behaviors. It interferes with your life, your jobs, your relationships.”

Ketamine was developed in the 1960s and has been used for decades as an anesthetic during surgery. It remains a mystery just how the drug works in the brain, and there are safety concerns. There is evidence from people who take the drug routinely — in much higher doses — that chronic, high-frequency ketamine use may be associated with increased risk of bladder inflammation and cognitive impairment, Rodriguez says. And if taken regularly, it can lead to dependence.

But researchers like Rodriguez are intrigued about the drug’s potential to help them identify a whole new line of medicines for fast-acting treatment of mental health disorders.

“What most excites me about ketamine is that it works in a different way than traditional antidepressants,” Rodriguez says. “Using ketamine, we hope to understand the neurobiology that could lead to safe, fast-acting treatments. I feel that is part of my mission as a physician and researcher.”

‘Right out of a movie’

Rodriguez’s interest in ketamine as a treatment for OCD was sparked about a decade ago when she was starting out as a research scientist at Columbia. A small, placebo-controlled study published in 2006 by a mentor of hers, Carlos Zarate, MD, now chief of the section on neurobiology and treatment of mood disorders at the National Institute of Mental Health, had shown that ketamine induced dramatic improvement in treatment-resistant depression within two hours of infusion. It was a landmark study, drawing attention among the psychiatric community and launching a new field of research into the use of ketamine to treat various mood and anxiety disorders.”What most excites me about ketamine is that it works in a different way than traditional antidepressants.”

Rodriguez, intent on searching for better, faster treatments for her patients like Rivas with OCD, took note. There was an emerging theory that ketamine affects the levels of the neurotransmitter glutamate in the brain and increasing evidence that glutamate plays a role in OCD symptoms, she says. Perhaps ketamine could help regulate OCD symptoms as well as depression.

In 2013, Rodriguez and colleagues published their results from that first clinical trial of ketamine in OCD patients. The trial randomized 15 patients with OCD to ketamine or placebo.

In those patients who were given ketamine, the effect was immediate. Patients reported dramatic decreases in their obsessive-compulsive symptoms midway through the 40-minute infusion, according to the study. The diminished symptoms lasted throughout the following week in half of the patients. Most striking were comments by the patients quoted in the study: “I tried to have OCD thoughts, but I couldn’t,” said one. Another said, “I feel as if the weight of OCD has been lifted.” A third said, “I don’t have any intrusive thoughts. … This is amazing, unbelievable. This is right out of a movie.” And while nearly all initially had dissociative effects like feelings of unreality, distortions of time or hallucinations, they were gone within two hours after the start of the infusion.

“Carolyn’s study was quite exciting,” Zarate says, adding that there were a number of similar, small but rigorous studies following his 2006 study that found fast-acting results using ketamine to treat bipolar disorder and post-traumatic stress disorder.

“We had no reason to believe that ketamine could wipe out any symptoms of these disorders within hours or days,” he says.

So how does it work?

Virtually all of the antidepressants used in the past 60 years work the same way: by raising levels of serotonin or one or two other neurotransmitters. Ketamine, however, doesn’t affect serotonin levels. Exactly what it does remains unclear.”There’s a recognition that people like me and others are using the drug to treat patients now. There’s an incredible need for something.”

Since coming to Stanford in 2015, Rodriguez has been funded by the National Institute of Mental Health for a large clinical trial of ketamine’s effects on OCD. This five-year trial aims to follow 90 OCD patients for as long as six months after they’ve been given a dose of ketamine or an alternative drug. Rodriguez and her research team want to observe how ketamine changes participants’ brains, as well as test for side effects.

Ultimately, Rodriguez says, she hopes the study will lead to the discovery of other fast-acting drugs that work in the brain like ketamine but without its addictive potential.

Recent research in the field indicates that the glutamate hypothesis that triggered her pilot study might be further refined.

“Ketamine is a complicated drug that works on many different receptor sites,” she says. “Researchers have fixated on the NMDA receptor, one of the glutamate-type receptors, but it might not be the only receptor bringing benefit.”

In May 2016, researchers from NIMH and the University of Maryland — Zarate among them — published a study conducted in mice showing that a chemical byproduct, or metabolite, created as the body breaks down ketamine might hold the secret to its rapid antidepressant actions. This metabolite, hydroxynorketamine, reversed depressionlike symptoms in mice without triggering any of the anesthetic, dissociative or addictive side effects associated with ketamine, Zarate says.

“Ideally, we’d like to test hydroxynorketamine and possibly other drugs that act on glutamate pathways without ketamine-like side effects as possible alternatives to ketamine in OCD,” Rodriguez says.

Beyond the clubs

Meanwhile, dozens of commercial ketamine clinics have popped up across the country, making treatments available to patients who are searching for help to stop their suffering now. Medical insurance companies usually cover ketamine’s FDA-approved use as an anesthetic but won’t cover its use for other purposes, such as mental health disorders. So patients who have run out of treatment options are paying hundreds of dollars a dose for repeated ketamine infusions.

“The fact that these clinics exist is due to the desperation of patients,” says Rodriguez.

She and other researchers are calling for guidelines to protect patients and more research to learn how to use the drug safely.

“I think it’s a game changer, and it’s here to stay,” says David Feifel, MD, PhD, professor emeritus of psychiatry at UC-San Diego, who studies the effect of ketamine on clinical depression. Feifel began prescribing the drug for patients with treatment-resistant depression in 2010.

“I’ve found it to be very safe,” Feifel says, adding that the American Psychiatric Association this year issued safety guidelines on how to use ketamine clinically for treatment of depression.

“There’s a recognition that people like me and others are using the drug to treat patients now,” he says. “There’s an incredible need for something.”

The drug hasn’t worked for everyone he’s treated, Feifel says, but for many it’s been “life-changing.”

Rodriguez says she understands what motivates the clinicians to prescribe the drug now to patients in dire straits — those who are suicidal or who have tried every possible medication and therapeutic option and continue to suffer each day.

“I see it as a way to treat people whose OCD is very, very severe,” she says. “People who can’t come out of the house, who are suicidal, who have no other options.

“I just don’t like the idea of people being in pain,” Rodriguez adds. “I want to see science translated into treatments now.”

Meanwhile, researchers are learning more about the drug. Janssen Pharmaceutical is testing the efficacy of a version of ketamine, known as esketamine, as a therapy for treatment-resistant depression and for major depressive disorder with imminent risk for suicide. The FDA has fast-tracked both investigations. At Stanford, Alan Schatzberg, MD, a professor of psychiatry and behavioral sciences, along with other faculty including Rodriguez, is studying the mechanism of action for ketamine in treating depression.

Rodriguez is also interested in using ketamine to kick-start a type of cognitive behavioral therapy called exposure and response prevention, an evidence-based psychological treatment designed to help patients overcome OCD. The therapy involves teaching patients with OCD to face anxieties by refraining from ritualizing behaviors, then progressing to more challenging anxieties as they experience success.

Relaxation and other techniques also help patients tolerate their anxiety — for example, postponing the compulsion to wash their hands for at least 30 minutes, then extending that time period.

“My goal isn’t to have people taking ketamine for long periods of time,” Rodriguez says. But perhaps a short-term course of ketamine could provide its own kind of exposure and response prevention by allowing patients to experience that it is possible not to be controlled by their OCD, she says.

Rivas well remembers that infusion of ketamine he received during Rodriguez’s first clinical trial to test the drug. The rush made him feel “like Superman.”

“I felt like my body was bigger, that I was more muscular, that I could tackle anything,” he says. But that feeling only lasted the duration of the 40-minute infusion. His OCD symptoms disappeared immediately and were still gone for two weeks after.

“I was amazed that something like that would work and work so fast,” he says. His OCD symptoms today are still intrusive, but he manages to keep them under control by taking antidepressants and seeing a therapist. Still, each day when he comes home from work, he has to put gloves on before he enters his apartment building, and as soon as he enters his apartment, he must wash his hands.

“It’s a ritual now,” he says. “There has never been a time that I haven’t done that, except those two weeks after the ketamine.”

When he heard that certain private ketamine clinics are now offering the drug as treatment for OCD, he said he understands why patients take the risks and pay the high prices. As more research has become available, he’s begun considering it himself.

“I’ve been suffering through my OCD for so long, I’ve gotten to the point where I’d try anything,” he says.

A Randomized Trial of a Low-Trapping Nonselective N-Methyl-D-Aspartate Channel Blocker in Major Depression. Zarate CA Jr, Mathews D, Ibrahim L, Chaves JF, Marquardt C, Ukoh I, Jolkovsky L, Brutsche NE, Smith MA, Luckenbaugh DA. Biol Psychiatry. 2012 Nov 30. pii: S0006-3223(12)00941-9. doi: 10.1016/j.biopsych.2012.10.019. PMID: 23206319.

A randomized trial of a low-trapping nonselective N-methyl-D-aspartate channel blocker in major depression.A randomized trial of a low-trapping nonselective N-methyl-D-aspartate channel blocker in major depression.

Rapid Resolution of Suicidal Ideation after a Single Infusion of an NMDA Antagonist in Patients with Treatment-Resistant Major Depressive Disorder. Nancy DiazGranados, MD, MS, Lobna Ibrahim, MD, Nancy Brutsche, MSN, Rezvan Ameli, PhD, Ioline D Henter, MA, David A Luckenbaugh, MA, Rodrigo Machado-Vieira, MD, PhD, and Carlos A Zarate, Jr, MD. J Clin Psychiatry. 2010 December; 71(12): 1605–1611. PMID: 20673547.

Rapid Resolution of Suicidal Ideation after a Single Infusion of an NMDA Antagonist in Patients with Treatment-Resistant Major Depressive Disorde

A randomized add-on trial of an N-methyl-D-aspartate antagonist in treatment-resistant bipolar depression. Diazgranados N, Ibrahim L, Brutsche NE, Newberg A, Kronstein P, Khalife S, Kammerer WA, Quezado Z, Luckenbaugh DA, Salvadore G, Machado-Vieira R, Manji HK, Zarate CA Jr. Arch Gen Psychiatry. 2010 Aug;67(8):793-802. doi: 10.1001/archgenpsychiatry.2010.90. PMID: 20679587.

Increased anterior cingulate cortical activity in response to fearful faces: a neurophysiological biomarker that predicts rapid antidepressant response to ketamine. Salvadore G, Cornwell BR, Colon-Rosario V, Coppola R, Grillon C, Zarate CA Jr, Manji HK. Biol Psychiatry. 2009 Feb 15;65(4):289-95. doi: 10.1016/j.biopsych.2008.08.014. Epub 2008 Sep 25. PMID: 18822408.

Increased anterior cingulate cortical activity in response to fearful faces a neurophysiological biomarker that predicts rapid antidepressant response to ketamine

A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Zarate CA Jr, Singh JB, Carlson PJ, Brutsche NE, Ameli R, Luckenbaugh DA, Charney DS, Manji HK. Arch Gen Psychiatry. 2006 Aug;63(8):856-64. PMID: 16894061.

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Is Ketamine Safe and Effective for Depression?

The anesthetic ketamine, used in both humans and animals, is perhaps best known as an illegal party drug due to its hallucinogenic effects. However, a growing body of research indicates that the drug may have a powerful new medical use: as a fast-acting antidepressant without the side effects seen in most prescription antidepressants.

As Nature reports, in many clinical trials to date people who have not responded to standard antidepressant treatment — such as SSRIs including Prozac — seem to respond to ketamine. And while it can take weeks to feel better after starting a prescription antidepressant, the therapeutic effects of ketamine are seen in a matter of hours.

Despite the seemingly “miracle drug” nature of ketamine, there are serious concerns about its use in depression. First, it is unclear how the drug works to alleviate depression. Second, there are no long-term studies on its long-term use. Studies that have already been done indicate the antidepressant effects of ketamine can last from between a few days to a few weeks.

And due to the addictive nature of ketamine itself, there are worries that sustained use of it may lead to dependence.

On May 4, Nature published the results of the latest trial involving ketamine, bolstering its potential as an antidepressant treatment. Researchers, examining the drug in mice, found that that the mood boosting effects may not be caused by ketamine itself, but instead by one of the metabolites ((2R,6R)-hydroxynorketamine) formed when the drug is broken down into smaller pieces.

Even more promising, the ketamine given to the rats did not increase side effects, even though the dose was much stronger than what would be given to humans for depression. The researchers say they want to take the metabolite into testing in humans, though that is likely years away.

The largest trial ever of ketamine in depression was done in 2013 with 73 participants. The drug lead to a decline in depression symptoms 24 hours after treatment in 64% of patients, all of whom had tried at least 3 other drugs without any results.  Antidepressant Efficacy of Ketamine in Treatment resistant depression

Despite the lack of clear-cut evidence of its benefits and unknowns about its long-term risk, many doctors are already offering ketamine as a depression treatments to patients, though this is an off-label use.

Side effects of ketamine can include confusion, lucid daydreaming, fuzzy vision, and a “high” feeling, though they tend to go away quickly, according to these doctors. Patients, who are usually given ketamine via infusion, are carefully monitored and must have pre-arranged transport home. They can’t drive or use heavy machinery for 24 hours.

Drug companies are even trying to cash in on the ketamine craze. Janssen Pharmaceutical is testing a form of ketamine it developed, called esketamine, in 5 clinical trials. It would be given via a nasal spray. Another is rapastinel, under development by Allergan. Both drugs had “breakthrough therapy designation” from the FDA, meaning they will go through the regulatory process at a much quicker rate.

NMDAR inhibition-independent antidepressant actions of ketamine metabolites

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New research is connecting genetic variations to schizophrenia and other mental illnesses

The conversation Article

We know that changes in our genetic code can be associated with an increased risk for psychiatric illnesses such as schizophrenia and bipolar disorder. But how can a genetic mutation lead to complex psychiatric symptoms such as vivid hallucinations, manic episodes and bizarre delusions?

To find out, researchers are trying to fill in the blanks between the genetic blueprint (genotype) and psychiatric disorder (psychiatric phenotype). Phenotypes are a set of observable characteristics that result when a particular genotype interacts with its environment. The phenotype is the eventual outcome of a specific genotype.

But between genotype and psychiatric phenotype lie many measurable traits that together are called endophenotypes. This is an aspect of genetics that scientists are just starting to understand.

The National Institute of Mental Health has recently begun an initiative to push researchers to study endophenotypes with a program called Research Domain Criterion (RDoC), described as an effort to study basic dimensions of functioning that underlie human behavior.

So what exactly are endophenotypes, and how might they contribute to psychiatric illnesses?

Endophenotypes lie between genes and psychiatric phenotypes

An endophenotype can refer to anything from the size and shape of brain cells, to changes in brain structure, to impairments in working memory. The term can refer to a physical trait or a functional one.

An endophenotype must be associated with a specific psychiatric illness, such as schizophrenia, and it must be heritable. It must also be present even if the illness is not active. Within families, the endophenotype must be more common in ill family members than in healthy family members. But the endophenotype must be more common among nonaffected relatives of people with the associated illness than among the general population.

Certain endophenotypes are thought to precede behavioral symptoms. For instance, in several conditions, such as schizophrenia and Alzheimer’s disease, changes in brain structure have been found years before the onset of symptoms.

Currently doctors diagnose a psychiatric disorder based on the patient’s symptoms. The underlying neurobiology isn’t usually considered, because we lack the data to really use it.

In the future, endophenotypes might let us detect who is susceptible to psychiatric illness before clinical symptoms develop. That means we could try to combat, or at least appease, the symptoms of the disorder before they start. And knowing how endophenotypes contribute to these disorders could lead to precision medicine treatments.

How do you study endophenotypes?

One way to study the endophenotypes is to focus on a specific genetic alteration that is associated with a psychiatric disorder. This way we can get a sense of what brain changes the genetic change causes.

The links leading from genetic alterations to psychiatric illness in 22q11.2 Deletion Syndrome. Rachel Jonas, CC BY

For instance, I study a genetic disorder called 22q11.2 Deletion Syndrome (also called 22q11DS). The syndrome is due to a deletion of up to 60 genes, many of which are linked to brain function. About 30 percent of individualswith 22q11DS will develop schizophrenia (the rate in the U.S. population overall is about one percent).

Studying 22q11DS lets us draw a line from a genetic alteration to a psychiatric phenotype, such as decreased neural function, brain structure changes or fewer neurons in certain parts of the brain, and to a psychiatric phenotype, such as schizophrenia.

Let’s go through some concrete examples of how this can be done.

22q11DS: a model syndrome to study endophenotypes

In one study researchers looked at a group of 70 children and adolescents with 22q11DS, and found deficits in executive function (which encompasses cognitive processes such as motivation, working memory and attention) in patients with 22q11DS.

In fact, researchers were actually able to predict subsequent development of psychotic symptoms in individuals with 22q11DS. This study shows that cognitive endophenotypes may underlie psychiatric phenotypes and demonstrates their predictive power. And, like all endophenotypes, it is invisible to the naked eye, but measurable in the lab.

Another study, using functional magnetic resonance imaging (fMRI), found reduced neural activity in patients with 22q11DS when they performed a working memory task compared to a group of healthy control subjects. What’s more, the magnitude of the decrease correlated with the severity of their psychotic symptoms. This suggests abnormalities in neural activity might underlie symptoms associated with schizophrenia.

Other studies have found an association between psychiatric illnesses such as schizophreniaand abnormalities in the size and shape of different brain regions. For instance, a recent study found that certain parts of the brain were thicker in patients with 22q11DS. What’s more, the degree of thickness was related to psychotic symptoms. Changes in brain structure have also been associated with psychiatric disorders, such as obsessive compulsive disorder.

Researchers can you use mice models to learn about endophenotypes. Mouse via www.shutterstock.com.

In order to gain a more in-depth understanding of the underlying physiology in 22q11DS, researchers can breed mice with the deletion syndrome by “knocking out” genes in the mouse genome.

Researchers have found that mice with 22q11DS had fewer neurons in a part of the brain associated with cognition compared to unaffected mice.

The number of neurons correlated with how well the mice performed on tasks measuring executive function. These results suggest that individuals with psychiatric illnesses might actually have microscopic changes in their brain cells. This is a significant finding, because we can’t study these effects directly in humans.

These are just some examples of how we can experimentally determine endophenotypes that underlie schizophrenia in 22q11DS. And while 22q11DS is a risk factor for schizophrenia, what we learn from studying this syndrome could help us understand the endophenotypes behind other illnesses.

Of course defining endophenotypes for psychiatric illness is just the first step. After that, researchers and scientists need to find ways to use these results to inform diagnosis, treatment and prevention strategies.

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New research, which features in the journal Neuron, shows that primates lose excitement in anticipation of a reward when a specific area of their brain becomes overactive. The study also shows that ketamine affects this brain region and prevents the loss of pleasure.

woman sitting on the edge of the bed seen from behind
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A loss of interest or pleasure in activities that were once exciting is one of the hallmarks of depression.

Depression is “the leading cause of disabilityworldwide” and one of the most commonmental health problems in the United States.

The symptoms of major depression include depressed mood and loss of interest or pleasure in daily activities. Some people may also experience difficulty sleeping, eating, and focusing or have intrusive thoughts of death or taking their own life.

The loss of interest, pleasure, or excitement in anticipation of activities that the individual once perceived as enjoyable is called anhedonia.

The brain mechanisms that underpin anhedonia in depression have remained unclear until now, and this lack of knowledge has hindered the success of many antidepressant treatments.

Now, a new study casts much-needed light on this symptom. Leading a team of researchers, professor Angela Roberts from the Department of Physiology, Development, and Neuroscience at the University of Cambridge, United Kingdom, and doctoral researcher and medical student Laith Alexander set out to study this phenomenon in marmosets.

Marmosets are a type of nonhuman primate with frontal lobes that are very similar to those of humans. This physical similarity means that the findings are more easily translatable to humans than they would be if the study involved rodents instead.

Prof. Roberts and colleagues tested the effects of ketamine, a hallucinogenic drug that has recently garnered interest as a potential treatment for depression, and found that it had a positive effect on the primates.

Studying anhedonia in primates

Prof. Roberts explains the motivation behind the study, saying, “Imaging studies of [people with depression] have given us a clue about some of the brain regions that may be involved in anhedonia, but we still don’t know which of these regions is causally responsible.”

“A second important issue,” she adds, “is that anhedonia is multi-faceted — it goes beyond a loss of pleasure and can involve a lack of anticipation and motivation, and it’s possible that these different aspects may have distinct underlying causes.”

To find out more about the brain mechanisms behind anhedonia, Prof. Roberts and her team devised an experiment in which they trained primates to react to two sounds. Sound A indicated that the marmosets would receive marshmallows as a treat while no treat followed sound B.

After the training, blood pressure measurements and head movements showed that the marmosets would get excited on hearing sound A but would not respond in this way to sound B.

Next, the scientists surgically implanted very thin metal tubes into the marmosets’ heads, through which they injected either a drug or a placebo into the brains of the primates.

The researchers targeted a specific brain region called “area 25,” which the drug made temporarily hyperactive. They used PET scans to study the primates’ brain activity.

Brain’s area 25 is key in anhedonia

The primates that received the drug showed increased activity in area 25 in the brain and also displayed significantly lower excitement in anticipation of the marshmallows.

In contrast, there was no change in either the brain activity or behavior of the primates that received the placebo.

In a second experiment, the primates had to work for their rewards. At first, they received a treat after touching a colored shape on a screen just once.

However, over the course of the experiment, the primates had to press the shape an increasing number of times before they received the marshmallow. Eventually, the animals would give up because the treat was no longer worth the effort.

The researchers found that the marmosets with a hyperactive area 25 gave up much more quickly. PET scans also revealed that abnormal activity in this brain area overflowed into other brain areas, which also became overactive when the anticipatory excitement dwindled.

How ketamine prevents the loss of pleasure

Finally, the researchers tested the effect that ketamine had on the primates. They gave the marmosets ketamine 24 hours before repeating the same experiments as before.

This time, ketamine blocked the activity of the drug that overactivated area 25. The brain activity of the primates that received ketamine looked normal in PET scans, and the primates continued to exhibit just as much excitement in anticipation of the marshmallow treats.

“Understanding the brain circuits that underlie specific aspects of anhedonia is of major importance,” says first author Laith Alexander, “not only because anhedonia is a core feature of depression but also because it is one of the most treatment-resistant symptoms.”

Studies show that as many as 30 percent of people living with depression have a form of the condition that does not respond to treatment.

“By revealing the specific symptoms and brain circuits that are sensitive to antidepressants like ketamine, this study moves us one step closer to understanding how and why patients may benefit from different treatments.”

Laith Alexander

Fractionating Blunted Reward ProcessingCharacteristic of Anhedonia by Over-ActivatingPrimate Subgenual Anterior Cingulate Cortex

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At NOVA Health recovery [703-844-0184 | Fairfax, Va 22306 ] we offer our patients cutting-edge treatment options for their depression, and one of our main stars is IV (intravenous) ketamine. But why does it have to be IV? “I don’t like needles, why can’t I just take this as a pill or as that nasal spray everyone is talking about?” you may be thinking. IV is the best route for your brain to receive ketamine because of something called bioavailability. In addition, it is also more effective, more precise, and safer for you.

What is bioavailability? It is the amount of medication that your body and brain is actually able to use, which is sometimes different than the amount of medication that your body receives. When you take any medication, parts of the active ingredients in them don’t go to your bloodstream; they get digested, altered into an unusable form, metabolized and excreted into your body. This is particularly prevalent in oral and intranasal medications. In fact, receiving a medication intravenously is the only way to have 100% bioavailability. Let’s take a look at the different bioavailability percentages based on what route you receive ketamine:

Intravenous: 100%

Intramuscular: 93%
Intranasal: 25-50%
Sublingual (under the tongue): 30%
Orally (by mouth): 16-24%

When we give ketamine intravenously, we know exactly where your entire dose is going: straight to your brain. The same cannot be said for other forms of ketamine. Intranasal ketamine has to bypass several layers of tissue before it can reach your brain, and too many things can happen that could cause you to lose some or most of your dose: sneezing, dripping, running down the back of your throat, etc. The same can be said for an oral pill and an intramuscular injection; these routes are just too unpredictable, and when it comes to treating your depression, we don’t want the results to be unpredictable.

When you receive IV ketamine in our office setting, it is given slowly over one hour. By doing this, we are able to monitor you closely, and if you experience any unpleasant side effects and want to stop the infusion, we are able to do that. By contrast, a dose of ketamine via intranasal spray would be done at home with no physician or nursing supervision, so side effects cannot be immediately addressed if they arise. The same is true for intramuscular or oral dosing – after you take the pill, or receive a shot of ketamine into your muscle, there is no way to stop the absorption of the medication into your bloodstream as the full dose is administered within seconds.

IV ketamine is by far the safest and most effective approach in using ketamine to treat depression. You are in a comfortable setting with healthcare providers with you the whole time, the potential for side effects is low, and you are certain that the dose you receive is the dose that is going to your brain, maximizing the benefits of this cutting-edge treatment.

However, we do offer the other routes of administration and take – home prescriptions for Ketamine therapies for those who are in our program. Contact us today at 703-844-0184 to get started on your treatment.

 

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Ketamine is emerging as a popular treatment for depression. New research suggests the drug acts like an opioid

Ketamine

Ketamine is emerging as a popular treatment for depression. New research suggests the drug acts like an opioid

  • Ketamine is emerging as a way to treat depression, but it appears to act like an opioid, Stanford researchers found.
  • Clinics are cropping up around the country where people receive ketamine infusions.
  • A handful of pharmaceutical companies, including Johnson & Johnson and Allergan, are using ketamine as inspiration for new prescription drugs to treat depression.

This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as "Special K."
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This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as “Special K.”

Ketamine is emerging as a way to treat depression, but it appears to act like an opioid — and it may carry similar risks, Stanford researchers found.

Clinics are cropping up around the country where people receive ketamine infusions. A handful of pharmaceutical companies are using ketamine as inspiration for new prescription drugs to treat depression. Yet the new research questions whether scientists know enough about chronic ketamine use to introduce it broadly.

The drug blocks NMDA receptors, which scientists think may treat depressive symptoms. Researchers wanted to test whether it was possible to elicit this reaction without activating the brain’s opioid receptors.

To block an opioid response, they gave participants naltrexone then infused them with ketamine. To compare that response with the normal response, they also gave participants a placebo before giving them the treatment.

Naltrexone so successfully blocked the anti-depressant effects of ketamine that researchers cancelled the study after the first interval because they felt it wasn’t ethical to continue it, said Dr. Nolan Williams, one of the study’s authors and a clinical assistant professor of psychiatry and behavioral sciences at Stanford University.

When patients took naltrexone, the opioid blocker, their symptoms did not improve, suggesting ketamine must first activate opioid receptors in order to treat depression, according to the study, published Wednesday in the American Journal of Psychiatry.

That’s not to say ketamine cannot be used occasionally, but it does raise questions about using it repeatedly over time, said Dr. Alan F. Schatzberg, co-author of the study and Stanford’s Kenneth T. Norris, Jr., professor of psychiatry and behavioral sciences. He likens it to opioid painkillers being an appropriate pain treatment when used once in the emergency room but posing problems, such as the risk of dependence, when used chronically.

“More studies need to be done to fully understand ketamine before it’s widely rolled out for long-term chronic use,” Schatzberg said.

Researchers planned on studying 30 adults but stopped enrolling patients once they decided combining ketamine and naltrexone was not only ineffective but also “noxious” for many participants. They tested a total of 12 people with both naltrexone and the placebo.

Of those 12, seven who received naltrexone experienced nausea after the ketamine infusion, compared to three in the placebo group. Two participants in each group also experienced vomiting.

Participants who received the placebo and ketamine treatment reported reduced depression symptoms. But those same participants did not see a decrease in depression symptoms after receiving ketamine and opioid-blocker naltrexone.

“We essentially blocked the mechanism for producing the anti-depressant effect, which were opioids,” said Williams.

The findings may have implications for clinics offering ketamine infusions and drug manufacturers trying to commercialize ketamine-like drugs.

Ketamine is meant to be used as an anesthetic. Since ketamine is currently not indicated to treat depression, insurance typically doesn’t cover the cost of infusions, so people tend to pay out of their own pocket. One session can run more than $500.

Meanwhile, drug giant Johnson & Johnson plans to seek approval from the Food and Drug Administration for its nasal spray esketamine this year after reporting positive results from a Phase 3 trial. Allergan plans to file its drug Rapastinel, which targets the NMDA receptors like ketamine, within the next two years. VistaGen Therapeutics is working on a similar drug.

In a statement, J&J said while the study reviewed ketamine and not esketamine, the findings “are difficult to interpret because of the study’s design.”

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Schizophrenia and Toxoplasmosis

 

 

Parasite May Play Role in Some Schizophrenia Cases

A parasite responsible for toxoplasmosis – Toxoplasma gondii – may be involved in the cause of around a fifth of schizophrenia cases in the US. This is according to a new study published in the journal Preventive Veterinary Medicine.

Definition of schizophrenia

University of Pennsylvania researcher Greg Smith calculated that around a fifth of schizophrenia cases may be attributable toT. gondiiinfection.

The Centers for Disease Control and Prevention (CDC) estimate that around 60 million people in the US may be infected with T. gondii. Infection most commonly occurs through eating undercooked, contaminated meat, drinking contaminated water and coming into contact with cat feces that contain T. gondii.

Most people with T. gondii infection are unaware they have it; people with healthy immune systems are usually able to stop the parasite causing illness. But for those with weaker immune systems, such as older people, pregnant women and those with immune system disorders, the parasite can cause toxoplasmosis.

Toxoplasmosis a disease characterized by flu-like symptoms, including swollen lymph glands and muscle aches and pains. In severe cases, toxoplasmosis can cause damage to the eyes, brain and other organs.

Some studies, however, have linked T. gondii infection to mental health conditions. In 2012, for example, Medical News Today reported on a study linking T. gondi to increased risk of self-harm or suicide among new mothers.

More recently, studies have linked T. gondii infection to schizophrenia, and some have found that antipsychotic medication may even stop the parasite from replicating. But such research has been met with much criticism.

In this latest study, Gary Smith, of the School of Veterinary Medicine at the University of Pennsylvania, wanted to gain a better understanding of the link between T. gondii infection and schizophrenia.

Link between T. gondii and schizophrenia ‘should be considered, not ridiculed’

Smith wanted to determine the proportion of schizophrenia cases that could be attributable to T.gondii infection. He did this by calculating the population attributable fraction (PAF) – a measure used by epidemiologists to understand the importance of a risk factor.

“In other words,” explains Smith, “we ask, if you could stop infections with this parasite, how many [schizophrenia] cases could you prevent?”

Smith calculated the PAF fraction throughout an average lifetime to be 21.4%, meaning that a fifth of all schizophrenia cases over a lifetime could be prevented by stopping T. gondiiinfections from occurring. “That, to me, is significant,” says Smith.

He notes that many countries have a much higher prevalence of T. gondii infections than the US, and such countries also have a higher prevalence of schizophrenia.

Schizophrenia is one of the leading causes of disability in the US, affecting more than 3.5 million people.

Smith believes that his findings indicate the importance of gaining a better understanding of the link between T. gondii infection and schizophrenia. He adds:

By finding out how important a factor T. gondii infection is, this work might inform our attitude to researching the subject.

Instead of ridiculing the idea of a connection between T. gondiiand schizophrenia because it seems so extraordinary, we can sit down and consider the evidence. Perhaps then we might be persuaded to look for more ways to reduce the number of people infected with toxoplasma.”

Common food preservative may help to treat schizophrenia

A new randomized trial from Taiwan shows that a common food preservative could enhance the effect of a schizophrenia drug, even in the case of people normally resistant to treatment.
older man taking pillsNew research suggests that a common food preservative could be the answer for treatment-resistant people with schizophrenia.

Schizophrenia is a chronic, sometimes disabling mental disorder characterized by delusions, flat affect, agitated movements, and a difficulty in sustaining activities.

Treatments include antipsychotic medication — such as brexpiprazole, clozapine, or risperidone — and psychosocial treatments.

Studies have shown that “one fifth to one half of [people with schizophrenia] are classified as refractory to pharmacological treatment,” meaning that they do not respond to antipsychotics.

Researchers from China Medical University in Taiwan may now have found a way of boosting the effectiveness of certain drugs, which may help some people living with schizophrenia to respond better to treatment.

The answer, says the study’s lead investigator Dr. Hsien-Yuan Lane, may be found in a common food preservative: sodium benzoate. Dr. Lane and team conducted a randomized, double-blind, placebo-controlled trial showing that this preservative could enhance the effects of the antipsychotic drug clozapine.

“Clozapine,” he explains, “is considered the last-line antipsychotic agent for patients with refractory schizophrenia.” Despite this, a significant number of people living with schizophrenia are resistant to this drug.

The new trial seems to confirm for the first time that sodium benzoate — which has successfully been used as an add-on to other antipsychotics — can be added to clozapine to improve the symptoms of drug-resistant patients.

Dr. Lane and colleagues’ findings were recently published in the journal Biological Psychiatry. “If the finding can be confirmed, this approach may bring hope for treating patients with the most refractory schizophrenia,” he suggests.

Sodium Benzoate, a D-Amino Acid Oxidase Inhibitor, Added to Clozapine for the Treatment of Schizophrenia_ A Randomized, Double-Blind, Placebo-Controlled Trial

D-Amino Acid Oxidase Inhibition A New Glutamate Twist for Clozapine Augmentation in Schizophrenia

A series of clinical trials
found that currently available NMDA-enhancing agents
including glycine, D-cycloserine, D-serine, and sarcosine were
efficacious in improving the overall psychopathology of
schizophrenia without side effect or safety concern.

16. Lin CH, Lane HY, Tsai GE (2012): Glutamate signaling in the pathophysiology and therapy of schizophrenia. Pharmacol Biochem Behav 100:665–677.
17. Heresco-Levy U (2005): Glutamatergic neurotransmission modulators as emerging new drugs for schizophrenia. Expert Opin Emerg Drugs 10:827–844.
18. Coyle JT (2012): NMDA receptor and schizophrenia: A brief history. Schizophr Bull 38:920–926.
19. Javitt DC, Schoepp D, Kalivas PW, Volkow ND, Zarate C, Merchant K, et al. (2011): Translating glutamate: From pathophysiology to treatment.Sci Transl Med 3:102mr102.

Cat ownership in childhood linked to greater risk of later-life mental illness

They are cute, fluffy and have that wide-eyed glare that few of us can resist; it is no wonder more than 95 million of us own a cat. But there may be a darker side to our four-legged friends. New research claims the animals could increase our risk of mental illnesses, including schizophrenia and bipolar disorder.
Cat using litter boxHumans can become infected with Toxoplasma gondii by accidentally swallowing the parasite after coming into contact with a cat’s feces.

Two studies published in the journals Schizophrenia Research and Acta Psychiatrica Scandinavica attribute this association to Toxoplasma gondii – a parasite found in the intestines of cats. Humans can become infected with the parasite by accidentally swallowing it after coming into contact with the animal’s feces.

T. gondii is the cause of a disease known as toxoplasmosis. According to the Centers for Disease Control and Prevention (CDC), more than 60 million people in the US are infected with the parasite, though the majority of people are not aware of it.

People with a healthy immune system often stave off T. gondii infection, so it does not present any symptoms. However, pregnant women and people with weakened immune systems are more susceptible to infection and may experience flu-like symptoms – such as muscle aches and pains and swollen lymph nodes – as a result, while more severe infection may cause blindness and even death.

Previous studies have also linked T. gondii infection to greater risk of mental disorders. In November 2014, for example, Medical News Today reported on a study claiming the parasite is responsible for around a fifth of schizophrenia cases. Now, new research provides further evidence of this association.

Link between T. gondii and schizophrenia ‘should be considered, not ridiculed’

Smith wanted to determine the proportion of schizophrenia cases that could be attributable to T.gondii infection. He did this by calculating the population attributable fraction (PAF) – a measure used by epidemiologists to understand the importance of a risk factor.

“In other words,” explains Smith, “we ask, if you could stop infections with this parasite, how many [schizophrenia] cases could you prevent?”

Smith calculated the PAF fraction throughout an average lifetime to be 21.4%, meaning that a fifth of all schizophrenia cases over a lifetime could be prevented by stopping T. gondiiinfections from occurring. “That, to me, is significant,” says Smith.

He notes that many countries have a much higher prevalence of T. gondii infections than the US, and such countries also have a higher prevalence of schizophrenia.

Schizophrenia is one of the leading causes of disability in the US, affecting more than 3.5 million people.

Smith believes that his findings indicate the importance of gaining a better understanding of the link between T. gondii infection and schizophrenia. He adds:

By finding out how important a factor T. gondii infection is, this work might inform our attitude to researching the subject.

Instead of ridiculing the idea of a connection between T. gondiiand schizophrenia because it seems so extraordinary, we can sit down and consider the evidence. Perhaps then we might be persuaded to look for more ways to reduce the number of people infected with toxoplasma.”

People with ‘rage’ disorder twice as likely to have toxoplasmosis

A disorder that causes the individual to fly off the handle unexpectedly, as in road rage, has been significantly linked with toxoplasmosis, a parasite commonly associated with cat feces, according to the Journal of Clinical Psychiatry.

[road rage]

People with IED are prone to sudden anger.

Intermittent explosive disorder (IED) has been defined as “recurrent, impulsive, problematic outbursts of verbal or physical aggression that are disproportionate to the situations that trigger them.”

Up to 16 million Americans are thought to have IED, more than the total number for bipolar disorder and schizophrenia combined.

Toxoplasmosis is a common and generally harmless parasitic infection that is passed on through the feces of infected cats, contaminated water or undercooked meat.

 

It affects around 30% of all humans but is normally latent1.

Research has revealed that the parasite is found in brain tissue, and it has been linked to a number of psychiatric conditions, including schizophrenia, bipolar disorder and suicidal behavior.

Researchers from the University of Chicago, led by Dr. Emil Coccaro, have been looking for more effective ways to diagnose and treat IED and impulsive aggression.

 

This is a scanning electron micrograph of the protozoan parasite Toxoplasma gondii, tissue cyst in brain of an infected mouse.
Credit: David Ferguson

Individuals with a psychiatric disorder involving recurrent bouts of extreme, impulsive anger–road rage, for example–are more than twice as likely to have been exposed to a common parasite than healthy individuals with no psychiatric diagnosis.

In a study involving 358 adult subjects, a team led by researchers from the University of Chicago found that toxoplasmosis, a relatively harmless parasitic infection carried by an estimated 30 percent of all humans, is associated with intermittent explosive disorder and increased aggression.

The findings are published in the Journal of Clinical Psychiatry on March 23, 2016.

“Our work suggests that latent infection with the toxoplasma gondiiparasite may change brain chemistry in a fashion that increases the risk of aggressive behavior,” said senior study author Emil Coccaro, MD, Ellen. C. Manning Professor and Chair of Psychiatry and Behavioral Neuroscience at the University of Chicago.

“However, we do not know if this relationship is causal, and not everyone that tests positive for toxoplasmosis will have aggression issues,” Coccaro said, adding that additional studies are needed.

Intermittent explosive disorder (IED) is defined by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, as recurrent, impulsive, problematic outbursts of verbal or physical aggression that are disproportionate to the situations that trigger them. IED is thought to affect as many as 16 million Americans, more than bipolar disorder and schizophrenia combined.

As part of their pioneering research to improve diagnosis and treatment for IED and impulsive aggression, Coccaro and his colleagues examined possible connections to toxoplasmosis, an extremely common parasitic infection. Transmitted through the feces of infected cats, undercooked meat or contaminated water, toxoplasmosis is typically latent and harmless for healthy adults. However, it is known to reside in brain tissue, and has been linked to several psychiatric diseases, including schizophrenia, bipolar disorder and suicidal behavior.

The research team recruited 358 adult subjects from the U.S., who were evaluated for IED, personality disorder, depression and other psychiatric disorders. Study participants were also scored on traits including anger, aggression and impulsivity. Participants fell into one of three groups. Roughly one third had IED. One third were healthy controls with no psychiatric history. The remaining third were individuals diagnosed with some psychiatric disorder, but not IED. This last group served as a control to distinguish IED from possible confounding psychiatric factors.

Hold your cats

The research team found that IED-diagnosed group was more than twice as likely to test positive for toxoplasmosis exposure (22 percent) as measured by a blood test, compared to the healthy control group (9 percent).

Around 16 percent of the psychiatric control group tested positive for toxoplasmosis, but had similar aggression and impulsivity scores to the healthy control group. IED-diagnosed subjects scored much higher on both measures than either control group.

Across all study subjects, toxoplasmosis-positive individuals scored significantly higher on scores of anger and aggression. The team noted a link between toxoplasmosis and increased impulsivity, but when adjusted for aggression scores, this link became non-significant. This finding suggests toxoplasmosis and aggression are most strongly correlated.

However, the authors caution that the study results do not address whether toxoplasmosis infection may cause increased aggression or IED.

“Correlation is not causation, and this is definitely not a sign that people should get rid of their cats,” said study co-author Royce Lee, MD, Associate Professor of Psychiatry and Behavioral Neuroscience at the University of Chicago. “We don’t yet understand the mechanisms involved–it could be an increased inflammatory response, direct brain modulation by the parasite, or even reverse causation where aggressive individuals tend to have more cats or eat more undercooked meat. Our study signals the need for more research and more evidence in humans.”

Coccaro and his team are now further examining the relationship between toxoplasmosis, aggression and IED. If better understood, this connection may inform new strategies to diagnose or treat IED in the future.

“It will take experimental studies to see if treating a latent toxoplasmosis infection with medication reduces aggressiveness,” Coccaro said. “If we can learn more, it could provide rational to treat IED in toxoplasmosis-positive patients by first treating the latent infection.”

People with rage disorder twice as likely to have latent toxoplasmosis parasite infection

Adjunctive Use of a Standardized Extract of Withania somnifera (Ashwagandha) to Treat Symptom Exacerbation in Schizophrenia

22% of subjects with IED tested positive for the parasite

In the current study, the authors evaluated 358 adult Americans for IED, personality disorderdepression and other psychiatric disorders and gave them scores for traits such as anger, aggression and impulsivity. They also screened for toxoplasmosis using blood tests.

Fast facts about toxoplasmosis

  • Around 60 million Americans are thought to have toxoplasmosis
  • If a woman catches it just before or during pregnancy, it can be dangerous for the baby
  • For those with a weakened immune system, there are medications to treat it.

They then classified the participants into three groups: approximately one third had IED, one third were healthy controls with no psychiatric history, and one third had received a diagnosis for a psychiatric disorder but not IED.

The purpose of the last group was to enable the team to distinguish IED from other psychiatric factors.

Findings showed that 22% of those with IED tested positive for toxoplasmosis exposure, compared with 9% of the healthy control group and 16% of the psychiatric control group.

The psychiatric group and the healthy group had similar scores for aggression and impulsivity, but the group with IED scored far higher on both counts than either of the other two groups.

An association emerged between toxoplasmosis and impulsivity. However, when the team adjusted for aggression scores, this association became non-significant, indicating a strong correlation between toxoplasmosis and aggression.

The authors point out that the findings do not mean that toxoplasmosis causes IED, or that people with cats are more likely to have the condition. It simply reveals a relationship.

T. gondii infection ‘may double schizophrenia risk’

For one study, Dr. Robert H. Yolken, of the Stanley Laboratory of Developmental Neurovirology at Johns Hopkins University School of Medicine in Baltimore, MD, and colleagues assessed the results of two previous studies.

These studies had identified a link between cat ownership in childhood and development of later-life schizophrenia and other mental disorders, comparing them with the results of a 1982 National Alliance for the Mentally Ill (NAMI) questionnaire.

The NAMI questionnaire – conducted around a decade before any data was published on cat ownership and mental illness – revealed that around 50% of individuals who had a cat as a family pet during childhood were diagnosed with schizophrenia or other mental illnesses later in life, compared with 42% who did not have a cat during childhood.

The questionnaire, the researchers say, produced similar results to those of the two previous studies, suggesting that “cat ownership in childhood is significantly more common in families in which the child later becomes seriously mentally ill.”

“If true,” the authors add, “an explanatory mechanism may be T. gondii. We urge our colleagues to try and replicate these findings to clarify whether childhood cat ownership is truly a risk factor for later schizophrenia.”

In another study, A. L. Sutterland, of the Academic Medical Centre in Amsterdam, the Netherlands, and colleagues conducted a meta-analysis of more than 50 studies that established a link between T. gondii and increased risk of schizophrenia.

They found that people infected with T. gondii are at more than double the risk of developing schizophrenia than those not infected with the parasite.

The team also identified a link between T. gondii infection and greater risk of bipolar disorderobsessive-compulsive disorder (OCD) and addiction.

“These findings suggest that T. gondii infection is associated with several psychiatric disorders and that in schizophrenia, reactivation of latent T. gondii infection may occur,” note the authors.

The CDC recommend changing a cat’s litter box every day to reduce the risk of T. gondii infection, noting that the parasite does not become infectious until 1-5 days after it has been shed in the animal’s feces.

They also recommend feeding cats only canned or dried commercial foods or well-cooked meats; feeding them raw or undercooked meats can increase the presence of T. gondii in a cat’s feces.

It is important to note that cat feces are not the only source of T. gondii infection. Humans can contract the parasite through consuming undercooked or contaminated meats and by drinking contaminated water.

How a cat parasite can change your personality

A new study suggests that infection with the cat-borne parasite Toxoplasma gondii could make people more risk-prone and likely to start their own business.
cute kitten

Your cute cat may host a parasite that could influence your behavior in surprising ways.

As humans who still inherit Enlightenment’s worship of rationality, we like to think that our decisions are autonomous and driven by reason alone.

However, science seems to contradict this popular belief. More and more research is showing that microorganisms such as bacteria and viruses influence our behavior and emotional states.

For instance, the bacteria in our guts may be responsible for states of anxiety and depression. Conversely, other studies have shown that some probiotic bacteria may relieve the effects of stress.

Now, a new study suggests that infection with the cat-borne parasite Toxoplasma gondii could make people change their behavior so that they become more prone to business and entrepreneurial ventures.

Stefanie K. Johnson, an associate professor at the University of Colorado (CU) Boulder’s Leeds School of Business, co-led the research in collaboration with Pieter Johnson, a professor in CU Boulder’s Department of Ecology and Evolutionary Biology.

The findings were published in the journal Proceedings of the Royal Society B.