We've all heard of Gremlins, those little pesky but cute looking little monsters that run amok throughout our world. But what Ghrelins? All things being equal, this peptide that lives in our gut, tips off our brain to signal that it's lunchtime and the need for satiation shortly follows that lead. However, how often are all things equal . . .
The complexity of Anxiety and its links to PTSD
Ghrelin is a peptide hormone in our gut that signals our brain that we are hungry but it is also present in the hypothalamus, a part of the brain that initiates the fight or flight response. Research at the NCBI (National Center Biotechnology Information), points to Ghrelin as having an antianxiety/stress effect, so this research, highlighting its potential to facilitate PTSD, is a surprise, seemingly even to the researchers!
My point in focusing on this peptide though is for another reason, one related to emotional eating. Essentially the brain is a pharmacy but, we are not pharmacists and playing around with diets, drugs, alcohol, even chocolate perhaps all feed into this pharmaceutical anomaly? Ordinarily, ghrelin tells us when we are hungry and its cousin, leptin, lets us know when we are full. Some have speculated that there may be a deficiency in the leptin side of the equation, that allowed us to keep on eating, when in fact, we were already full. However, research on ghrelin is proving interesting because while it tells us we are hungry, it is also stimulated by stress. One hypothesis is that it helps to mitigate the effects of stress (an antianxiety effect), as in, it is a part of the counter stress process (relaxation response), initiated by the parasympathetic nervous system. It's as if Ghrelin may act as a kind of balancing system in restoring homeostasis. Albeit this research kind of throws a spanner in the works. However, if 46 soldiers were in a PTSD provoking situation, statistics say that 1 of those would develop PTSD. So, in that context, there may need to be further research.
Since stress, unless produced for the right reasons, e.g. danger or threat, has the potential to really play havoc with our lives, it seems logical that keeping stress under control is a good thing. Going back to my earlier statement about the brain being a pharmacy. Essentially we need to do some specific things in order to let the pharmacy regulate itself and we can go on and have a happy life. But what do we need to do to make this happen? The answer, to some extent, lays in Maslow's hierarchy of needs, specifically, the basic needs, air, liquids, food. Providing we breathe properly, as in diaphragmatically, not just as an anti-anxiety procedure but all the time. Liquids hydrate the brain and the body and this is critical for normal brain/body function. Lastly food, food is the way we put into the brain the 9 amino acids that the brain cannot synthesise. Amino acids play a critical role in protein synthesis and are the essential building blocks of the pharmacy in our head.
When it comes to what we do after our pharmaceutical supply chain has been satisfied, relaxation is the order of the day and nothing can help you to relax more than hypnosis, although meditation comes a close second. The challenge for most people though, is that meditation is a lot harder to master! Apart from its ability to help you be calm, hypnosis is also uniquely able to help you unravel the life events that are causing the particular issue that is blighting your life. From there a solution is found and applied and normal service can be restored!
Hypnosis is a proven and effective way to achieve change at the level of your brain. Hypnotherapy can effectively rewrite the neural code that changes the way memory, or memories, expresses themselves, change that, and you change everything! Once these memories have been rewritten, the new neural code becomes mostly permanent.
Hypnotherapy stands out as one of the most effective strategic life management methods there is, especially in its ability to promote clear thinking and good states of mental wellness. The behaviours that make life challenging are often a result of too much stress, too little sleep and too little by way of clarity! So, to get or take back control of your mind and your life, it makes perfect sense to use a methodology that addresses the subconscious mind's role in perpetuating negative, vague and ambiguous states of mind. Hypnosis helps us to create calm relaxing states of mind that make life work better! If you would like to address any concerns you have in this direction, or, if you just want to make your life feel better, then why not make an appointment for a Free Consultation? Hypnosis gives you the ability to have a good life!
The objective here is to help people understand how and why we become illogically trapped into irrational emotional experiences that may actually be happening for reasons different to that which we would imagine! If you want to know more about how Hypnotherapy can help you; why not make an appointment for a Free Consultation?
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The Research:
About a dozen years ago, scientists discovered that a hormone called ghrelin enhances appetite. Dubbed the "hunger hormone," ghrelin was quickly targeted by drug companies seeking treatments for obesity -- none of which have yet panned out.
MIT neuroscientists have now discovered that ghrelin's role goes far beyond controlling hunger. The researchers found that ghrelin released during chronic stress makes the brain more vulnerable to traumatic events, suggesting that it may predispose people to posttraumatic stress disorder (PTSD).
Drugs that reduce ghrelin levels, originally developed to try to combat obesity, could help protect people who are at high risk for PTSD, such as soldiers serving in the war, says Ki Goosens, an assistant professor of brain and cognitive sciences at MIT, and senior author of a paper describing the findings in the Oct. 15 online edition of Molecular Psychiatry.
"Perhaps we could give people who are going to be deployed into an active combat zone a ghrelin vaccine before they go, so they will have a lower incidence of PTSD. That's exciting because right now there's nothing given to people to prevent PTSD," says Goosens, who is also a member of MIT's McGovern Institute for Brain Research.
The lead author of the paper is Retsina Meyer, a recent MIT PhD recipient. Other authors are McGovern postdoc Anthony Burgos-Robles, graduate student Elizabeth Liu, and McGovern research scientist Susana Correia.
Stress and fear
Stress is a useful response to dangerous situations because it provokes action to escape or fight back. However, when stress is chronic, it can produce anxiety, depression and other mental illnesses.
At MIT, Goosens discovered that one brain structure that is especially critical for generating fear, the amygdala, has a specific response to chronic stress. The amygdala produces large amounts of growth hormone during stress, a change that seems not to occur in other brain regions.
In the new paper, Goosens and her colleagues found that the release of the growth hormone in the amygdala is controlled by ghrelin, which is produced primarily in the stomach and travels throughout the body, including the brain.
Ghrelin levels are elevated by chronic stress. In humans, this might be produced by factors such as unemployment, bullying, or the loss of a family member. Ghrelin stimulates the secretion of growth hormone from the brain; the effects of growth hormone from the pituitary gland in organs such as the liver and bones have been extensively studied. However, the role of growth hormone in the brain, particularly the amygdala, is not well known.
The researchers found that when rats were given either a drug to stimulate the ghrelin receptor or gene therapy to overexpress growth hormone over a prolonged period, they became much more susceptible to fear than normal rats. Fear was measured by training all of the rats to fear an innocuous, novel tone. While all rats learned to fear the tone, the rats with prolonged increased activity of the ghrelin receptor or overexpression of growth hormone were the most fearful, assessed by how long they froze after hearing the tone. Blocking the cell receptors that interact with ghrelin or growth hormone reduced fear to normal levels in chronically stressed rats.
When rats were exposed to chronic stress over a prolonged period, their circulating ghrelin and amygdalar growth hormone levels also went up, and fearful memories were encoded more strongly. This is similar to what the researchers believe happens in people who suffer from PTSD.
"When you have people with a history of stress who encounter a traumatic event, they are more likely to develop PTSD because that history of stress has altered something about their biology. They have an excessively strong memory of the traumatic event, and that is one of the things that drives their PTSD symptoms," Goosens says.
"This study breaks new ground by showing how ghrelin and growth hormone modulates the output of the amygdala, a brain area implicated in key affective symptoms of stress-related psychiatric disorders. These findings also hold considerable promise in designing new therapeutic strategies against the stress-induced increase in fear," says Shona Chattarji, a professor of neurobiology at the National Centre for Biological Sciences in Bangalore, India, who was not part of the research team.
New drugs, new targets
Over the last century, scientists have described the hypothalamic-pituitary-adrenal (HPA) axis, which produces adrenaline, cortisol (corticosterone in rats), and other hormones that stimulate "fight or flight" behaviour. Since then, stress research has focused almost exclusively on the HPA axis.
After discovering ghrelin's role in stress, MIT researchers suspected that ghrelin was also linked to the HPA axis. However, they were surprised to find that when the rats' adrenal glands -- the source of corticosterone, adrenaline, and noradrenaline -- were removed, the animals still became overly fearful when chronically stressed. The authors also showed that repeated ghrelin-receptor stimulation did not trigger the release of HPA hormones, and that blockade of the ghrelin receptor did not blunt the release of HPA stress hormones. Therefore, the ghrelin-initiated stress pathway appears to act independently of the HPA axis. "That's important because it gives us a whole new target for stress therapies," Goosens says.
Pharmaceutical companies have developed at least a dozen possible drug compounds that interfere with ghrelin. Many of these drugs have been found safe for humans, but have not been shown to help people lose weight. The researchers believe these drugs could offer a way to vaccinate people entering stressful situations, or even to treat people who already suffer from PTSD because ghrelin levels remain high long after the chronic stress ends. The researchers have applied for a patent for the use of anti-ghrelin treatments to treat and prevent stress-exacerbated psychiatric disorders.
PTSD affects about 7.7 million American adults, including soldiers and victims of crimes, accidents, or natural disasters. About 40 to 50 per cent of patients recover within five years, Meyer says, but the rest never get better.
The researchers hypothesize that the persistent elevation of ghrelin following trauma exposure could be one of the factors that maintain PTSD. "So, could you immediately reverse PTSD? Maybe not, but maybe the ghrelin could get damped down and these people could go through cognitive behavioural therapy, and over time, maybe we can reverse it," Meyer says.
Working with researchers at Massachusetts General Hospital, Goosens' lab is now planning to study ghrelin levels in human patients suffering from anxiety and fear disorders. They are also planning a clinical trial of a drug that blocks ghrelin to see if it can prevent the relapse of depression.
Story Source:
Materials provided by Massachusetts Institute of Technology. Note: Content may be edited for style and length.
Journal Reference:
- RM Meyer, A Burgos-Robles, E Liu, S S Correia, K A Goosens. Ghrelin–growth hormone axis drives stress-induced vulnerability to enhanced fear. Molecular Psychiatry, 2013; DOI: 10.1038/mp.2013.135
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