Although psychiatric disorders are primarily considered brain diseases, the influence of the digestive system on brain health and the occurrence of mental disorders was first mentioned in traditional Chinese medicine, Ayurveda, and Hippocratic medicine. As nutrition has a great influence on the microbiological composition and function of the human intestine, the idea that nutrition can play a causal role in changes in the intestinal microbiome with an impact on human emotional and cognitive functions has become an exciting research topic in psychiatry, and the term nutritional psychiatry has been proposed.
Lack of macro- and micronutrients in early life can compromise the development of brain function. Previous research on the impact of nutrition on brain development has focused mainly on amino acids and micronutrients that are absorbed in the proximal small intestine. However, large molecules that are not absorbed in this way are gaining more and more importance. Their absorption depends on the metabolism of intestinal microbiota in the distal small intestine and large intestine. So the health benefit of these molecules depends on the composition of the intestinal microbiome. 
The so-called nutritional psychiatry developed from preclinical observations and epidemiological studies in which the connection between nutrition and mental health was determined. The results of these studies support the role of nutrition and the possibility of a beneficial role of dietary changes in various mental disorders. This includes Alzheimer's disease, depression, cognitive decline, and epilepsy, but the possibilities do not end there. Some research also points to the potential of dietary changes in autism, Parkinson's disease, anxiety, etc. 
There are three pathways of communication between the gut microbiome and the brain. These are the neural, immunoregulatory, and endocrine pathways. The central nervous system directly influences the composition and function of the microbiome through the autonomic nervous system, or indirectly through the regulation of gastrointestinal (GI) motility and transit, mucus secretion and intestinal barrier permeability, and luminal release of neurotransmitters. 
Neuroendocrine communication channel
In preclinical studies, it has been shown that many microbes can produce metabolites (from body secretions, food components, or chemical substances) that affect brain function. One such process is the conversion of the amino acid tryptophan into metabolites that play an important role in neuroendocrine signaling by neuroimmune mechanisms. Tryptophan is a precursor of serotonin and other important metabolites. .
About 95% of the serotonin in the body is produced and stored in the ECC (enteroendocrine cells) and plays an important role in modulating the activity of the enteric nervous system and in signaling to the brain via different subtypes of vagal afferents that form synaptic contacts with the ECC. Microbial metabolites stimulate serotonin production and release by ECC. While serotonergic neurons located in the brainstem play an important role in the regulation of functions such as sleep, food intake, mood regulation, and pain, gut-based serotonin plays an important role in gastrointestinal motility and secretion .
Kynurenine is also an important Trp metabolite. In a rodent model of chronic variable stress, higher brain kynurenine concentrations were correlated with increased depression-like behavior. This behavior is reduced by the use of Lactobacillus, which regulates the synthesis of kynurenine. Kynurenine, which can cross the blood-brain barrier, has been shown to cause neuroinflammation and neurodegeneration, which has also been reported in Alzheimer's disease and depression .
Another type of Trp metabolites is indoles, which are produced exclusively by intestinal microbes since only certain microbes possess the enzyme tryptophanase necessary for their production from Trp. Although many indoles are known to positively affect both systemic and intestinal homeostasis, preclinical studies have shown that some indole metabolites may also have negative effects on brain health, such as inducing depression-like behavior. Indoles are precursor molecules for many compounds critical to brain health and function. They have been detected in the GI tract, brain, and systemic circulation. One such metabolite, indoxyl sulfate, may play a role in the pathophysiology of several brain disorders, including Alzheimer's disease and depression. 
Interactions of gut microbes with dietary tryptophan that lead to the generation of multiple neuroactive metabolites, some of which have been implicated in several brain disorders, clearly demonstrate the intricate relationship between diet, the gut, and certain gut microbes and brain disease.
The immune communication channel
There is a close link between immune activation in the gut and neuroinflammation in the brain, as the gut microbiome can directly influence the maturation and function of microglia in the CNS as part of immunoregulatory pathways. Microglia make up the majority of immune cells in the brain, and gut bacteria play an important role in their proper functioning. Dysregulation of microglia and gut microbial dysbiosis has been implicated in several psychiatric disorders, such as anxiety, depression, neurodegenerative disorders, such as Parkinson's and multiple sclerosis, and neurodevelopmental disorders, such as ASD. 
The close relationship between inflammatory signals originating from the gut in response to certain diets and the key roles of the gut microbiota in generating both pro- and anti-inflammatory signals highlight the important interactions between diet, the gut microbiome, and brain disease.
There are several ways in which nutrition promotes healthy brain structure and function, including the reduction and prevention of metabolic endotoxemia, neuroactive metabolites, and essential micronutrients.
Low-grade inflammation due to increased circulating endotoxins is called metabolic endotoxemia. Dietary factors that increase the relative abundance of these anti-inflammatory and other health-promoting bacteria include prebiotics. Several clinical studies have shown the beneficial effects of a diet rich in prebiotics on the diversity and richness of the gut microbiome, and the reduction of systemic immune activation. Such Mediterranean-like diets can promote healthy brain function as demonstrated in a variety of dietary intervention trials in depression and cognitive decline .
Omega-3 fatty acids and zinc may have important effects on brain development and function independently of the gut microbiome. Nutrients obtained from the diet, such as vitamins, minerals, polyunsaturated fats, and amino acids, support healthy brain function. Many of these nutrients serve as cofactors for enzymes, supporting neurotransmitter synthesis, myelination, cell signaling, and metabolic pathways. Several specific nutrients have been extensively studied for their antidepressant effects, such as omega-3 fatty acids, folic acid, s-adenosyl-methionine, inositol, and vitamins B3, B6, and C, and may even be beneficial when added to supplements, but only if as a supplement to a gut-healthy diet. Furthermore, low omega-3 fatty acid intake has been linked to mental illnesses such as depression.
In summary, a healthy diet rich in fiber, polyphenols, and micronutrients has been shown to have a positive effect on gut microbiota, reduce metabolic endotoxemia and neuroinflammation, and is associated with improved brain health. Fiber has been associated with improved health and brain function in several small observational and interventional studies .
Diet, the brain-gut-microbiome (BGM) system, and brain disorders.
In several psychiatric and neurological disorders, a connection between changes in diet and interaction of the BGM system has been observed.
Diet and depression
Recent studies show that patients with depressive disorders have an altered gut microbiome compared to healthy individuals. One study investigated the association between gut microbiota composition, depressive symptoms, and quality of life indicators. The study found that the bacterial species Flavonifractor is deficient in individuals with reduced physical functioning. The bacterial species Coprococcus and Dialister were positively associated with quality of life and are lacking in people with untreated depression. Participants with low Bacteroides levels showed a poorer quality of life and higher incidence of depression. 
Several mouse studies have shown that transferring the microbiome of a depressed individual to a healthy one can induce depressive behavior in the recipient. That indicates the possibility of a causative role of microbiota in the pathophysiology of depression. As a diet has an important influence on the gut microbiome, and changes in the gut microbiome have been linked to depression-like behaviors, the diet has emerged as a potential treatment strategy for depression. The study found evidence for a statistically significant relationship between unhealthy eating patterns and poorer mental health, as well as for quality nutrition and better mental health in children and adolescents. 
However, in cross-sectional studies, there are no conclusions about the relationship between diet and mental health. The reason can be that subjects with depressive disorders eat more unhealthy food to self-medicate. Another possible reason is the influence of early eating habits on brain development. There is evidence that nutrient-poor diets can lead to nutrient deficiencies, which are linked to mental health problems. Folate, zinc, and magnesium intakes are inversely associated with depressive disorders, while omega-3 fatty acids are inversely associated with anxiety disorders. 
Yet, several studies have confirmed a correlation between mental well-being and a healthy diet rich in fresh fruits, vegetables, and whole grains. The benefits of a plant-based diet in depression are anti-inflammatory effects due to increased production of short-chain fatty acids and polyphenols and improvement of intestinal permeability. That leads to a reduction in metabolic endotoxemia. Increased intake of omega-3 fatty acids and minerals can alleviate deficiencies in nutrients for mood and brain health. 
Diet and Alzheimer’s disease
Studies have pointed to a neural connection between the gut microbiome and areas of the brain affected by Alzheimer's disease.
Neuroinflammation, which precedes cognitive impairment and depends on the composition of the intestinal microbiome, is already associated with Alzheimer's disease. It has been shown that patients with this disease have reduced levels of systemic primary products of intestinal microbial metabolism and increased levels of various secondary products compared to healthy individuals, which is directly related to cognitive impairment and glucose mechanism in the brain. As bile acid synthesis is crucially dependent on dietary factors, and as secondary bile is generated by gut microbes, these findings suggest a possible role of diet and the gut microbiome in the observed changes in the relationship between primary and secondary products of gut microbial metabolism. Secondary levels were associated with the progression of mild-to-severe Alzheimer's disease symptoms and poorer cognitive function. 
Ketogenic diet and Alzheimer's disease
Clinical studies have shown a positive effect of the ketogenic diet on patients with AD or mild cognitive impairment. Preclinical findings from these studies indicated that diets that can induce high blood ketone levels may also improve cognition and memory in these patient groups. 
Diet and Autism
Autism spectrum disorder (ASD) is often combined with gastrointestinal symptoms, anxiety, and immune dysregulation. GI symptoms often associated with ASD include diarrhea, abdominal pain and discomfort, gastric reflux, and changes in bowel habits.
Several preclinical and clinical studies have revealed increased levels of inflammatory markers in the systemic circulation of individuals with ASD. Intestinal permeability has also been proven in these people. These observations, together with the common comorbidity of GI symptoms and anxiety, suggest that gut dysbiosis may be part of the underlying pathophysiology of ASD.
Several smaller studies have investigated nutrition as a treatment option for ASD. In one, 70 children with ASD participated, and the effect of a 12-month dietary intervention consisting of a gluten- and casein-free diet was examined. Improvement was found for 81% of participants after three months. 
Microbial transfer therapy has emerged as a promising treatment approach for patients with ASD. A transplant of microbiota from a healthy donor is inserted into the patient. A study with children with ASD who underwent this therapy found significant reductions in GI and ASD symptoms. Also, this study confirmed favorable changes in the abundance of beneficial bacterial strains, including Bifidobacteria, Prevotella, and Desulfovibrio. This study indirectly suggests that dietary manipulation of the gut microbiome may have a therapeutic effect mediated by gut microbes. 
Diet and Epilepsy
Intestinal dysbiosis can be included in the pathophysiology of epilepsy. That makes the ketogenic diet a potential therapy that may have antiepileptic effects. The study in mouse models of epilepsy showed that a ketogenic diet protected against refractory epileptic seizures only in mice colonized with a specific gut microbiota compared to mice treated with antibiotics. The underlying mechanism involved a change in microbial abundance, which led to a decrease in GABA synthesis in the periphery, while an increase in GABA in the CNS showed an anti-seizure effect. 
The study of 14 children with drug-resistant epilepsy and 30 healthy individuals showed that a week-long ketogenic diet led to a 50% reduction in seizure frequency in infants, which was associated with reduced levels of Proteobacteria and increased levels of beneficial strains of Bifidobacterium, Bacteroides and Prevotella compared to baseline, correlated with suppression of seizure activity. 
The results of studies examining the role of nutrition in improving psychiatric disorders remain mixed. However, one of the main challenges of nutritional psychiatry research is to gradually change the prevailing way of thinking that psychiatric disorders are diseases of the brain and do not involve the gut and its microbiome. Educating mental health professionals about the critical role of nutrition and its impact on brain-gut microbiome interactions is necessary to make progress in this area of psychiatry.
There is emerging evidence that diet has a major modulatory influence on brain-gut-microbiome (BGM) interactions with important implications for brain health and for several psychiatric disorders including depression.
Interested how changing you’d diet can improve your BGM and reduce symptoms such as fatigue, depression, and anxiety? Call CPC @ 561-531-7818 to make an appt with Jessica Coote, APRN, Weight Management And Holistic Approach Specialist.
A technIcal primer on Over-The-Counter Pregnenolone vs Prescription Allopregnanolone and Their Use in Psychiatric and Pain Disorders
Pregnenolone (PREG) is a prohormone synthesized in the adrenal glands. It is called a prohormone because it is a precursor to other hormones such as cortisol, estrogen, testosterone, and progesterone. Given it affects many chemical processes and chemicals in the brain, it has an important role in psychiatric diseases including postpartum depression, major depression, and post-traumatic stress disorder (PTSD). 
PREG is also a neurosteroid. More broadly, steroids affect cellular functions by binding to cytosolic and nuclear receptors that bind to DNA and induce changes in gene transcription. More specifically neurosteroids are most often synthesized from cholesterol in the CNS independently of the endocrine system. Neurosteroids pharmacologically modulate neurotransmission by non-genomic mechanisms through specific interactions with neurotransmitter receptors. Pregnenolone modulates N-methyl-D-aspartate (NMDA), γ-aminobutyric acid type A (GABAA), glycine, and calcium-permeable transient receptor potential (TRP) channels. PREG stimulates the trafficking of functional NMDA receptors to the cell surface at relatively low nanomolar concentrations, resulting in a delayed onset of potentiation of the NMDA response, consistent with its overall role as a potentiator of excitatory synaptic activity. PREG likely plays a significant role in the modulation of glutamatergic excitatory synaptic transmission that underlies learning and memory. The burden of evidence supports PREG as an antidepressant and cognitive enhancer for a range of neurological disorders. 
INTRAVENOUS ALLOPREGNANOLONE (APREG)
One of the most important applications of the neurosteroid allopregnanolone (APREG) is the treatment of postpartum depression (PPD). APREG is one of the many derivatives of PREG. Confusing as it is, APREG is called brexanolone when used as a medication and Zulresso when marketed by the drug company. For our purposes we will refer to all of the above as APREG.
APREG has neurogenetic, neuroprotective, antidepressant, and anxiolytic effects. Decreased levels of APREG are associated with major depression, anxiety disorders, premenstrual dysphoric disorder, and Alzheimer's disease.  In trials for the treatment of postpartum depression, APREG yielded positive results as a positive modulator of the GABAA receptor. [2,3,4] APREG is thought to mimic the progesterone metabolite that fluctuates after childbirth). 
In one study, two double-blind, randomized, placebo-controlled phase 3 trials were conducted at 30 clinical research centers and specialized psychiatric units in the United States. Eligible women were aged 18-45 years, with postpartum depression and qualifying Hamilton Depression Rating Scale (HAM-D). At the end of the study, the administration of APREG injection for postpartum depression resulted in a significant and clinically significant reduction in the HAM-D total score compared to placebo. APREG is a drug with a rapid onset of action and a sustained response to treatment during the study period. The results suggested intravenous APREG therapy has significant potential in treating women with with postpartum depression.  The rapid onset of action of APREG is faster than most FDA-indicated treatments and may lead to improved quality of life for both mother and child. APREG was designated a breakthrough treatment by the FDA and is a 2019 FDA-approved drug for PPD.
ORAL PREGNENOLONE (PREG)
Although allopregnanolone (APREG) is currently only available as a prescription intravenous therapy, APREG levels also increase with the use of pregnenolone (PREG). Pregnenolone is available as a non-prescription-needed or over-the-counter drug. The usual therapeutic dose is 50 or 100 mg, taken early in the morning. Certainly, pregnenolone therapy should be under the supervision of a doctor.
Pregnenolone and Mood:
In a clinical trial comparing PREG with placebo (19 PREG subjects, 18 placebo subjects), PREG supplementation resulted in significantly greater reductions in depressive symptoms in mono- and bipolar depressed patients with a history of substance abuse.
Pregnenolone was also studied in a 2014 study. It has been used at a dose of 500 mg per day for 12 weeks in patients suffering from bipolar depression. The comparison group received a placebo. Depression remission rates were higher in the PREG group (61%) compared to the placebo group (37%). The authors concluded that the results suggest that PREG can improve symptoms of depression in patients with bipolar disorder and that it can be safely administered because it is well tolerated. 
Steroid compounds may act as neuromodulators in various functions of the central nervous system. One study analyzed the levels of the neuroactive steroids pregnenolone and progesterone, as well as the neuropeptide diazepam binding inhibitor from the cerebrospinal fluid obtained by lumbar puncture from 27 people with affective illness vs 10 healthy volunteers. Subjects with a mood disorder who were clinically depressed had a lower cerebrospinal fluid (CSF) PREG compared with healthy volunteers. In addition, PREG was lower in all affectively ill subjects, regardless of mood state at the time of lumbar puncture, than in healthy volunteers. No differences were found for progesterone or neuropeptide diazepam binding inhibitor levels by mood state or diagnosis. The study authors concluded that CSF PREG is reduced in individuals with affective illness, particularly during episodes of active depression. 
Pregnenolone and Pain:
Ninety-four war veterans with chronic low back pain participated in the research in North Carolina. Pregnenolone and placebo were administered in escalating doses of 100 mg for one week, 300 mg for one week, and 500 mg for two weeks. After only four weeks of treatment, there was a significant improvement in pain and mobility. Side effects were negligible. The authors of this study concluded that PREG might be a safe and potentially effective treatment for chronic low back pain. 
Pregnenolone for schizophrenia:
Use of pregnenolone has also produced positive results in schizophrenia both in reducing negative and positive symptoms, while simultaneously increasing serum levels of PREG, PregS, AlloP, DHEAS, and progesterone. 
Highly sensitive and specific methods are starting to elucidate different steroid metabolomes. Multiple studies have reported more significant changes in PREG than other steroids in extra physiological or pathological conditions, suggesting that PREG plays a highly functional role.  Beneficial effects of oral PREG have been demonstrated in preclinical and clinical studies but do they compare to the intravenous APREG treatment that has been FDA approved? Only time will tell as more evidence emerges. Drug and administration costs for APREG are over $38,000  whereas a bottle of PREG may cost less than $20. At this time, PREG is highly accessible to patients as an over-the-counter nutraceutical, and we predict its use will rapidly increase given its unique mechanism that is unlike most prescription and over-the-counter therapies. Therein, both providers and interested patients should understand the differences between the risks/benefits of both therapies.
Please consult your psychiatric provider before treatment with any therapy. If you need a psychiatric provider in the state of Florida, please visit www.cpc.care or call 561-531-7818
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2. ZULRESSO Prescribing Information. Cambridge, MA: Sage Therapeutics, Inc; 6/2019.
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4. Powell JG, Garland S, Preston K, Piszczatoski C. Brexanolone (Zulresso): Finally, an FDA-Approved Treatment for Postpartum Depression. Ann Pharmacother. 2020 Feb;54(2):157-163. doi: 10.1177/1060028019873320. Epub 2019 Sep 3. PMID: 31476884.
5. Meltzer-Brody S, Colquhoun H, Riesenberg R, Epperson CN, Deligiannidis KM, Rubinow DR, Li H, Sankoh AJ, Clemson C, Schacterle A, Jonas J, Kanes S. Brexanolone injection in post-partum depression: two multicentre, double-blind, randomised, placebo-controlled, phase 3 trials. Lancet. 2018 Sep 22;392(10152):1058-1070. doi: 10.1016/S0140-6736(18)31551-4. Epub 2018 Aug 31. Erratum in: Lancet. 2018 Sep 29;392(10153):1116. PMID: 30177236
6. Edinoff AN, Odisho AS, Lewis K, Kaskas A, Hunt G, Cornett EM, Kaye AD, Kaye A, Morgan J, Barrilleaux PS, Lewis D, Viswanath O, Urits I. Brexanolone, a GABAA Modulator, in the Treatment of Postpartum Depression in Adults: A Comprehensive Review. Front Psychiatry. 2021 Sep 14;12:699740. doi: 10.3389/fpsyt.2021.699740. PMID: 34594247; PMCID: PMC8477036.
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By Mike Makosiej
Anxiety Couples/Marriage Depression General
alone coffee at the cornerstone depression gracelessness ketamine infusion treatment mental health Seasonal Affective Disorder stress therapy
We have this awesome coffee pot at our office, though once I describe it, your opinion of it may differ. It has this unique trait that when you pour it, for some reason, it spills out coffee unless you pour it very carefully and slowly. Today, as I prepared and made my morning coffee, it struck me that the pot pours perfectly fine if you just take the time it requires of you to pour carefully. If you pour with patience, you are rewarded with a delicious cup of coffee; but pour too quickly and a mess soon follows. What prompted this line of thought this morning was what I have often called ‘gracelessness’. Sometimes there are days when I feel clumsy: I spill things, drop things, and generally can’t get into a groove. Today, that was me. I spilled coffee, dropped my keys, lost my glasses, dropped a clock on the floor – you get the idea. I was relying too much on myself. Has that ever happened to you? You feel like all gracefulness is gone or lacking and everything you do is a struggle or in some way a difficult hindrance? This blog attempts to marry those unique ideas and provide some autumnal reflections.
I love the fall. Even though down here the leaves don’t change like they used to when I lived up North, I still like to make a hot coffee latte and reflect on changing seasons. Today, as we reflect on patience and gracefulness, it occurs to me that sometimes in the autumn of our lives, we can struggle with patience and grace in a different way than we might when we’re younger or in a different phase of our lives. It’s easy, afterall, to feel impatient when you feel as though your youth is dwindling. You’re not alone in feeling like your best days are behind you. That feeling of nostalgia can really get to you. But if you focus too much on what was, and not enough on what can be, you may find it difficult to slow down and reflect.
How do I ‘slow down’?
Think about that quirky coffee pot for a moment. If you take your time to pour yourself a cup of Joe, you end up with the perfect cup; if you rush, you spill it everywhere. Slowing down can be difficult, especially when you feel like you need to keep going to stay with-it or fresh. That’s not always the case, however. Sometimes, when our bodies seem a half-second off from our brains, what we need most is to slow down for a minute. Slowing down isn’t simply you picking up your keys in slow-motion, but rather, you taking the time to pause and reflect on the many blessings you have. During moments of gracelessness, that’s when I find I most need to reflect on how it is a miracle that I accomplish anything at all when relying solely on my own abilities. If you take the time to be thankful for what you have and the many blessings present in your life, oftentimes, that’s the key to slowing down for a moment.
What if I’m depressed or feel like I can’t break free from this ‘gracelessness’?
You might be thinking, gee Mike, sounds great but no. I get it. Depression is real. And over prolonged periods, it can effect you in deep ways. Gracelessness can add up, after all. It can become a part of your mindset; it can bring about a deep depression. You aren’t alone in this. Countless people struggle with depression and anxiety. You might have even tried a combination of therapy and anti-depressants to no avail. This is also not as uncommon as you might think. In fact, many people come to our clinic for that exact reason! We specialize in treatment resistant depression. Our therapists work with countless patients who struggle to overcome their depression. Our nurses and psychiatrists specialize in innovative treatments, such as ketamine infusion therapy and Spravato, in order to help those who suffer most from depression and suicidal ideations and ensure they are cared for with the utmost sensitivity.
Why all this coffee talk?
Aside from being one of Justin and Marc’s favorite beverages, our coffee pot really is quirky. In other news, however, we at Cornerstone are going to be releasing a podcast designed to address a lot of the common issues you face each and every day. Coffee at the Cornerstone is our attempt to continue to provide a service to you whilst also encouraging the growth of this community we are dedicated to building with you. In the new year, we’ll be releasing our new podcast, and we look forward to including you as a part of our community!
By Mike Makosiej;
Posted: October 11, 2021
Categories: Anxiety Depression Trauma / PTSD, anxiety, counseling, depression, ketamine infusion treatment, mental health.
Tags: Seasonal Affective Disorder, therapy, vitamin infusion therapy
Coping with life’s lemons...Make lemonade?
How many times have you heard that, or has someone you know tried to make you feel better by saying such platitudes? The fact is that when you’re struggling with anxiety and depression, the last thing you need is trite platitudes. Just as you might struggle to cope with depression, you may also be struggling with anxiety. You might worry about how you’re going to pay the bills, if your children are safe, if you can truly forgive your spouse or loved one for possible indiscretions. These are common problems that face most modern-day Americans. But anxiety and depression, at their heart, can also be so much more than that. You may feel like you don’t belong or struggle with feelings of worthlessness; at the same time, you may worry that because you’re not feeling any better, that there’s something inherently wrong with you.
This could not be farther from the truth!
In previous blogs, our partner's at Cornerstone Counseling have discussed the many difficulties that you face when dealing with and coping with depression. We at Cornerstone recognize the many struggles you might be dealing with when it comes to anxiety and depression, and we want you to know that we’re here to help. At their root, anxiety and depression are many times co-occuring conditions. Evidence-guided research suggests that both can be treated together.
What strategies can I use to help deal with these struggles?
There are a number of effective strategies that can be used to help you cope with these co-occurring conditions:
Uncontrollable crying for no reason was my sign. The slap in the face I needed to finally admit I needed help. But let me back up and start from the beginning.
I used to be the happy girl. If you asked my friends, the first thing they would say was that the party didn’t start until I walked into the room. I was the vivacious smiling girl, bubbling over with enthusiastic excitement. It was always easy for me to walk into a room full of strangers and befriend them. I woke up happy, with or without a boyfriend. I loved waitressing and bartending all through school and, after graduation, I loved nursing even more. I was 33 when my husband died, but I pressed on and fell in love and suffered break-up’s more than once. I don’t say this to brag; rather, I say this to explain who I used to be before my dark depression.
I had never experienced depression before. Sure, I had had sad moments and I had experienced grief, but neither were depression. In my early 20’s I struggled with PMDD (premenstrual dysphoric disorder), when my PMS turned me into an irritable, angry person for a few days every month. Thanks to an advertisement in a magazine, I tried Sarafem (aka Prozac/fluoxetine) for a brief time, and once again my life was sunshine and rainbows ... until it wasn't.
I met my future ex-husband on Labor Day of 2017, and we were married exactly one year later. I was blissfully happy but, apparently, I had ignored the signs that he never was … less than a year later, I found myself divorcing the man of my supposed dreams. My second year of graduate school was suddenly becoming insanely difficult. I was diagnosed with ADHD that had gone unnoticed my entire life. I have since learned that depression and anxiety are closely linked to ADHD because our disability is a glaring reminder of our seeming ineptitude as compared to our 'normal' or 'neurotypical' peers. My life seemed to be unraveling before my eyes. The 4.0 honors student in me was now struggling to cope every day, lacking any sense of purpose, sad for no tangible reason, avoiding friendships, and nearly failing grad school.
My brain believed that the ‘nurse’ in me had failed. I felt beyond embarrassed and ashamed of my inability to accept and overcome my increasingly depressed mood. My psychiatrist prescribed Prozac again since it had once worked but, as is not uncommon, it let me down the second time around. (This is often referred to as the 'poop-out syndrome'). Then he prescribed Wellbutrin, then Lexapro, then Pristiq, all with sub-effective results and miserable side effects (insomnia, headaches, fatigue, sexual side effects, etc.).
But one day, I remembered how Ketamine infusions had changed a former colleague's life. Firsthand, I had witnessed her practically overnight transition from near catatonic depression to happiness. That was the day I picked up the phone and spoke to Jessica, my former colleague and current dear friend, who worked at the same Ketamine clinic my friend had visited (Cornerstone Psychiatric Care). When I expressed hesitation at the cost for Ketamine infusions, which she recommended as the gold standard for depression and PTSD, I will never forget what Jessica said to me: “Sure, you might be better on your own in a year ... but do you really want to waste a year of your life being depressed? How much is your life worth to you?”
You see, dear reader, at this point and for the first time in my life, I suddenly understood the meaning of the word ‘depression’. Despite what you may think, mine was no ‘situational’ depression; it had persisted for over one year before it became impossible for me to pretend anymore. My passive suicidal ideation was growing by the day and, while my pride refused to share the extent of my seemingly shameful secret with even my bestest of friends, I was suddenly overcome by the seriousness of it all. And so, as a last-ditch effort, I decided to try Ketamine infusions.
To this day there do not exist adequate words to express my gratitude at Jessica and Dr. Ettensohn's compassion during what I perceived to be my flawed state of depression. Realize that I was the nurse who encouraged patients to seek help; yet that same nurse in me so arrogantly lacked the courage to take my own advice until it was almost too late. Their kind-hearted empathy made all the difference in my sad heart.
During his amazing TED talk, "Depression, The Secret We Share," Andrew Solomon so presciently stated, "... but the brain lies". To this day, when I listen to his incredibly perceptive talk, I still shed tears at the realization of how close I came to giving up … but my tears turn to sobs when I ponder the mental struggles endured by so many others; by patients whose faces I can’t forget who have cried in front of me. And then I weep for people I will never know for whom the struggles were unendurable, and for the loved ones I have lost including my beloved nephew, and my niece's husband.
In the very near future, the USA will witness the FDA's approval of Ketamine, as it has already approved its stepsister, intranasal Esketamine. When this happens, and I promise you that it will as evidence-based research concurs, I hope against hope that other depressed individuals, as I once was, will be educated regarding this fast-working life-saving treatment option. That their psychiatrists or psych NP's, or their family and friends, will suggest and encourage them to try Ketamine. That people will learn how Ketamine infusions are currently being used in select Emergency Departments nationwide for patients presenting with suicidality. How on earth do we expect depressed and often suicidal patients to wait 4-6 weeks for an antidepressant to work?
I am writing this in an effort to stop the shame associated with depression and mental illness. There is a reason that you are still reading my experience and so I implore you to grab onto this life preserver called Ketamine ... because it will undoubtedly save your life as it once did mine.
-- [Cornerstone Psychiatric Care removed the patient’s name and contact for compliance purposes.]
If you or your loved one suffers from mental illness, give us a call at (561) 531-7818 or email us at firstname.lastname@example.org to learn more about how ketamine can help.
Obsessive compulsive disorder (OCD) is a diagnosis that has been subject to frequent indiscriminate use outside the mental health field; however, The National Comorbidity Survey Replication estimates lifetime prevalence of OCD to be 2.3 percent in a 2010 study by Ruscio AM et al.
OCD is defined by the presence of obsessions, compulsions or both. Obsessions are defined as recurrent, persistent thoughts that are intrusive and unwanted. They can include things like fear of dirt and/or contamination by germs, fear of causing harm to another, fear of thinking evil thoughts, and the need (obsession) for order, symmetry, or exactness. Those suffering from OCD often attempt to ignore or suppress such thoughts but find it difficult to do so. Compulsions are defined as behaviors or mental acts (like counting or repeating words) that the person feels driven to perform in response to an obsession. These compulsions can be attempts at reducing anxiety/distress but are excessive. Often times, patients diagnosed with obsessive compulsive disorder have obsessions or compulsions that last on average at least one or more hours per day.
Patients with OCD frequently take selective serotonin reuptake inhibitors (SSRIs) such as fluvoxamine, fluoxetine, sertraline, or citalopram. Such SSRIs have been a boon to OCD patients, however response can take up to several months and dosages often have to be quite high, leading to increased risk of unpleasant side effects.
In 2013, Rodriguez et al. examined ketamine treatment for OCD patients who were not taking standard treatment with serotonin reuptake inhibitors. Although the study only involved 15 patients the design was randomized, double-blinded, placebo-controlled, and utilized patients with "near constant obsessions". Results from this study showed that 50% of the patients receiving ketamine met criteria for treatment response, while 0% of those who did not receive ketamine met this same criteria. In this case, “treatment response” meant a 35% reduction in OCD symptoms, including things like: distress from obsessive thoughts, time occupied by obsessive thoughts, amount of control over obsessive thoughts and effort put forth to resist obsessions amongst other OCD symptoms.
Perhaps more striking, however, is that Rodriguez et al. published some patient reactions to the remarkable effects of ketamine:
Psychotherapy, and in particular a type of cognitive behavioral therapy called exposure therapy, has always been considered a major and necessary treatment for OCD patients. After receiving ketamine treatments, exposure therapy may help OCD patients maximize their therapeutic gain. Given ketamine may help facilitate neuroplasticity, or the brain's ability to form new connections, patients often times find ketamine and therapy to be synergistic when used in conjunction.
As of now, a ketamine protocol similar to that used with major depressive disorder is used when treating OCD. This protocol has provided relief to many patients suffering with OCD. Further studies will be helpful in elucidating a standard protocol that may be more specific to obsessive-type and compulsive-type OCD. This may be sooner rather than later as multiple OCD related ketamine trials are currently underway.
If you or your loved one suffers from continued symptoms of Obsessive Compulsive Disorder following interventions from your psychiatrist, psychologist, or other mental health provider, give us a call at (561) 531-7818 or email us at email@example.com to learn more about how ketamine can help with OCD.
Major Depression (Major Depressive Disorder) is one of the most common mental health disorders, but how often are we working up sleep as a cause or contributing factor? A large epidemiologic study by Ford DE et al in 1989 found that at least 40% of patients with either insomnia or hypersomnia had a concurrent psychiatric disorder, such as depression. Along the same lines, more complicated sleep disorders such as obstructive sleep apnea and restless leg syndrome are more likely to be found in the population of depressed patients compared to the general population.
Evidence suggests a bidirectional relationship between common sleep disorders and depression, meaning that one may elevate the risk for the other. Although we do not understand the exact mechanisms, sleep seems to ‘clean the brain’ at night (Xie et al. 2013); depression can lead to worsening cognitive function. It is hard to deny that improving sleep is important for brain health and for alleviating depressive symptoms! In fact sleep studies demonstrated that after patients were treated for depression, there were positive brain changes on polysomnography and electroencephalogy. In such studies, slow wave sleep (what we will term "good" sleep) is increased and REM sleep (what we will term "not-as-good" sleep) is decreased.
Interestingly, antidepressants have been linked to decreased total REM sleep. Although some antidepressants play a positive role in sleep disorders, it is important to talk to your psychiatrist about the positive and negative effects of your antidepressant on any given sleep disorder. Some antidepressants may be more useful for certain types of sleep disorders but vary largely based on the type of sleep disorder. For example, extended release bupropion may worsen insomnia disorder but help regimented patients overcome hypersomnia (sleeping too much) that accompanies circadian rhythm dysregulation. Bupropion may be more neutral and even beneficial for restless legs syndrome, whereas other antidepressants can worsen restless legs syndrome.
As more evidence becomes available regarding the importance of sleep, it is becoming more important for patients and physicians to become educated on sleep disorders. Because sleep disorders and depressive disorders both produce similar symptoms of excessive daytime sleepiness, fatigue, poor concentration, weight gain and irritability, among many others, we must not overlook sleep disorders before coming to the conclusion that depression is the only cause of such common symptoms.
An important note on obstructive sleep apnea: Although there many different types of sleep disorders, obstructive sleep apnea has a high prevalence in the general population and especially in depressed patients. It is worth noting that this sleep apnea frequently goes untreated and can be harmful to the brain over a long period of time. This disorder causes hypoxic episodes, meaning that your body and brain do not get enough oxygen for short periods of time. This is why patients with sleep apnea frequently have headaches in the morning. If you have depressive symptoms such as those mentioned in the paragraph above in addition to snoring, along with certain risk factors such as obesity, diabetes, hypertension and heart disease, you should consider talking with your doctor about a referral to a sleep physician or sleep study. In fact, you can find a number of sleep apnea screeners online such as http://www.stopbang.ca/osa/screening.php, but please remember that it is not diagnostic and only your physician can rule sleep apnea in or out.
If you suffer from continued depression despite following interventions from your sleep and/or other physician(s), give us a call at (561) 531-7818 or email us at firstname.lastname@example.org to learn about how ketamine can help with depression. Of note, ketamine is not a treatment for primary sleep disorders.
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