Thursday, 12 May 2016

Low Serotonin



Serotonin is a powerful brain chemical that profoundly affects your mood so knowing if you are deficient is a key first step to overcoming troubling mood and impulse control problems. Having one or more of these 8 serotonin deficiency symptoms will be a strong clue that you may indeed be serotonin deficient. Serotonin is one of the so-called inhibitory neurotransmitters that serves to balance any excessive excitatory (stimulating) neurotransmitter (like dopamine) firing in the brain. With adequate serotonin levels in the brain and its proper functioning, you will be positive, happy, confident, flexible, and easy-going. With low levels of serotonin, you will begin to display serotonin deficiency symptoms by becoming negative, obsessive, worried, irritable, sleepless or depressed.


PMS characterized by hypoglycemia, sugar carvings, sweet carvings, and/or depression

Make Peace with Your Blood Sugar

In the setting of diets high in refined carbs (flour) and sugar, and/or low cortisol from stress control of blood sugar and cellular energy burning may be disturbed. Cortisol is responsible for mobilizing stored sugar to the bloodstream and maintaining fat storage of sugar when it is unused in the blood stream. Thus, when it is low, one experiences everything that comes with hypoglycemia including:
•         Poor morning appetite
•         Night waking
•         Energized by eating
•         Forgetfulness
•         Need for caffeine, cravings for sugar
When cortisol runs high as it tends to in acute stress or the early stages of adrenal burnout, it promotes high blood sugar and symptoms of insulin resistance including:
•         Morning sugar cravings
•         Persistent hunger
•         Abdominal weight
•         Frequent urination
•         Fatigue after meals
•         Insomnia
•         Irregular periods
•         Acne
•         Body hair growth/head hair thinning



Protect Progesterone

 In functional medicine,  is referred to as a cumulative load of estrogen effects that outpace progesterone. This state is thought to underlie symptoms of PMS, per menopause, and some cases of postpartum psychiatric disorders. Estrogen can come from our environment in the form of xenoestrogens found in plastics, pesticides, and cosmetics. Its excretion can be impaired by abnormal gut flora and by poor methylation status/use of B vitamins. Stress, as referenced above, can lead to shunting of progesterone to make cortisol, called a pregnenolone steal. If the body determines that it is in a state of alarm, those stress hormones are more important than conception hormones!
In my practice, I start with, a mineral and phytonutrient-rich Peruvian vegetable that has adapt genic properties in supporting the signaling around hormone production, called the Hypothalamic Pituitary Axis. This root helps to support the body’s ability to produce and balance hormones, buffering the effects of the stress hormone cortisol as demonstrated .

Temperament-regulating Thyroid

While there is not a clear relationship between low thyroid function and PMS/PMDD, some  demonstrated thyroid “volatility” and increased the hormonal responsiveness of the gland. Intervention studies have focused on T4/levothyroxine, but it is T3, the active thyroid hormone that is active at the cellular level enhancing the functioning of every tissue and promoting adequate energy production. There is scientific speculation that low progesterone relative to estrogen may inhibit thyroid hormone uptake at the cell. When the above interventions are of limited yield, and there are other symptoms like cold intolerance, fatigue, cloudiness, weight fluctuations, constipation, and depression, thyroid is an important place to focus.
There are a number of single nutrients like Calcium,  These days, many women embark on conception and pregnancy apprehensive about the potential for postpartum depression or anxiety to descend upon them in those early, exhausting, new baby months.
Since the characterization and treatment of postpartum anxiety, depression, and psychosis remain largely incomplete, prevention is where it’s at.

Make Peace With Your Blood Sugar

In the setting of diets high in refined carbs (flour) and sugar, and/or low cortisol from stressed, control of blood sugar and cellular energy burning may be disturbed. Cortisol is responsible for mobilizing stored sugar to the bloodstream and maintaining fat storage of sugar when it is unused in the blood stream. Thus, when it is low, one experiences everything that comes with hypoglycemia including:
•              Poor morning appetite
•              Night waking
•              Abdominal weight
•              Frequent urination
•              Fatigue after meals
•              Insomnia
•              Irregular periods
•              Acne
•              Body hair growth/head hair thinning

Protect Progesterone




In functional medicine, is referred to as a cumulative load of estrogen effects that outpace progesterone. This state is thought to underlie symptoms of PMS, perimenopause, and some cases of postpartum psychiatric disorders. Estrogen can come from our environment in the form of xenoestrogens found in plastics, pesticides, and cosmetics. Its excretion can be impaired by abnormal gut flora and by poor methylation status/use of B vitamins. Stress, as referenced above, can lead to shunting of progesterone to make cortisol, called a pregnenolone steal. If the body determines that it is in a state of alarm, those stress hormones are more important than conception hormones

Feeling wired at night


A new, peculiar hybrid form of waking consciousness has been emerging in recent years. Because so many of us struggle nightly with inadequate sleep and dreams, we become chronically tired. At the same time, the excessive stimulation and hyperbole emblematic of modern life drives us to feel persistently wired. We are tired — simultaneously tired and wired.
Although it’s unnerving, being tired is the new normal for millions of us. I see tired people everywhere. Among my friends, family, neighbors, and colleagues. And in public figures such as politicians, celebrities, heroes and even cartoon icons (e.g., Homer Simpson). And I routinely encounter the ramifications of wired consciousness in most of my insomnia patients.
Despite their chronic struggles with poor sleep, people with insomnia commonly report feeling energized during the day. But they are quick to add that beneath the surface they also feel persistently tired — exhausted, spent, or fatigued. This incongruity has been examined scientifically. It turns out that, as a group, people with chronic insomnia actually appear to be less sleepy during the day than normal sleepers.
Research confirms that insomnia is commonly associated with hyper arousal, a kind of excessive, turbo-charged wakefulness. Hyper arousal is characterized by racing brain waves, a rapid heart rate, over heated core body temperature and dysfunctional hormonal rhythms — all of which serve to both hinder nighttime sleep and mask daytime sleepiness.
While hyper arousal strongly draws us upward, sleepiness and fatigue simultaneously drag us down. We are uncomfortably stretched, pulled painfully in opposite directions by equally potent forces. I think of this as the psychological equivalent of being on the rack. Not surprisingly, insomnia and hyper arousal are strongly linked to depression — which is commonly characterized by a persistent sense of feeling stuck.
We are stuck in relentlessness. Modern lifestyles impose a harsh, unremitting quality onto our days. We are deluged with information and entertainment options and virtually addicted to activity and productivity. We are walking and talking and driving and thinking faster and faster. Speeding, in fact, is the most common infraction of the law. And sleeplessness is an epidemic.


Lack of sweating

                             

Anhidrotic sometimes referred to as hyperhidrosis, sudomotor dysfunction or sweating dysfunction is an abnormal lack of sweat in response to heat - the person's body is unable to sweat normally. Anhidrotic is the complete absence of sweating while hyperhidrosis is sweating less than normal.



Poor memory


Memory loss affects most people in one way or another.  More often than not, it is a momentary memory lapse; nothing to worry about – it happens to the best of us.  However, when memory lapses begin to become a regular occurrence, it is wise to dig a little deeper and seek medical advice.


Causes and Development


Memory can be affected by a number of factors and there are many possible causes of patches of memory being lost, some more sinister than others.  A high fever, an attack of epilepsy, severe alcohol intoxication or surgery can erase the memory.  A stroke can cause sudden memory loss (accompanied by other neurological symptoms, such as dizziness, visual changes, buckling knees or slurred speech.) A passing loss of short-term memory, or ischemic attack, lasts only a few minutes and can precede a stroke.
Memory problems can also be the result of deeper-rooted issues such as brain disease,tumors, or the onset of a disease such as Alzheimer's that causes brain cell deterioration. Alzheimer's disease and senile dementia are sources of memory loss in older persons and are associated with the gradual erosion of the personality.  Sufferers who have any doubts at all should always seek medical advice with regards to continued memory loss.


Lose of libido

Men don't like to talk about it; neither do their partners. But loss of libido in men or inhibited sexual desire stresses a marriage more than any other sexual dysfunction, according to Barry McCarthy, co-author of Rekindling Desire: A Step by Step Program to Help Low-Sex and No-Sex Marriages.
Losing interest in sex may not be as common an occurrence for men as it is for women: It affects about 15% to 16% of men and at least double that many women. "But when men lose interest in sex it scares them more than women -- their masculinity is so linked to their sexuality that it is very threatening," says Esther Perel, a couples therapist in New York city and author of Mating in Captivity.
Lose of libido also makes men more unhappy about the rest of their lives than it does women. Only 23% of men with loss of libido say they still feel very happy about live in general vs. 46% of women, says Edward Laumann, professor of sociology at the University of Chicago co-author of The Social Organization of Sexuality: Sexual Practices in the United States. "It bothers men more."

Depression, anxiety, irritability, or seasonal affective disorder


Seasonal affective disorder (SAD) is a syndrome characterized by recurrent depressions that occur annually at the same time each year. We describe 29 patients with SAD; most of them had a bipolar affective disorder, especially bipolar II, and their depressions were generally characterized by hypersomnia, overeating, and carbohydrate craving and seemed to respond to changes in climate and latitude. Sleep recordings in nine depressed patients confirmed the presence of hypersomnia and showed increased sleep latency and reduced slow-wave (delta) sleep. Preliminary studies in 11 patients suggest that extending the photoperiod with bright artificial light has an antidepressant effect.

Loss of motivation or competitive edge

                                               

The ability to transfer best practices internally is critical to a firm's ability to build competitive advantage through the appropriation of rents from scarce internal knowledge. Just as a firm's distinctive competencies might be difficult for other firms to imitate, its best practices could be difficult to imitate internally. Yet, little systematic attention has been paid to such internal stickiness. The author analyzes internal stickiness of knowledge transfer and tests the resulting model using canonical correlation analysis of a data set consisting of 271 observations of 122 best-practice transfers in eight companies. Contrary to conventional wisdom that blames primarily motivational factors, the study findings show the major barriers to internal knowledge transfer to be knowledge-related factors such as the recipient's lack of absorptive capacity, causal ambiguity, and an arduous relationship between the source and the recipient.

Low self-esteem



                             

 Society and the Adolescent Self-Image by Morris Rosenberg (1965). No one from psychiatry, the social sciences or the educational field who thoughtfully reads this volume will fail to come away from the experience without having his understanding of the formation and the impact of the self-image upon the individual broadened and enriched. The reader should be warned, however, that because of the large number of tables distributed throughout the volume this is not the easiest book to read. These are appropriately distributed, however, and are interspersed with lucid descriptive discussions that relate to the nearby tables. This volume is a presentation of the research results on 5 ,024 high school juniors and seniors from 10 high schools in New York state. The results as tabulated and discussed on the whole are not inconsistent with expectations from clinical judgment. The religious preponderance of a social community in which the person lived clearly demonstrates the impact of the social milieu. The last section of the volume is devoted to the impact of the self-concept upon the members' participation in society, first in his leadership in the high school community and then the part he plays in public affairs.

Inability to make decisions


The right of patients to accept or refuse recommended treatment requires careful reassessment when their decision-making capacities are called into question. Patients must be informed appropriately about treatment decisions and be given an opportunity to demonstrate their highest level of mental functioning. The legal standards for competence include the four related skills of communicating a choice, understanding relevant information, appreciating the current situation and its consequences, and manipulating information rationally.

Obsessive-compulsive disorder

Obsessive-compulsive disorder is a severe and disabling clinical condition that usually arises in late adolescence or early adulthood and, if left untreated, has a chronic course. Whether this disorder should be classified as an anxiety disorder or in a group of putative obsessive-compulsive-related disorders is still a matter of debate. Biological models of obsessive-compulsive disorder propose anomalies in the serotonin pathway and dysfunctional circuits in the orbit-striatal area and dorsolateral prefrontal cortex. Support for these models is mixed and they do not account for the symptomatic heterogeneity of the disorder. The cognitive-behavioural model of obsessive-compulsive disorder, which has some empirical support but does not fully explain the disorder, emphasizes the importance of dysfunctional beliefs in individuals affected. Both biological and cognitive models have led to empirical treatments for the disorder—ie, serotonin-reuptake inhibitors and various forms of cognitive-behavioral therapy. New developments in the treatment of obsessive-compulsive disorder involve medications that work in conjunction with cognitive-behavioral therapy, the most promising of which is D-cycloserine.


Bulimia or binge eating

                                             
Thirty-two patients who complained of episodes of ravenous overeating which they felt unable to control (bulimia) were asked to describe their behavior and symptoms. There was considerable variation both between and within individuals, but a number of factors were defined which appeared to be common to all with the complaint. It is difficult to set up strict criteria for the recognition of bulimia, and those that have recently been proposed are criticized in the light of our present findings.

Fibromyalgia

Musculoskeletal aching and concomitant soft-tissue rheumatism are the most common rheumatic disorders. They are rarely identified as “diseases” or “disorders” in population surveys because of the difficulty in reliable diagnosis. Clinicians have similar troubles. Pain in the arm, leg, buttock, or chest, for example, is often difficult to understand and explain, and can be attributed to disk disorders, neuritis, bursitis, tendonitis, myositis, arthritis, myofascial pain, and psychologic disturbance. Few validation studies relating to diagnostic accuracy have been performed in these conditions and, although they remain common in the clinic, their vagueness and lack of adequate definition and validated criteria has generally excluded them as subjects for valued research.

Increased pain or poor pain tolerance

The purposes of this study were to test the feasibility of the Cancer Total Quality Pain Management Patient Assessment Tool in a population of oncology inpatient and outpatients; identify factors associated with poor pain relief. The Cancer TQPM Tool was adapted from the American Pain Society’s Quality Assurance Standards on Acute Pain and Cancer Pain and was tested in a convenience sample of 200 patients. The majority of patients reported that the TQPM Tool was easy to understand and to use, providing evidence for the feasibility of the tool. Factors associated with higher pain intensity included the inpatient setting, the presence of metastatic disease, hesitancy in bothering the nurse, and concerns regarding tolerance and addiction. Although there was a strong relationship between concerns about addiction and concern about tolerance, fear of tolerance appeared to have a greater effect on pain intensity scores than did fear of addiction. The findings from this study suggest that the Cancer TQPM Patient Assessment Tool can be used effectively in both inpatients and outpatients to determine outcomes and the quality of cancer pain management, as well identify factors associated with poor pain control. Clinical implications include more effective education of patients and caregivers, including equivalent emphasis on tolerance and addiction.

Headaches or migraines

We set out to examine associations between ambient air pollution concentrations and emergency department (ED) visits for migraine/headache in a multi-city study. Materials and Methods: We designed a time-series study of 64 839 ED visits for migraine (ICD-9: 346) and of 68 495 ED visits for headache (ICD-9: 784) recorded at hospitals in five different cities in Canada. The data (days) were clustered according to the hierarchical structure (location, year, month, day of week). The generalised linear mixed models technique was applied to fit the logarithm of clustered daily counts of ED visits for migraine, and separately for headache, on the levels of air pollutants, after adjusting for meteorological conditions. The analysis was performed by sex (all, male, female) and for three different seasonal periods: whole (January—December), warm (April—September), and cold (October—March). Results: For female ED visits for migraine, positive associations were observed during the warm season for sulphur dioxide (SO2), and in the cold season for particulate matter (PM2.5) exposures lagged by 2-days. The percentage increase in daily visits was 4.0% (95% CI: 0.8-7.3) for SO2 mean level change of 4.6 ppb, and 4.6% (95% CI: 1.2,-8.1) for PM2.5 mean level change of 8.3 μg/m3. For male ED visits for headache, the largest association was obtained during the warm season for nitrogen dioxide (NO2), which was 13.5% (95% CI: 6.7-20.7) for same day exposure. Conclusions: Our findings support the associations between air pollutants and the number of ED visits for headache.

Cravings for sweets or carbohydrates

                                        

                                  

This pilot study tested the relation between food cravings and food intake in the laboratory. Participants (n = 91; mean BMI = 35.1 kg/m2) completed the Food Craving Inventory to measure cravings for sweets, fats, carbohydrates, and fast food fats, and a taste test consisting of four foods (jelly beans, M&M's®, regular potato chips, and baked low-fat potato chips). Thereafter, participants could eat the items ad libitum. Specific food cravings were significantly correlated with consumption of corresponding types of foods. The sweets scale correlated with M&M® and jelly bean intake, but not chip intake. The fats scale correlated only with intake of regular potato chips.

Constant hunger or increased appetite
                                  

                                 


 Four young patients who developed weight gain induced by carbamazepine therapy are described. The patients received the carbamazepine as anticonvulsant treatment, and soon after starting the drug, abruptly developed an increase in appetite with a concomitant increase in food intake. During a period of 2 months, the patients' weights rose by between 7 and 15 kg. Dietary restriction during the carbamazepine treatment was ineffective in promoting weight loss, and lose of the excess weight was achieved only when the drug was discontinued. These patients demonstrate an as yet unpublished adverse effect of carbamazepine. In carbamazepine-induced weight gain, the overeating and fat deposition must be taken into consideration as a differential diagnosis to the hitherto described water retention and edema.

Inability to sleep in, no matter how late going to bed

                                

Sleep hygiene, relaxation therapy, and some cognitive interventions make a good package that can often be administered conjointly. I typically use an individualized mix of them in my initial treatment sessions with chronic insomniacs.

Less than 7-5 hours of sleep per night

We measured ear oxygen saturation (SaO2), chest wall movement, and oronasal air flow, and took electroencephalographic tracings during nocturnal sleep in 20 healthy subjects and 20 similarly aged patients with chronic obstructive pulmonary disease (COPD), none of whom was obese. Thirteen of the patients with COPD were persistently hypoxemic and hypercapnic when awake (“blue and bloated”, Type B); the remaining 7 maintained relatively normal arterial gas tensions when awake despite equally severe airways obstruction (“pink and puffing”, Type A). Hypoxemic episodes (HE) (SaO2 falls of greater than 10%) occurred during sleep in all the blue bloaters but in only 3 of 7 pink puffers and 3 of 20 normal subjects. However, the maximal change in arterial oxygen tension (PaO2) (calculated from SaO2 values assuming normal pH) was similar in all 3 groups, averaging 24 mmHg. Furthermore, the cumulative duration of apnea and hypopnea was the same in each group. Only one patient with COPD had more than 2 apneas per night, and obstructive apnea was seen only in the healthy subjects. Sleep apnea syndromes thus appear to be rare in nonobese patients with COPD. Of the 40 HE in patients with COPD, 29 occurred during periods of hypoventilation. In 10 blue bloaters whose arterial blood was sampled during sleep, the measured fall in PaO2 during the HE (mean, 11.2 mmHg) was greater than the rise in PaCO2 (mean, 4.2 mmHg). Although these changes in arterial gas tensions could be produced by an increase in ventilation-perfusion imbalance during the HE, it is suggested that unsteady-state gas exchange during transient hypoventilation could provide an alter.

Irritable bowel




A questionnaire to establish the presence of 15 symptoms thought to be typical of the irritable bowel syndrome (IBS) was given to 109 unselected patients referred to gastroenterology or surgery clinics with abdominal pain or a change in bowel habit or both. Review of case records 17--26 months later established a definite diagnosis of IBS in 32 patients and of organic disease in 33. Four symptoms were significantly more common among patients with IBS--namely, distension, relief of pain with bowel movement, and looser and more frequent bowel movements with the onset of pain. Mucus and a sensation of incomplete evacuation were also common in these patients. The more of these symptoms that were present the more likely was it that the patient's pain or altered bowel habit, or both, was due to IBS. We conclude that a careful history can increase diagnostic confidence and reduce the amount of investigation in many patients with chronic abdominal pain. Native explanation.

Constipation

                           

The evaluation of chronic constipation with or without encopresis must begin with a careful history. The intervals between bowel movements and the size and consistency of stools deposited into the toilet should be noted. Encopresis may be manifested as dirtying the underwear. The physical examination should include a rectal and neurological examination. No specific organic cause can be found in the majority of children. One or several anorectic physiological abnormalities have been found by us and others in 95% of children with idiopathic constipation. These abnormalities include impaired rectal and sigmoid sensation and decreased rectal contractility during rectal distention. The external anal sphincter and pelvic floor muscles may be abnormally contracted during straining, and the child may be unable to defecate a rectal balloon. Most patients will benefit from a program designed to clear stools, to prevent further impaction, and promote regular bowel habits. Fifty percent of patients will be cured after 1 year and 65%-70% after 2 years.

Nausea
             
                                     
                                

In a recent editorial, Kapur described perioperative nausea and vomiting as "the big 'little problem' following ambulatory surgery."257 Although the actual morbidity associated with nausea is relatively low in health outpatients, it should not be considered an unavoidable part of the perioperative experience. The availability of an emesis basin for every patient in the postanesthesia recovery unit is a reflection of the limited success with the available therapeutic techniques.257 There had been little change in the incidence of postoperative nemesis since the introduction of halothane into clinical practice in 1956. However, newer anesthetic drugs appear to have contributed to a recent decline in the incidence of emesis. Factors associated with an increased risk of postoperative emesis include age, gender (menses), obesity, previous history of motion  or postoperative vomiting, anxiety, gastroparesis, and type and duration of the surgical procedure (e.g., laparoscopy, strabismus, middle ear procedures). Anesthesiologists have little, if any, control over these surgical factors. However, they do have control over many other factors that influence postoperative emesis (e.g., pre-anesthetic medication, anesthetic drugs and techniques, and postoperative pain management). Although routine antiemetic prophylaxis is clearly unjustified, patients at high risk for postoperative emesis should receive special considerations with respect to the prophylactic use of antiemetic drugs. Minimally effective doses of antiemetic drugs can be administered to reduce the incidence of sedation and other deleterious side effects.
Potent nonopioid analgesics  can be used to control pain while avoiding some of the opioid-related side effects. Gentle handling in the immediate postoperative period is also essential. If emesis does occur, aggressive intravenous hydration and pain management are important components of the therapeutic regimen, along with antiemetic drugs. If one antiemetic does not appear to be effective, another drug with a different site of action should be considered. With the availability of new ant serotonin drugs, the incidence of recurrent (intractable) emesis could be further decreased. Research into the mechanisms of this common postoperative complication may help in improving the management of emetic sequelae in the future. As suggested in a recent editorial, improvement in antiemetic therapy could have a major impact for surgical patients, particularly after ambulatory surgery. Patients, as well as those involved in their postoperative care, look forward to a time when the routine offering of an emesis basin after surgery becomes a historical practice.

Use of corticosteroids

                                   

                                

Controversy remains as to whether low-dose corticosteroids can reduce the mortality and morbidity of acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS) without increasing the risk of adverse reactions. We aimed to evaluate all studies investigating prolonged corticosteroids in low-to-moderate dose in ALI or ARDS.
Data Sources: MEDLINE, EMBASE, Current Content, and Cochrane Central Register of Controlled Trials, and bibliographies of retrieved articles.
Study Selection: Randomized controlled trials (RCTs) and observational studies reported in any language that used 0.5–2.5 mg•kg−1•d−1 of methylprednisolone or equivalent to treat ALI/ARDS.
Data Extraction: Data were extracted independently by two reviewers and included study design, patient characteristics, interventions, and mortality and morbidity outcomes.
Data Synthesis: Both cohort studies (five studies, n = 307) and RCTs (four trials, n = 341) showed a similar trend toward mortality reduction (RCTs relative risk 0.51, 95% CI 0.24–1.09; p = 0.08; cohort studies relative risk 0.66, 95% CI 0.43–1.02; p = 0.06). The overall relative risk was 0.62 (95% CI 0.43–0.91; p = 0.01). There was also an improvement in length of ventilation-free days, the length of intensive care unit stay, Multiple Organ Dysfunction Syndrome Score, Lung Injury Scores, and improvement in Pao2/Fio2. There was no increase in infection, neuromyopathy, or any major complications. There was significant heterogeneity in the pooled studies. Subgroup and meta-regression analyses showed that heterogeneity had minimal effect on treatment efficacy; however, these findings were limited by the small number of studies used in the analyses.