Тестирование тиреоидной функции у больных депрессией

In Depression & Your Thyroid, Ross lays out a step-by-step guide for testing and diagnosis. The first step is to figure out if you have any of the symptoms of low thyroid and to discuss this with your doctor. These are some of the signs of thyroid dysfunction. (You may experience only a few of these.)

• Fatigue
• Puffy face
• Oversensitivity to cold
• Difficulty concentrating or remembering things
• Tingling or numbness in hands and legs
• Hair loss
• Dry skin
• Weight gain
• Difficulty breathing
• Low blood pressure
• Low body temperature
• Slow pulse
• Slow reflexes
• Infertility or repeated miscarriages

Next, your doctor should conduct a physical examination, which will include checking your blood pressure, pulse, reflexes and thyroid gland. In people with low thyroid, blood pressure and pulse are low and reflexes are sluggish. Ross notes that during your physical exam, your thyroid gland tends to be normal.
Because people with low thyroid typically get cold easily and have a low temperature, Ross suggests keeping a record of your temperature every morning for five days. Keep a thermometer by your bed and check it before getting up or moving.
The first round of tests should include: Free T3; free T4; TSH (thyroid-stimulating hormone); antiperoxidase antibody and antithyroglobulin antibody. (Learn more here.)
The second round of tests includes a 24-hour urine sample for T3 and T4 hormones. (Sometimes the tests will include a TBII or thyroid-binding inhibitory immunoglobulin, but it’s not typically ordered.)
Doctors perform the third round of tests to absolutely confirm that a person has hypothyroidism. They may look at adrenal function, male and female hormones, virus and bacterial infections, intestinal parasites, molds, food sensitivities, minerals, toxic metals, liver, coagulation, antioxidants, amino acids and organic acids. Whether you have any of these tests will depend on your symptoms and the previous tests.

 Is Thyroid Dysfunction Driving Your Depression?

Лабораторная диагностика РДА

The urine test, which detects elevated levels of compounds called porphyrins, costs $50 to $100. Heyer said the test would become less expensive if used frequently as a way to screen babies.
James Woods, a researcher at the University of Washington who worked on the project with Battelle researchers, noted that everybody has the compounds in their urine, but the levels were clearly higher in certain children in the study. Also, although the study included only boys (who are much more likely to have autism than girls), Woods said that the test would likely work for both genders based on other research.
Heyer noted that although there’s been speculation that elevated porphyrin levels are related to mercury exposure in autistic children, the research team found no link to increased exposure to mercury. This leaves the question open of why the compounds are higher in some children with autism.

 Pilot Study: Urine Test Detects One-Third of Autism Cases

Ответ на провокацию углекислым газом при социофобии и паническом расстройстве

The 35% carbon dioxide (CO2) challenge is a well-established model of panic. This study aimed to investigate 35% CO2 sensitivity in patients with social anxiety disorder (SAD) compared with patients with panic disorder (PD) and normal controls. First, a 35% CO2 challenge was conducted including 16 patients with generalized SAD, 16 with PD and 16 normal subjects. Outcome was assessed by a Visual Analogue Scale for Fear (VAS-F) and the Panic Symptom List (PSL). Second, meta-analyses of fear and panic scores were performed, including data from the present experiment and from previous 35% CO2 challenge studies in patients with SAD. The present 35% CO2challenge found equal increases in VAS-F and PSL in patients with SAD compared with normal controls, whereas the CO2 response in patients with PD was significantly stronger than in controls. The meta-analyses confirmed the experimental data from this study, and in addition showed an intermediate panic rate in SAD patients, in between that of normal controls and patients with PD. In conclusion, neither our experiment nor the meta-analyses found evidence for a similarly exaggerated 35% CO2 sensitivity in SAD and PD, suggesting that the pathogenesis of SAD is different from PD, although patients with SAD may be slightly more sensitive than non-anxious controls.

35% CO2 sensitivity in social anxiety disorder 

Антитела к глиадину у больных шизофренией

The present work measured circulating antibodies against native gliadins, deamidated gliadin–derived epitopes, and transglutaminase 2 (TGM2) in 473 patients with schizophrenia and 478 control subjects among a Chinese population. The results showed that 27.1% of patients with schizophrenia were positive for the IgA antibody against native gliadins compared with 17.8% of control subjects (χ2 = 11.52, P = .0007, OR = 1.72, 95% CI 1.25–2.35), although this significant difference appeared to be due mainly to low IgA gliadin antibody levels in female controls. A total of 27.6% of female patients were positive for IgA gliadin antibodies compared with 13.9% of female controls (χ2 = 10.46, P = .0012, OR = 2.36, 95% CI 1.39–4.01), and 26.4% of male patients were positive for IgA antibodies compared with 19.8% of male controls (χ2 = 3.26, P = .071, OR = 1.46, 95% CI 0.97–2.19). Of 128 patients who were positive for the IgA antibody against native gliadins, 8 were positive for the IgA antibody against deamidated gliadin epitopes and 1 was positive for IgA anti-TGM2 antibody. However, quantitative analysis demonstrated that the mean levels of IgA antibodies against deamidated gliadin epitopes and TGM2 were significantly lower in patients with schizophrenia than the control subjects (P < .001 and P = .008, respectively). The prevalence of IgG antibodies against native gliadins was not significantly different between the patient group and the control group (χ2 = 2.25, P = .134, OR = 1.32, 95% CI 0.92–1.88). This study suggests that specific gliadin-derived epitopes may be involved in schizophrenia.

 A Study of Circulating Gliadin Antibodies in Schizophrenia Among a Chinese Population

Пиколинат хрома, депрессия и контроль массы тела

A Duke University study validated that adding chromium supplements to diet significantly improved symptoms of atypical depression, and patients’ tendency to overeat. In the study, 75 people with atypical depression, most of whom were overweight or obese, received either 600 mcg per day of chromium (as chromium picolinate) or a placebo for eight weeks. The proportion of people who improved by at least 50% (responders) was greater in the chromium group than in the placebo group (54% versus 36%), although this difference was not statistically significant. However, significant differences were seen when the analysis was restricted to those people who reported that they had severe carbohydrate craving (a possible indicator of abnormal glucose metabolism). In that subset, the proportion of responders was 65% in the chromium group and only 33% in the placebo group, a statistically significant difference. No significant side effects were observed in people taking chromium.

 Chromium, Depression, and Weight Management

Применение статинов снижает риск возникновения депрессии у пациентов с ИБС

Background: Statins are among the most commonly prescribed medications worldwide. Although their benefits for cardiovascular disease are well established, the effects of statins on depressive symptoms are unknown.
Method: We examined the association between baseline statin use (2000–2002) and subsequent depressive symptoms in a prospective cohort study of 965 outpatients with coronary disease from 12 outpatient clinics in the San Francisco Bay Area. Depressive symptoms were assessed annually for 6 years using the Patient Health Questionnaire (PHQ) (primary outcome measure). We evaluated the cross-sectional association between statin use and risk of depressive symptoms at baseline and the longitudinal association between baseline statin use and risk of depressive symptoms during follow-up.
Results: Of the 965 participants, 629 (65%) used statins. At baseline, statin users had lower mean ± SE PHQ depression scores than nonusers (4.8 ± 0.2 vs 5.9 ± 0.3, P < .01). Statin users were less likely than nonusers to have depression (PHQ score ≥ 10) at baseline (17% vs 24%; P = .02) and during follow-up (28% vs 40%; P < .01). Among the 776 patients without depressive symptoms at baseline (PHQ < 10), statin use was associated with a 48% decreased odds of developing depression during follow-up (odds ratio [OR], 0.52; 95% CI, 0.38–0.73; P < .01). After we adjusted for potentially confounding variables, statin use remained associated with a 38% decreased odds of subsequent depression (adjusted OR, 0.62; 95% CI, 0.41–0.95; P = .02).
Conclusions: We found that statin use was associated with a decreased risk of subsequent depressive symptoms in patients with coronary heart disease. Whether use of statins prevents depressive symptoms deserves further study.

 Statin Use and Risk of Depression in Patients With Coronary Heart Disease: Longitudinal Data From the Heart and Soul Study

Когнитивное снижение при приёме статинов: распространенность и методы коррекции

DATA SYNTHESIS: Reports of statin-associated cognitive impairment were found primarily in observational studies (eg, case reports/series). One randomized controlled trial demonstrated that simvastatin impaired some measures of cognition compared to placebo. Conversely, in the majority of randomized controlled trials and observational studies, statins were found to have either a neutral or beneficial effect on cognition. Preliminary data suggest that statins that are less lipophilic (ie, pravastatin and rosuvastatin) may be less likely to contribute to cognitive impairment due to limited penetration across the blood-brain barrier. These drugs would be a logical alternative in cases where cognitive impairment secondary to another statin is suspected.
CONCLUSIONS: Despite several reports of statin-associated cognitive impairment, this adverse effect remains a rare occurrence among the totality of the literature. If statin-associated cognitive impairment is suspected, a trial discontinuation can reveal a temporal relationship. Switching from lipophilic to hydrophilic statins may resolve cognitive impairment. The vascular benefits and putative cognitive benefits outweigh the risk of cognitive impairment associated with statin use; therefore, the current evidence does not support changing practice with respect to statin use, given this adverse effect.

 Is Statin-Associated Cognitive Impairment Clinically Relevant? A Narrative Review and Clinical Recommendations

Аугметация антидепрессантов ингибиторами холинэстеразы

STUDY SELECTION AND DATA EXTRACTION: English-language clinical trials were evaluated. Studies that included subjects with Alzheimer's disease, dementia, Parkinson disease, bipolar disorder, or schizophrenia were excluded. Four clinical studies met our criteria.
DATA SYNTHESIS: We identified 4 randomized, double-blind, placebo-controlled trials that ranged in sample size from 20 to 130. Galantamine 16 mg daily was evaluated in 2 trials lasting 8 and 24 weeks. Neither study found a statistically significant difference in measures of cognition or Hamilton Rating Scale for Depression scores. Donepezil augmentation was evaluated in a 1-year and a 2-year trial. Donepezil was found to improve global cognition at 1 year, but the benefit did not persist at year 2. Subjects with mild cognitive impairment at baseline who received donepezil experienced higher depression recurrence than did those who took placebo (p = 0.03); this effect was not observed in cognitively intact subjects (p = 0.39).
CONCLUSIONS: There is no clear benefit for ChEI therapy as an adjunct to antidepressant therapy for depressed older adults.

Cholinesterase Inhibitor Adjunctive Therapy for Cognitive Impairment and Depressive Symptoms in Older Adults with Depression 

Гомоцистеин и депрессия

Objective: Elevated serum levels of the amino acid homocysteine (HCY) are associated with a variety of diseases. To resolve conflicting findings in studies that suggest a relationship between elevated serum HCY levels and depression, we examined the relationship between HCY levels and depressive symptoms in the largest sample studied to date.
Method: We conducted a cross-sectional study of 11,757 participants (68.9% men) aged 20 to 90 years who completed preventive health examinations at the Cooper Clinic, Dallas, Texas, from 2007 to 2010. Currently experiencing depression was defined as a 10-item Center for Epidemiologic Studies Depression Scale (CES-D) score of ≥ 10. Serum HCY levels were obtained. Data were analyzed in a multiple logistic regression model of CES-D score of ≥ 10.
Results: When controlling for age, sex, body mass index, exercise, education, smoking, antidepressant use, creatinine level, alcohol use, and chronic medical conditions, elevated HCY was associated with 26% greater odds of currently experiencing depressive symptoms (P = .007) as defined by CES-D score.
Conclusions: In the largest sample examined to date, we found a significant positive relationship between elevated serum HCY levels and currently experiencing depressive symptoms. Given the cross-sectional nature of the study, it is not possible to determine the direction of the relationship or whether lowering HCY levels will ameliorate depressive symptoms. Thus, longitudinal studies are needed.

Relationship Between Serum Homocysteine Levels and Depressive Symptoms: The Cooper Center Longitudinal Study

Случай отравления витаминно-минеральным комплексом

When she elaborated that the experiments were taking plance in a hidden hospital annex on the other side of the picture on the wall of her room, and that her dear friend Oliver Sacks was overseeing them, her delusional state was exposed. Her lab tests showed shockingly high levels of calcium, up to 19.0 mg/dL (the normal range is 9.0 to 10.5) and vitamin D levels of 127 mg/dL (the normal range is 15 to 42). She was vitamin toxic and had likely been so for the last several months. As she weakened, she ate and drank less, but she carefully took her pills. These combined to send her vitamin levels spiraling up to life-threatening levels. Low potassium from the diuretic and not eating only worsened the toxicity. Since she hadn't seen her internist in over a year, her vitamin levels had remained untested. And when he checked them, her imperious manner and world-class medical reputation discouraged him from overriding her irrational refusal of care.

In retrospect, her decline was classic for hypercalcemia, not only the confusion progressing through delirium to stupor and toward coma, but also the weakness I had noticed when she coughed. Hypercalcemia contributed to the drooping eyelids, the nasal voice, the falls, and at the end, complete disability. Her high calcium had passed unnoticed during the first hospitalization at Christmas. Likely the doctors found confusion, weakness, and falls unremarkable in an 84-year-old and they did not look too hard for specific causes.

 Almost Losing My Mother: From Doctor to Patient and Back Again

Нарушение циркадных ритмов у больных шизофренией

In order to take a systematic look at the circadian rhythms of people with schizophrenia, Foster and his colleagues recruited 20 people with the disease and instructed them to wear movement-detecting wristwatches for six weeks. The amount of motion detected can be analyzed to determine whether the person is asleep or awake, given the vastly different movement patterns between the two states.
The patients also filled out questionnaires and kept daily diaries of their sleep and activities. All of the patients were taking medication to control their symptoms, and they had all been stable on that medication for at least three months. Finally, the patients gave 48 hours work of urine samples to be tested for melatonin, a hormone that regulates sleep (melatonin makes a person sleepy).
For comparison, the researchers asked another 21 mentally healthy but unemployed adults to wear the same watches and keep the same records as the people with schizophrenia. Unemployed people were chosen because the patients with schizophrenia were all unemployed, and employment can alter sleep patterns by forcing people to get up with an alarm clock.

A comparison between the two groups revealed that while unemployed people keep fairly regular sleep hours, every person with schizophrenia in the sample had a sleep problem.
"What became very clear is that they are massively and completely disrupted," Foster said.
This disruption did not follow a common pattern. Some people with schizophrenia went to bed late and got up late, with their melatonin release patterns delayed by several hours compared with healthy counterparts. Others would get up later and later every day, their circadian rhythms "drifting" through time. The most severely affected showed no normal 24-hour sleep-wake pattern at all. They'd alternate sleep and activity throughout the day and night.

The results weren't the result of unemployment, because the unemployed-but-healthy group did not show them. Nor could they be linked to any specific medication or dosage level, Foster said.

Better Sleep May Help Improve Schizophrenia