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Depression and vasoconstriction: do you have cold, blue hands?

depression vasoconstriction

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#1 xxxxxxxx

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Posted 06 November 2015 - 09:55 PM


Does anybody with unmedicated depression (without the influence of possibly vasoconstricting drugs/ supplements/ psych meds) experience extremely cold limbs with blue nail beds? This is not Raynaud's phenomenon, as the symptoms are not transient and not *that* severe. It is also not made better by soaking my hands/feet in really hot water. It is not made worse by exposure to cold (except they turn white from their usual blue). 

 

I've been medically cleared of:

+Anemia, with or without B12 deficiency

+thyroid disease (even did a short trial of thyroxine, which made me hyperthyroid and still did not address the cold, blue hands)

+autoimmunity/ markers of inflammation

+heart and blood pressure abnormalities

+high cholesterol

+cortisol extremes (I did score high-normal on morning cort, but passed a dexamethasone suppression test) 

+my lung function is fine and I don't have any respiratory symptoms anyway

+I do not have any anxiety with my depression, just anhedonia

+I'm not underweight or malnourished. We checked most vitamins.

 

However, I do have PCOS which is giving me a slightly elevated A1C/ abnormal glucose tolerance. I'm young, thin, and do not have actual overt T2 diabetes yet. It would be highly unlikely that the problem is from diabetic neuropathy or vasculopathy (peripheral artery disease, etc). I'm not on any drugs (quit my 2 weeks of tianeptine) except hormonal birth control for the PCOS. 

 

Surely there should be a mechanism linking depression to a functional circulatory abnormality? I did see one study where depressives showed absence of visible nail lunulae (those white arcs near the base of your nail), which was a result of some kind of circulatory "changes" the abstract neglected to explain. 



#2 Junk Master

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Posted 15 November 2015 - 05:17 PM

Actually,  I don't think I experience the phenomenon as severely as you, but I do experience "unusually" cold hands and feet; and, have overcome bouts of depression in the past, have taken numerous SSRI'S and SNI'S for depression, and in the past have been in CBT for depression.

 

Lately, as the weather turns, I've been noticing the symptoms again.

 

No clue as to why, but I will say when I was taking high amounts of Niacin I felt the symptoms were diminished.



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#3 NinefingerJoe

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Posted 23 November 2015 - 03:30 PM

Now that I think about it, my cold hands clear up whenever I have a manic episode. Or since now I'm on Mirtazepine. Odd.

#4 gamesguru

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Posted 23 November 2015 - 11:39 PM

Depression is also associated with mitochondrial and endoplasmic stress. 

So good diet (which also helps cardiovascular health)... foods with PQQ, CoQ10, melatonin[1], etc might help.

 

The A1C/glucose might throw other things off. 

 

Ginger lowers blood pressure through blockade of voltage-dependent calcium channels.
Ghayur MN1, Gilani AH.  2005.
The vasodilator effect of crude extract of ginger (Zo.Cr) was endothelium-independent because it was not blocked by L-NAME (0.1 mM) or atropine (1 microM) and also was reproduced in the endothelium-denuded preparations at the same dose range. These data indicate that the blood pressure-lowering effect of ginger is mediated through blockade of voltage-dependent calcium channels.

 

Antidepressant-like synergism of extracts from magnolia bark and ginger rhizome alone and in combination in mice.
Yi LT1, Xu Q, Li YC, Yang L, Kong LD.  2009.
Magnolia bark and ginger rhizome is a drug pair in many prescriptions for treatment of mental disorders in traditional Chinese medicine (TCM). However, compatibility and synergism mechanism of two herbs on antidepressant actions have not been reported. The aim of this study was to approach the rationale of the drug pair in TCM. We evaluated antidepressant-like effects of mixture of honokiol and magnolol (HMM), polysaccharides (PMB) from magnolia bark, essential oil (OGR) and polysaccharides (PGR) from ginger rhizome alone, and the possibility of synergistic interactions in their combinations in the mouse forced swimming test (FST) and tail suspension test (TST). Serotonin (5-HT) and noradrenaline (NE) levels in prefrontal cortex, hippocampus and striatum were also examined. 30 mg/kg HMM decreased immobility in the FST and TST in mice after one- and two-week treatment. OGR (19.5 or 39 mg/kg) alone was ineffective. The combination of an ineffective dose of 39 mg/kg OGR with 15 mg/kg HMM was the most effective and produced a synergistic action on behaviors after two-week treatment. Significant increase in 5-HT and synergistic increase in NE in prefrontal cortex were observed after co-administration of HMM with OGR. These results demonstrated that HMM was the principal component of this drug pair, whereas OGR served as adjuvant fraction. Compatibility of HMM with OGR was suggested to exert synergistic antidepressant actions by attenuating abnormalities in serotonergic and noradrenergic system functions. Therefore, we confirmed the rationality of drug pair in clinical application and provided a novel perspective in drug pair of TCM researches.

Effect of Treatment with Ginger on the Severity of Premenstrual Syndrome Symptoms
Samira Khayat, 1 , 2 , 3 Masoomeh Kheirkhah, 4 , 5 ,* Zahra Behboodi Moghadam, 2 Hamed Fanaei, 6 Amir Kasaeian, 7 , 8 and Mani Javadimehr 9.  2014.
Based on the results of this study, maybe ginger is effective in the reduction of severity of mood and physical and behavioral symptoms of PMS and we suggest ginger as treatment for PMS.

Green and black tea are equally potent stimuli of NO production and vasodilation: new insights into tea ingredients involved.
Lorenz M1, Urban J, Engelhardt U, Baumann G, Stangl K, Stangl V.  2009.
Epidemiological studies suggest that consumption of tea is associated with beneficial cardiovascular effects. Since different types of tea are consumed throughout the world, a question of much interest is whether green tea is superior to black tea in terms of cardiovascular protection. We therefore compared the effects of green and black tea on nitric oxide (NO) production and vasodilation and elucidated the tea compounds involved. We chose a highly fermented black tea and determined concentrations of individual tea compounds in both green and black tea of the same type (Assam). The fermented black tea was almost devoid of catechins. However, both teas stimulated eNOS activity and phosphorylation in bovine aortic endothelial cells (BAEC) as well as vasorelaxation in rat aortic rings to a similar extent. In green tea, only epigallocatechin-3-gallate (EGCG) resulted in pronounced NO production and NO-dependent vasorelaxation in aortic rings. During tea processing to produce black tea, the catechins are converted to theaflavins and thearubigins. Individual black tea theaflavins showed a higher potency than EGCG in NO production and vasorelaxation. The thearubigins in black tea are highly efficient stimulators of vasodilation and NO production. Green and black tea compounds induced comparable phosphorylation of eNOS and upstream signalling kinases. Whereas stimulation of eNOS activity by EGCG was only slightly affected by pretreatment of cells with various ROS scavengers, TF3(theaflavin-3',3-digallate)-induced eNOS activity was partially inhibited by PEG-catalase. These results implicate that highly fermented black tea is equally potent as green tea in promoting beneficial endothelial effects. Theaflavins and thearubigins predominantly counterbalance the lack of catechins in black tea. The findings may underline the contribution of black tea consumption in prevention of cardiovascular diseases.

Dietary modulation of uptake transporters
Naccarati, Chiara (2014)
Transporters play a determinant role in creating and maintaining physiological balance within the cells. Though, not much information exists on the modulation of transporters, especially in terms of polyphenols and other dietary components. Initially, a comprehensive database was created, using the high-performance search engine Genevestigator. The database summarises the existing knowledge on selected transporters (OAT1, OAT3, OATP1A2, OATP1B1, OATP1B3, OATP4C1, MRP2, MRP3, BCRP, MCT1, MCT7 and SMCT1). The anatomical distribution of the latters was investigated in the human heart, kidney, liver and intestine. Transcriptional modulation was also assessed, in response to biological mediators, disease, chemicals and drugs. It was shown that while some transporters were modulated from a large number of conditions, others only responded to few. Interestingly, not many dietary compounds were tested, highlighting the limited knowledge existing in this area. Subsequently, expression of a transporter of interest, the organic anion transporter 3 (OAT3), was assessed in liver HepG2 cells. It was predicted, on the basis of the Ct value, that OAT3 was expressed in the cell line at low levels. Modulation of OAT3, in response to stressors (hydrogen peroxide, tert-butyl hydroperoxide and ethanol) at various concentrations and for different time lengths was assessed. It was shown that none of the stressors affected the transporter. In the same cell line, uptake of the metabolite kaempferol-3-O-glucuronide was assessed, to establish whether uptake occurred in a carrier-mediated manner or through passive diffusion mainly. Uptake resulted to be carrier-mediated, although the low Vmax of the transport, close to detection limit, did not make possible further studies to identify the transporter(s) involved in its uptake. Finally, intestine Caco-2 cells were used to assess modulation of the serotonin transporter from green tea and coffee. For the first time, it was reported that green tea and coffee acted as modulators of serotonin uptake. Whole extracts showed to act in a concentration-dependent way. Physiological concentrations of individual green tea components showed not to have a significant effect on the uptake, however significant effect was observed when using supplement concentrations (equivalent to 7 cups). Physiological concentrations of several coffee components showed to modulate serotonin uptake. Among them, ferulic acid and 5-feruloylquinic acid showed to act in a competitive manner.

Neurobiological effects of the green tea constituent theanine and its potential role in the treatment of psychiatric and neurodegenerative disorders.
Lardner AL.  2014.
Theanine (n-ethylglutamic acid), a non-proteinaceous amino acid component of green and black teas, has received growing attention in recent years due to its reported effects on the central nervous system. It readily crosses the blood-brain barrier where it exerts a variety of neurophysiological and pharmacological effects. Its most well-documented effect has been its apparent anxiolytic and calming effect due to its up-regulation of inhibitory neurotransmitters and possible modulation of serotonin and dopamine in selected areas. It has also recently been shown to increase levels of brain-derived neurotrophic factor. An increasing number of studies demonstrate a neuroprotective effects following cerebral infarct and injury, although the exact molecular mechanisms remain to be fully elucidated. Theanine also elicits improvements in cognitive function including learning and memory, in human and animal studies, possibly via a decrease in NMDA-dependent CA1 long-term potentiation (LTP) and increase in NMDA-independent CA1-LTP. Furthermore, theanine administration elicits selective changes in alpha brain wave activity with concomitant increases in selective attention during the execution of mental tasks. Emerging studies also demonstrate a promising role for theanine in augmentation therapy for schizophrenia, while animal models of depression report positive improvements following theanine administration. A handful of studies are beginning to examine a putative role in attention deficit hyperactivity disorder, and theoretical extrapolations to a therapeutic role for theanine in other psychiatric disorders such as anxiety disorders, panic disorder, obsessive compulsive disorder (OCD), and bipolar disorder are discussed.


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#5 Dichotohmy

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Posted 24 November 2015 - 05:33 AM

It's a ridiculous stretch to suggest depression (or bipolar depression) causes an overt physical symptom like this. Its also short sighted to suggest a link between cold blue hands and depression without the existance of a third condition causing the first two. On the other hand, it is common for depression to be a symptom of the conditions you list as medically cleared of.

Because you mention it being transient, is the coldness and blue appearance spurred by anything specifically? Does the same thing happen to your feet? Does blood pool in your extremities - IE swelling?

#6 PalmAnita

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Posted 24 November 2015 - 05:53 AM

Yeah, somehow I thought about this too previously. When I'm depressed, I tend to have really cold clammy hands and feet and this goes away when the mood lift from NMDA antagonists sets in - one of many small pieces that are easily overlooked but when I search for them, they can get puzzled together. 

 

Can't say anything about what's the cause and what's the symptom, but I really think that the split between mental and physical disorders is obsolete - it's all about neurobiology in the end. One can lead to the other.

 

Annoying thing I have is a somewhat fast heartbeat, my resting pulse is usually above 75 and often 80-95 bpm ... don't know if this is dangerous, but I should certainly do more sports. Curiously on (very) small dosages of dexamphetamine I happened to have the lowest bpm's of 71 or so. This made me think about a somewhat derailed adrenergic system, which would fit with my anxiety problems too ...



#7 gamesguru

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Posted 24 November 2015 - 03:16 PM

Brain blood flow changes in depressed patients treated with interpersonal psychotherapy or venlafaxine hydrochloride: preliminary findings.
Regional cerebral blood flow abnormalities in depressed patients with cognitive impairment.
Cerebral Blood Flow Abnormalities Persist in Major Depression

Brain Blood Flow Gives Clues To Treating Depression
Date:  August 14, 2007
Source:  Society of Nuclear Medicine
Share:  Total shares:  70


FULL STORY
The usefulness of established molecular imaging/nuclear medicine approaches in identifying the “hows” and “whys” of brain dysfunction and its potential in providing immediately useful information in treating depression are emphasized in a study in the August Journal of Nuclear Medicine.

“Individuals in a depressed emotional state have impaired cerebral (brain) blood flow,” explained Omer Bonne, head of inpatient psychiatry and associate professor in the Department of Psychiatry at Hadassah-Hebrew University Medical Center in Jerusalem, Israel. “Clinical improvement in depression is accompanied by diverse changes in cerebral blood flow, according to whether patients are treated with medication or electroconvulsive treatment,” he noted.

“We found that antidepressant medicines normalized decreased brain blood flow usually seen in patients with depression, while electroconvulsive treatment was associated with additional decreases in blood flow,” he reported. “Currently, clinical psychiatry is based almost solely on subjective observer-based judgment. Our findings suggest that objective imaging evaluations could support subjective clinical decisions,” he said.

Using SPECT (single photon emission computed tomography)—a molecular imaging/nuclear medicine procedure in which injected radiotracers are utilized to produce three-dimensional, computer-reconstructed images that reveal information about both structure and function—investigators confirmed already published findings that cerebral blood flow in depressed patients is lower than in healthy control subjects, especially in frontal, limbic and subcortical brain regions.

“We wanted to see whether improvement in clinical depression is accompanied by changes—increases—in cerebral blood flow,” he said. “We found that cerebral blood flow increased only in patients whose depression improved. In contrast, cerebral blood flow remained unchanged in patients whose depressed condition persisted,” detailed Bonne.

Depression is a serious and debilitating—yet treatable—disease that affects every aspect of a person’s health. Estimates indicate that 19 million Americans are affected by depression each year, along with their family members, friends and co-workers. Depression may be related to a chemical imbalance in the brain that makes it hard for the cells to communicate with one another.

A variety of antidepressant medications and psychotherapies are used to treat depression. Sometimes electroconvulsive therapy—applying an electric current briefly to produce a seizure—is useful, especially for those whose depression is severe or life threatening or for whom repeated treatment trials with antidepressant drugs failed.

“Interestingly, patients’ response to two different classes of antidepressant medicines that target different neurotransmitters is associated with a similar improvement in cerebral blood flow,” he noted. “However, cerebral blood flow continued to deteriorate in patients who responded to electroconvulsive therapy,” added Bonne, who helped implement functional brain imaging research in psychiatry at Hadassah. Israeli researchers studied 33 depressed patients and 25 healthy control subjects with SPECT and the radiotracer 99mTc-HMPAO.

“Our findings may aid in elucidating the mechanism of depression and its treatment,” said Bonne. “There may be more than one mechanism responsible for the development of depression and for mediating response to its treatment,” he added. Additional research could examine whether it’s possible to use functional imaging techniques to determine which patients would benefit from drug treatment and which would respond better to electroconvulsive therapy, explained Bonne. Future research should also examine the differences in brain blood flow in patients at later time points, he said.

“99mTc-HMPAO SPECT Study of Cerebral Perfusion After Treatment With Medication and Electroconvulsive Therapy in Major Depression” appears in the August issue of the Journal of Nuclear Medicine, which is published by SNM, the world’s largest molecular imaging and nuclear medicine society. Co-authors include Yoav Kohn and Bernard Lerer, Department of Psychiatry, and Nanette Freedman, Hava Lester, Yodphat Krausz and Roland Chisin, Department of Medical Biophysics and Nuclear Medicine, at Hadassah-Hebrew University Medical Center in Jerusalem, Israel.

 

 

Table 1.

Mechanisms Contributing to Poor Prognosis After Heart Attack

Not taking medications as prescribed Continuing to smoke Less physical activity Increased stress hormone levels Increased blood sugar and lipid levels Increased tendency of blood to clot

Increased inflammatory cytokine levels

 

and generally medical diagnoses are associated with increased depression.
after all, who wants to be diagnosed with some shitty disease?


Depression After Heart Attack: Why Should I Be Concerned About Depression After a Heart Attack?
Depression and Coronary Heart Disease


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#8 gamesguru

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Posted 25 November 2015 - 02:30 PM

Found this on diabetes/A1c.

Efficacy of ginger for treating Type 2 diabetes: A systematic review and meta-analysis of randomized clinical trials
James W. Dailya, Mini Yangb, Da Sol Kimb, Sunmin Parkb.  2015.
Background/Purpose
Few clinical trials have investigated the antidiabetic effects of ginger to date. Several recent clinical trials published in 2013 and 2014, although small, have added contradictory but compelling new evidence about the use of ginger in treating diabetes in humans. Therefore, a systematic review and meta-analysis was conducted to clarify the evidence for using ginger to treat diabetes.
Methods
Five randomized clinical trials (RCTs) were identified and included in the meta-analysis. Four of the RCTs were considered high quality and lasted ≥8 weeks; one lasted only 30 days and was considered low quality. Outcomes measured included fasting blood glucose and insulin, homeostatic model assessment (HOMA)-insulin resistance (IR), and hemoglobin A1c (HbA1c) levels, and were assessed as mean differences in the meta-analysis.
Results
Ginger supplementation significantly lowered fasting blood glucose concentrations and HbA1c levels, but did not significantly lower fasting blood insulin or HOMA-IR.
Conclusion
Ginger root supplementation significantly lowers blood glucose and HbA1c levels. When combined with dietary and lifestyle interventions it may be an effective intervention for managing Type 2 diabetes mellitus.



#9 MarianVB

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Posted 05 December 2015 - 12:45 PM

I have ptsd, depression and psychotic symptoms. When symptoms flare up, i (and others too) notice i have cold, blue hand and feet, tingling sensations and chills. Also when withdrawing from meds i had severe mood swings and My father noticed when i got depressed and scared My hands turned extremely cold and blue.
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#10 aonyx

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Posted 05 December 2015 - 06:23 PM

I had a mild form of Reynaud's but I guess that doesn't count.







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