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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 8 of 8. This is the beginning of the thread.
Posted by mogger on June 14, 2012, at 12:04:14
I saw this interesting article today that I wanted to share with everyone. Not exactly what it means but if anyone can put it into layman's terms that would be great!
Posted by bleauberry on June 14, 2012, at 14:31:47
In reply to Yeast Cell Reaction to Zoloft Suggests..., posted by mogger on June 14, 2012, at 12:04:14
I tried the link but it isn't there.
Posted by Phillipa on June 14, 2012, at 15:37:05
In reply to Re: Yeast Cell Reaction to Zoloft Suggests..., posted by bleauberry on June 14, 2012, at 14:31:47
So it wasn't just me? I also tried. Hey blue is doxycycline good after three years of storage? Thanks P
Posted by mogger on June 14, 2012, at 17:52:20
In reply to Yeast Cell Reaction to Zoloft Suggests..., posted by mogger on June 14, 2012, at 12:04:14
http://www.sciencedaily.com/releases/2012/04/120424121900.htm
sorry you two I have cut and pasted it again it didn't work for me as well. If you go on sciencedaily.com and click on mind and brain and then depression the article will come up. Not sure why it isn't working.
Posted by Raisinb on June 14, 2012, at 22:05:21
In reply to Yeast Cell Reaction to Zoloft Suggests..., posted by mogger on June 14, 2012, at 12:04:14
Cool article. Since the Zoloft caused reactions in the yeast cells, and yeast cells don't have any serotonin in them, it suggests that Zoloft does something besides inhibit the reuptake of serotonin, which could possibly mean that depression is more than just a lack of serotonin. I think most scientists have been pretty doubtful about that for several years. It is obviously too simplistic a theory to explain most people's experience.
Posted by mogger on June 15, 2012, at 0:00:46
In reply to Re: Yeast Cell Reaction to Zoloft Suggests... » mogger, posted by Raisinb on June 14, 2012, at 22:05:21
Bleauberry and Phillipa here is the article. I couldn't copy it on my phone but I am at my computer. Thanks Raisinb for explaining that. I think it is interesting that they are hypothesizing "that depression might also be linked to diminished secretions of brain-derived neurotrophic factor (BDNF), a protein that regulates brain-cell growth."
ScienceDaily (Apr. 24, 2012) Princeton University researchers have observed a self-degradation response to the antidepressant Zoloft in yeast cells that could help provide new answers to lingering questions among scientists about how antidepressants work, as well as support the idea that depression is not solely linked to the neurotransmitter serotonin.
In findings published in the journal PLoS ONE, researchers based in the lab of Ethan Perlstein, an associate research scholar in Princeton's Lewis-Sigler Institute for Integrative Genomics and lecturer in molecular biology, report that sertraline -- trademarked as Zoloft -- accumulated in the internal membranes of baker's yeast cells.
This buildup caused a swelling and sharp curvature in the membranes of vesicles, bubble-like cell components with a hand in cell metabolism, movement and energy storage. The vesicles then went into autophagy, a protective response in which cells recycle excess or damaged membrane.
But yeast cells lack serotonin, which is the primary target of antidepressants, Perlstein said. By observing a reaction to sertraline in an organism that does not contain the drug's conventional target, Perlstein and his co-authors have found significant evidence suggesting that antidepressants engage in pharmacological activity beyond regulating serotonin. Perlstein worked with co-first authors Jingqui Chen and Daniel Korostyshevsky, as well as Sean Lee, all three senior research specialists in Perlstein's lab.
Although antidepressants are known to regulate serotonin, it is not completely understood how antidepressants interact with the body's brain cells and what effect, if any, this activity has on treating depression, Perlstein said. Antidepressant accumulation has been observed in the membranes of human cells, the researchers report, but is considered benign.
If, however, the membrane curvature the researchers found has therapeutic significance in treating depression, then the cell membrane could present an additional target for next-generation antidepressants. More immediately, Perlstein said, the activity of the drug in a serotonin-free organism supports existing research suggesting that depression might also be linked to diminished secretions of brain-derived neurotrophic factor (BDNF), a protein that regulates brain-cell growth. Perlstein explains his findings as follows: "The key finding of this paper is that the antidepressant sertraline/Zoloft accumulates within an organism lacking serotonin and induces autophagy, which is a protective mechanism cells use to recycle excess or damaged cell membrane. Specifically, we observed distortions, bulging and buckling in the membrane layer of vesicles inside cells treated with sertraline. "We saw these effects in the yeast species Saccharomyces cerevisiae, or baker's yeast. Despite it being a simple, single-cell organism, the basic cellular 'plumbing' of yeast has been preserved by evolution in more complex organisms, including humans. "In fact, the gene networks that we found modify vesicle formation in yeast cells in response to sertraline also exist in human cells, specifically neurons. Vesicle formation heavily influences the ability of neuronal synapses -- the tiny gapped connections between nerve cells -- to package neurotransmitters and prepare them for use in nerve-cell communication. "Our finding that sertraline affects vesicle formation suggests a more expansive view of antidepressant function than is currently accepted. "Dominant now is the monoamine hypothesis of antidepressant function, which was originally formulated in the 1960s and 1970s. It states that depression is the result of a chemical imbalance of neurotransmitters in the brain that may be corrected by artificially increasing the levels of serotonin, or other monoamine neurotransmitters, in the synapses. Sertraline belongs to a class of drugs called selective serotonin reuptake inhibitors (SSRI) that are thought to block the function of specific proteins that normally decrease serotonin levels in the synapses. "However, the monoamine hypothesis fails to account for several key clinical observations of antidepressant activity, notably the lag time between the start of antidepressant treatment in patients and the onset of relief. Moreover, the monoamine hypothesis cannot explain the unexpected biological activity of antidepressants in simple organisms that lack serotonin such as baker's yeast. "The work out of my lab captures a specific non-serotonin-based biological reaction to an SSRI. Granted, the synaptic serotonin transporter is one site where these drugs interact, but we show that's likely not all they do. These drugs have multiple effects on various targets in the cell -- and one of the targets might be cell membranes themselves.
"In addition, our work provides some grounding for the neurotrophic hypothesis of depression, which states that the loss of neural connectivity in specific brain regions such as the hippocampus may actually be the root of depression. The neurotrophic hypothesis fills in many of the gaps of the monoamine hypothesis, including the therapeutic time lag. Since the 1990s, neuroscientists have known that chronic, extended antidepressant treatment can result in the proliferation of brain cells, possibly via a mechanism that involves the growth protein BDNF.
"Altogether, our work suggests that the serotonin-based theory might be an oversimplification and that the cause of depression is not a closed story. "In my lab, future research will aim to integrate the multiple, interwoven strands that make up the totality of antidepressant pharmacology -- including but also beyond serotonin -- and translate this knowledge into better antidepressants and diagnostic tools for depression."This research was published online April 18 in PLoS ONE and was supported by the Lewis-Sigler Institute.
Posted by bleauberry on June 15, 2012, at 7:23:34
In reply to Re: Yeast Cell Reaction to Zoloft Suggests... » bleauberry, posted by Phillipa on June 14, 2012, at 15:37:05
> So it wasn't just me? I also tried. Hey blue is doxycycline good after three years of storage? Thanks P
Absolutely NOT. Throw it away..
Most meds are fine after they expire. They lose potency but don't usually go rancid or toxic.
Doxycycline however does go bad and can damage the kidneys. It can be a deadly drug after expiration.
If you want some it is pretty easy and cheap to order on the web from overseas pharmacies. In your case a dose of 200mg twice a day would be standard. In someone with non-lyme history 200mg is usually the max. But in lyme all the llmds agree that Doxy needs to be at least 400mg a day. Personally I find tolerating that is no different than tolerating 200mg, feels the same, and it has been an easy med to handle after I got through the first few months of touch-and-go herxing, start, stop, restart, break, restart, up dose, back dose, up dose, up dose....but now it is like taking a placebo. Except if I try stopping it, I crash hard and lyme symptoms come back with a vengeance.
Anyway, off track, sorry, but no, Doxy is not safe after expiration.
Posted by Phillipa on June 15, 2012, at 20:30:56
In reply to Re: Yeast Cell Reaction to Zoloft Suggests... » Phillipa, posted by bleauberry on June 15, 2012, at 7:23:34
Thanks will throw away. Phillipa
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