23 hours ago, guitarman01 said:I skimmed through that article pretty fast looking for the headline. I'm still not quite clear on how doxycycline is having an effect.
This seems like a more digestible summary, you summed it up pretty well though.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452046/
Reprogramming adult, fully differentiated cells to pluripotency in vivo via Oct3/4, Sox2, Klf4 and cMyc(OSKM) overexpression has proved feasible in various independent studies and could be used to induce tissue regeneration owing to the proliferative capacity and differentiation potential of the reprogrammed cells. However, a number of these reports have described the generation of teratomas caused by sustained reprogramming, which precludes the therapeutic translation of this technology. A recent study by the IzpisºaBelmonte laboratory described a cyclic regime for shortterm OSKM expression in vivo that prevents complete reprogramming to the pluripotent state as well as tumorigenesis. We comment here on this and other studies that provide evidence that in vivo OSKM induction can enhance tissue regeneration, while avoiding the feared formation of teratomas. These results could inspire more research to explore the potential of in vivo reprogramming in regenerative medicine."When such animals were fed with doxycycline for extended periods of time, ubiquitous and sustained expression of OSKM caused uncontrolled proliferation and disorganized differentiation followed by extensive tumorigenesis and death"
^just looking at that line right there, this seems a long way off from any type of commercialization. Or a person walking into a doctors office saying I need a prescription for this. 10 years will probably turn into 20 at the least. Although this is nothing i've been looking at, so Im sure you have more knowledge then me.
The mice were genetically engineered to respond to doxycycline by producing the pluropotency-inducing factors. The genes for the pluropotency factors were artificially inserted into the genome in a way they they would be copied into useful products in the presence of docycycline.
https://en.wikipedia.org/wiki/Tetracycline-controlled_transcriptional_activation
Due to this programming, the TetR repressor (that keeps the genes turned OFF) is released from the regulatory region when exposed to doxycycline (turning the genes ON) and Oct3/4, Sox2, Klf4 and cMyc(OSKM) are transcribed, rather than the shRNA (silencing RNA) insert shown in the diagram.
...In the study, bad things didn't start to happen unless the genes were consistently turned on by repeated doxycycline administration. Not sure why they don't use something more subtle than doxycycline for this since it has its own deleterious off-target effects on mitochondria.
Something similar to this may be needed to truly "cure" us, but reliable in-vivo reprogramming of whole organisms is years away. They are at least working on this now utilizing technologies like CRISPR.
On 2/18/2018 at 9:26 PM, mariovitali said:According to the hypothesis, Vitamin K is very important. However there are many more pathways that need to be looked at. What we are dealing with is a vicious cycle of Inflammation, Oxidative Stress, Endoplasmic Reticulum Stress and impaired Phagocytosis (list not inclusive).
Im sure you are, but id keep your mind open to other possibilities as well (as am I) as opposed to the liver being the originating source of the problem. I still keep the liver as a target in mind of course.
Liver stiffness starts to sound a lot like artery stiffness, hence blood flow, tissue death.
You can look at kidney dysfunction possibly being related as well.
Heart diseases affecting the liver and liver diseases affecting the heart.
Clinical Predictors of Hepatic Fibrosis in Chronic Advanced Heart Failure
Jan 19, 2010 -ConclusionsHepatic fibrosisis common inpatientswith advancedheart failure. Renal dysfunction, significant tricuspid regurgitation and abnormalliverfunction tests are associated withhepatic fibrosis, but the predictive value of other clinical features is limited.
Liver stiffness assessed by Fibrosis-4 index predicts ... - Open Heart
ObjectiveLiverdysfunction due toheart failure(HF) is known as congestive hepatopathy. It has recently been reported thatliverstiffness assessed by transient elastography reflects increased central venous pressure. TheFibrosis-4 (FIB4) index (age (years) aspartate aminotransferase (IU/L)/platelet count
Association between liver fibrosis and coronary heart disease risk in ...
Dec 18, 2017 -Nonalcoholic fattyliverdisease (NAFLD) is being increasingly recognized as the most common cause of chronicliverdisease worldwide. It has been shown that NAFLD in adults is associated with increased risk of coronaryheart disease(CHD). Because of the limitations ofliverbiopsy, noninvasive scoring...
Interactions of the heart and the liver
In chronic and acute cardiac hepatopathy, owing tocardiac failure, a combination of reduced arterial perfusion and passive congestion leads to cardiaccirrhosisand cardiogenic hypoxic hepatitis. These conditions may impair theliverfunction and treatment should be directed towards the primaryheart diseaseand seek to...
On 2/18/2018 at 11:29 PM, Dubya_B said:
Maybe this is what Im looking at. Does bacteria play a role?
I dont really plan on spending much time on this personally, because to me, this is sort of science fiction for the next decade or so. Im looking for solutions and answers now, hopefully not in the distant future when it wont matter as much.
Tetracycline-controlled gene expression is based upon the mechanism of resistance to tetracycline antibiotic treatment found inGram-negative bacteria. In nature, the Ptetpromoterexpresses TetR, therepressor, and TetA, the protein that pumps tetracycline antibiotic out of the cell
Q: What is CRISPR? A: CRISPR (pronounced crisper) stands for Clustered Regularly Interspaced Short Palindromic Repeats, which are the hallmark of a bacterial defense system that forms the basis forCRISPR-Cas9 genome editing technology.
1 hour ago, sirhc30 said:I got visual disturbances from accutane and had brain MRI's (with contrast-agents) with normal result........
Perhaps its not an MRI we need to do but some other scan??
its like what a lot of guys on here are now saying about the liver, they are now saying fibroscan specifically not just a normal liver scan which Ive done twice only to conclude a fatty liver....
Similar with what we now should be asking in the way of hormone testing. Weve all done many blood tests only to conclude some highs and lows here and there but nothing conclusive- time we now looked at pituitary scans to dig deeper at the mechanism that actually controls the hormones.
16 hours ago, guitarman01 said:Maybe this is what Im looking at. Does bacteria play a role?
I dont really plan on spending much time on this personally, because to me, this is sort of science fiction for the next decade or so. Im looking for solutions and answers now, hopefully not in the distant future when it wont matter as much.Tetracycline-controlled gene expression is based upon the mechanism of resistance to tetracycline antibiotic treatment found inGram-negative bacteria. In nature, the Ptetpromoterexpresses TetR, therepressor, and TetA, the protein that pumps tetracycline antibiotic out of the cell
Q: What is CRISPR? A: CRISPR (pronounced crisper) stands for Clustered Regularly Interspaced Short Palindromic Repeats, which are the hallmark of a bacterial defense system that forms the basis forCRISPR-Cas9 genome editing technology.
Bacteria's only involvement in this is that we take from them to make our lives better.
i.e.: The control region was taken from the tetracycline/doxycycline antibiotic-resistance gene-set in bacteria, genes that induce pluripotency were added in place of the normal a-b resistance genes, then the whole deal was injected into early-stage embryos of the mice, or their progeny, used in the study Frage posted about reversing epigenetic marks.
The CRISPR system was taken from bacteria and is used to routinely perform procedures like the one mentioned above with high precision and accuracy, with far less steps. Bacteria use it to find and cut viral DNA with high specificity, we use it to cut and paste gene inserts into animals.
This stuff isn't science fiction! It's every day science. There are people out there who could do this during their lunch break. j/k
It's all moot since we don't know what specifically happened to us yet and medicine is 30 years behind the times anyway,
They can't even be bothered with 23andMe-level genetic analysis in clinical studies for drugs yet! ...Something that would drastically reduce the number of people on medicines causing them severe side effects ...Pathetic.
.
3 hours ago, Dubya_B said:This stuff isn't science fiction! It's every day science.
Sorry, I meant too far off in the distance even if its fact based. For me at the end of the day the science doesn't matter as much as what can we do about this based on the science, or how do we further look into this?
Meaning immediate solutions for health, or resolutions legally. Some might not apply to you or me at this point but information that can at least be passed on.
Then again, maybe we have already dabbled in this, and didn't have the greatest outcome afterwards. A roll of the dice.
Vitamin A/Retinol and Maintenance of Pluripotency of Stem Cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3967188/
Retinol, the alcohol form of vitamin A is a key dietary component that plays a critical role in vertebrate development, cell differentiation, reproduction, vision and immune system. Natural and synthetic analogs of retinol, called retinoids, have generally been associated with the cell differentiation via retinoic acid which is the most potent metabolite of retinol. However, a direct function of retinol has not been fully investigated. New evidence has now emerged that retinol supports the self-renewal of stem cells including embryonic stem cells (ESCs), germ line stem cells (GSCs) and cancer stem cells (CSCs) by activating the endogenous machinery for self-renewal by a retinoic acid independent mechanism. The studies have also revealed that stem cells do not contain enzymes that are responsible for metabolizing retinol into retinoic acid. This new function of retinol may have important implications for stem cell biology which can be exploited for quantitative production of pure population of pluripotent stem cells for regenerative medicine as well as clinical applications for cancer therapeutics.
Now again looking at this very quickly, i could take a page from those studies. After treatment cellular chaos or dysregulation could ensue.
For thoughts about tumor genesis, maybe its plausible.
^also looking at this systemic bacteria was altered. Obviously the acne bacteria is gone or greatly reduced. systemic microbiome changes also occurred in the skin, nose, throat, and intestinal tract as all of this happened.
Reprogramming of human somatic cells by bacteria. - NCBI
Apr 10, 2015 -We previously showed that when human dermal fibroblast (HDF) cells were incorporated with lactic acidbacteria(LAB), the LAB-incorporated HDF cells formed clusters and expressed a subset of commonpluripotentmarkers. Moreover, LAB-incorporated cell clusters could differentiate into cells derived...
Again this is very quick, but these are my quick thoughts.
I went back and looked at this study. Alot of good information here.
Looking at it more, it's talking about a function for Vitamin A/retinol that's independent of Retinoic Acid.
Meaning it has its own function as retinol, before any type of conversion to Retinoic Acid.
Funny how you continue to see the paradox of retinoic acid toxicity with retinol deficiency.
I just dont think supplementing Vitamin A is the answer though. Ive tried this on numerous occasions.
I didnt have eye floaters until I tried supplementing with vitamin a, many years after accutane.
In that regard this might be a false lead, but your seeing everything that relates.
Vitamin A/Retinol and Maintenance of Pluripotency of Stem Cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3967188/
retinol has a direct retinoic acid independent function in stem cell biology [12,13,14,15,16] and metabolic fitness of mitochondria
Inside the cytoplasm, vitamin A/retinol binds to a 15 kDa cellular retinol binding protein (CRBP) and is converted into retinoic acid by two sequential oxidation steps that convert first retinol into retinaldehyde and then to retinoic acid. Though the conversion of retinol into retinaldehyde is reversible, the retinoic acid cannot be reduced back to retinol. Retinol is converted into retinaldehyde by retinol dehydrogenases (Rdh10) whereas the enzymes that metabolize retinaldehyde into retinoic acid include retinaldehyde dehydrogenases Ralhd1 (Aldhd1), Ralhd2 (Alhd1A2) and Ralhd3 (Alhd1A3) [26,27].
retinoid X receptor (RXR) which belong to the superfamily of ligand-inducible transcriptional regulators that include steroid hormone receptors
vitamin A/retinol also has a direct function in the maintenance of self-renewal and prevention of differentiation of pluripotent stem cells
the alcohol form of vitamin A influences the biological functions without conversion into its acid metabolite.
This is maybe more of what I thought I was posting. You can find conflicting studies for just about everything if you look hard enough.
@Dubya_B
Short-term retinoic acid treatment sustains pluripotency and suppresses differentiation of human induced pluripotent stem cells
https://www.nature.com/articles/s41419-017-0028-1?elqTrackId=3af3934dbb0f49deb9ff3180a6035632
Cell Death & Diseasevolume9, Articlenumber:62018
@Frage
This is from your study.
"pluripotency reverses cellular age"
How is this different from your study?
Anyone feel free to chime in as well.
Here's something new.
Does oral isotretinoin prevent Propionibacterium acnes resistance?
This paper reports preliminary data demonstrating that oral isotretinoin (Roaccutane/Accutane) significantly reduces total numbers of resistant P. acnes on the skin of all patients.
Frustrated by Acne? New Research Shows Skin Microbiome Makes a Difference
- BYCYNTHIA WALLENTINE
- 04/07/2017 1:21 PM
Recent research, presented at the Microbiology Society's Annual Conferenceby a team from the David Geffen School of Medicine in UCLA, may open doors for new options in the treatment of acne.
The findings of the study offer some hope for those who suffer acne:
- For good and forever,P. acnes:The bacteria commonly blamed for acne are present in the skin microbiome of those with and without acne. But the strains ofP. acneswere different between the two groups. In the group without acne, theP. acnesstrains support bacterial metabolism, and are considered important for healthy skin. In the group of participants with acne, there were less helpful strains ofP. acnesthat were more likely to trigger skin damage.
@guitarman01
I couldn't find that exact quote in the studies I posted, but yeah, inducing a cell to a pluripotent state will eliminate most epigenetic marks and thus a giant amount of cellular age. This is a big reason why we as a race can span time infinitely. Even though mom and dad are old, their kid won't be, even though that kid started out as a single cell FROM the mother.
Other parts of cellular age could be like, random bad proteins floating around, mDNA damage, or damaged enzymes? Not exactly positive on all the forms of cell damage, but DNA and epigenome mutations are key players.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3967188/
^This study you posted is specifically about using retinol/retonic acid to increase populations of stem cell colonies in vitro. Some differences being: It's probably unlikely to work well in vivo, they only looked at already pluripotent cells, and it mostly increased gene expression associated with sustaining pluripotency and not inducing it (except maybe OCT4). The gist being that it's very unlikely this would result in the type of cellular reprogramming we would want in vivo, something that seems very tricky to do.
This topic is still really interesting to me anyway and something I'll look into more. And keep an eye on as the medical world progresses.
edit: At least some folks are getting awful good with CRISPR:
[Edited link out]
Just hope this can translate to us some day.
Also, Cell publishes great studies.
On 19.2.2018 at 2:02 AM, TrueJustice said:Perhaps its not an MRI we need to do but some other scan??
After Accutane I got the Visual Snow syndrome. People with Visual Snow also have many symptoms (it's a Syndrome!!!!!!), such as pain, fatigue, brain fog etc. and I see similarities to post-accutane. I don't even know if the cause of all the disorders is the same as yours or if I got Visual Snow Syndrome, which has different causes than your post-accutane-problems.
I see all the similarities and think it's worth watching the Visual Snow research too. With Visual Snow, a pet scan shows that certain regions of the brain have altered metabolism: https://www.nyheadache.com/blog/visual-snow-and-migraine/.
@sirhc30 United States
6 hours ago, sirhc30 said:After Accutane I got the Visual Snow syndrome. People with Visual Snow also have many symptoms (it's a Syndrome!!!!!!), such as pain, fatigue, brain fog etc. and I see similarities to post-accutane. I don't even know if the cause of all the disorders is the same as yours or if I got Visual Snow Syndrome, which has different causes than your post-accutane-problems.I see all the similarities and think it's worth watching the Visual Snow research too. With Visual Snow, a pet scan shows that certain regions of the brain have altered metabolism: https://www.nyheadache.com/blog/visual-snow-and-migraine/.
What did your specialist say after these findings??
What was the follow up?
@Frage
When I'm looking through alot of these studies, I look at what might be possible.
On 2/19/2018 at 0:53 PM, guitarman01 said:
For example this right here. I don't necessarily have to explore this in depth to think what might be possible and ask myself questions.
Can the microbiome that resides in and on a person alter human genetic expression?
Possibly.
I do also zoom in on certain topics, thoughts, possibilities.
You brought up anti aging treatments. I was already sort of aware of some anti aging properties of Accutane, (even though it seems to be the opposite)
So I looked for this information. Those last two studies, while maybe not quite the same (and I don't claim to understand some of this at this point)
Seem like they could be similar enough, combined with other studies that are out there, to ask the question does Accutane have anti aging properties?
Possibly.
So maybe we took something that had anti aging properties, but something else still wasn't right about it for a certain group of people.
Again you can find conflicting studies for everything.
To me it's what holds up to scrutiny? What can you try to tear down and what's still left standing?
I've said it before, if we really do find something, it might not be in any studies yet.
It could be a combination of knowledge across many topics that keep peeling back the layers to see whats left.
Thanks for the posts.
7 hours ago, sirhc30 said:After Accutane I got the Visual Snow syndrome. People with Visual Snow also have many symptoms (it's a Syndrome!!!!!!), such as pain, fatigue, brain fog etc. and I see similarities to post-accutane. I don't even know if the cause of all the disorders is the same as yours or if I got Visual Snow Syndrome, which has different causes than your post-accutane-problems.I see all the similarities and think it's worth watching the Visual Snow research too. With Visual Snow, a pet scan shows that certain regions of the brain have altered metabolism: https://www.nyheadache.com/blog/visual-snow-and-migraine/.
I have Visual Snow as well as tinnitus. Both suggest a hypermetabolism of the brain.
Here's the thing: The two most dominant side effects affecting peoples well being I'd say are people with ED or Depression. Both we can assume relate to alterations of the limbic system in the brain (at least what I assume). That isn't to say there are the rare few that have circulation issues post accutane, or digestive organ problems, or persistent dry skin/hair, which I can see why studies relating to micro biome, or genetic cellular transcription would interest those people, but we should try to focus on what is practical and what symptoms we can mediate.
I think that would be more practical than trying to find the mechanisms of action. From my experience, doctors aren't interested in linking side effects to accutane, the more you do, the more they shy away, rather they just want to attenuate symptoms best they can. We need more experimentation of treatments from people and more empirical evidence gathering. But theory is fine, but provide some treatment after posting theory, or we aren't gonna get anywhere anytime soon.
2 hours ago, macleod said:I have Visual Snow as well as tinnitus. Both suggest a hypermetabolism of the brain.Here's the thing: The two most dominant side effects affecting peoples well being I'd say are people with ED or Depression. Both we can assume relate to alterations of the limbic system in the brain (at least what I assume). That isn't to say there are the rare few that have circulation issues post accutane, or digestive organ problems, or persistent dry skin/hair, which I can see why studies relating to micro biome, or genetic cellular transcription would interest those people, but we should try to focus on what is practical and what symptoms we can mediate.
I think that would be more practical than trying to find the mechanisms of action. From my experience, doctors aren't interested in linking side effects to accutane, the more you do, the more they shy away, rather they just want to attenuate symptoms best they can. We need more experimentation of treatments from people and more empirical evidence gathering. But theory is fine, but provide some treatment after posting theory, or we aren't gonna get anywhere anytime soon.
Almost all people with visual snow have depression and anxiety disorders and many also have ED. I guess that studiesare in progress, to find treatment strategies on on Visual Snow . There are experts who predict that Visual Snow can eventually be successfully treated nearly. If there are any treatment strategies for Visual Snow soon, maybe these will help many people here who have ED or anxiety disorders etc. or maybe it doesn't help, but I think it's worth to think about it. Maybe we should keep that in mind and observe news about Visual Snow regularly, because there are so many similarities.
@Jorcruz24
Something to keep in mind.
FibromyalgiaCommon inHeartFailure Patients, Study Finds
Patients with coronary artery disease, a heart condition in which blood vessels become blocked with plaque, often have fibromyalgia. A study found that the severity of fibromyalgia followed the severity of the heart disease.
Among them, 22.8% fulfilled diagnostic criteria for fibromyalgia. Even more 31% had widespread musculoskeletal pain, with at least 11 tender points. In addition, 19.3% had depression. When this number was split for those with and without fibromyalgia, slightly more patients in the fibromyalgia group were affected by depression.
In addition, the team found that all other central sensitivity diseases investigated, including temporomandibular joint (TMJ) dysfunction, irritable bowel disease (IBD), headache, and chemical sensitivity were more common in people with both heart failure and fibromyalgia.
Fibromyalgia is associated with coronary heart disease: a population ...
Is fibromyalgia a cardiovascular disease? A comment on Martinez ...
Fibromyalgia associated with coronary heart disease and stroke risk ...
Jul 12, 2016 -There are many factors that could contribute to this increased risk ofheart diseaseinfibromyalgia. Some researchers believe it may be a result of genetics, while others believe the conditions contributes to greater health problems as it progresses. At this time, the researchers have only found an association...
Study Says Accutane Worse for Heart, Liver Than Thought | Fox News
Most dermatologists already knew the drug also could increase levels of cholesterol, liver enzymes and blood fats calledtriglycerides[Edited link out]that can raise the risk of heart disease. But the new study found higher than expected percentages of patients developing these abnormal lab results.
Among patients with normal lab tests before they started taking the drug, 44 percent developed high levels of triglycerides. The package insert, by contrast, cites high triglycerides in 25 percent of patients.
Thirty-one percent of healthy patients in the study developed highcholesterollevels [Edited link out] and 11 percent developed abnormal liver tests.
Roche representatives did not reply to an e-mail seeking comment on the study
Acne DrugAccutaneNo Longer Sold. ... Generic versions of the acne drug, calledisotretinoin, are still available from several manufacturers. But Roche, which has sold the drug to 13 million patients since 1982, will not be one of them. The decision was made for "business reasons," Roche announced in a news release.Jul 8, 2009
Theres always a chance they found out something. Of course they would never be able to tell if they did.
Here's another possible link with SSRI's.
Antidepressants linked to thicker arteries -- ScienceDaily
Researchers at the Emory School of Medicine have found real correlating data discovering that taking antidepressants, namely SSRIs, thicken the lining of your carotid arteries by 400 times normal. The carotid arteries are the arteries coming from your heart to your brain, bringing your brain freshly oxygenated blood to keep it functioning at optimum levels. People with carotid artery disease from thickening of the walls to plague build up have a decreased blood flow and this causes several unwanted conditions including stroke and death.
Effects of Long Term Sertraline Treatment and Depression on Coronary Artery Atherosclerosis in Premenopausal Female Primates
long term treatment with SSRI's promote Coronary Artery Atherosclerosis.
"these data suggest that a conservative approach to prescribing SSRIs for a broad range of disorders or for long time periods may be warranted, and that further study is critical given the widespread use of these medications."
Isotretinoin increased carotid intima-media thickness in acne patients
Background:Isotretinoin(Iso) in acne treatment may cause dyslipidemia and increase in liver enzymes. Moreover, its effect on lipid and glucose metabolism may induce atherosclerotic complications. The aim of this study was to evaluatecarotidintima-media thickness(CIMT), osteopontin (OPN), lipid, high sensitive...
Now how about 5ar inhibitors?
a recent clinical study with a 5--reductase type 1 and type 2inhibitorshowed clinical responsessimilarto those seen with finasteride.
"We hypothesize that the lower prostate cancer incidence observed in men taking warfarin is due to the ability of warfarin toreduce AR activity,similar to the effect of 5-alpha reductase inhibitors"
Previously, we identified warfarin and other vitamin K antagonists as AR inhibitors in a high-throughput screen for novel AR regulators [18]
@mariovitali@Dubya_B@Frage and company.
On 15/02/2018 at 11:09 PM, Colinboko said:Kind of starting to get worried with this whole water retention/kidney thing..
Really want to get an MRI done after some blood tests to rule out any type of pituitary tumor. Ive seen lots of correlation between Accutane and adenomas. A pituitary tumor would be a blessing actually. That way something could at least be fucking treated. Would also explain a lot of the balance issues/dizziness/pressure behind eyes/light sensitivity
I must be releasing a SHIT ton of ADH because Im holding onto every sip of water I take but when I drink things that inhibit ADH, I pee it right out. Such as coffee, alcohol...
My urineis rarely clear also.. Like I said it seems like every ounce of water is being stored somewhere
You need to get tested for this
https://en.wikipedia.org/wiki/Diabetes_insipidus?wprov=sfti1
40 minutes ago, Perene said:You need to get tested for this
https://en.wikipedia.org/wiki/Diabetes_insipidus?wprov=sfti1
Opposite for me. This is from a lack of vasopressin. I seem to have too much! Im not frequently urinating.
4 hours ago, guitarman01 said:Here's another possible link with SSRI's.
Antidepressants linked to thicker arteries -- ScienceDaily
Researchers at the Emory School of Medicine have found real correlating data discovering that taking antidepressants, namely SSRIs, thicken the lining of your carotid arteries by 400 times normal. The carotid arteries are the arteries coming from your heart to your brain, bringing your brain freshly oxygenated blood to keep it functioning at optimum levels. People with carotid artery disease from thickening of the walls to plague build up have a decreased blood flow and this causes several unwanted conditions including stroke and death.https://www.sciencedaily.com/releases/2011/04/110402163856.htmApr 2, 2011 -Researchers measured carotid intima-media thickness -- the thickness of theliningof the mainarteriesin the neck -- by ultrasound. Among the 59 pairs of twins where only one brother tookantidepressants, the one taking the drugs tended to have higher carotid intima-media thickness (IMT), even when...Effects of Long Term Sertraline Treatment and Depression on Coronary Artery Atherosclerosis in Premenopausal Female Primates
long term treatment with SSRI's promote Coronary Artery Atherosclerosis.
"these data suggest that a conservative approach to prescribing SSRIs for a broad range of disorders or for long time periods may be warranted, and that further study is critical given the widespread use of these medications."Isotretinoin increased carotid intima-media thickness in acne patients
Background:Isotretinoin(Iso) in acne treatment may cause dyslipidemia and increase in liver enzymes. Moreover, its effect on lipid and glucose metabolism may induce atherosclerotic complications. The aim of this study was to evaluatecarotidintima-media thickness(CIMT), osteopontin (OPN), lipid, high sensitive...
Now how about 5ar inhibitors?
a recent clinical study with a 5--reductase type 1 and type 2inhibitorshowed clinical responsessimilarto those seen with finasteride."We hypothesize that the lower prostate cancer incidence observed in men taking warfarin is due to the ability of warfarin toreduce AR activity,similar to the effect of 5-alpha reductase inhibitors"
Previously, we identified warfarin and other vitamin K antagonists as AR inhibitors in a high-throughput screen for novel AR regulators [18]
@mariovitali@Dubya_B@Frage and company.
Does alcohol thin the blood??
Is that why we sometimes feel better during and after alcohol or is that more to do with releasing endorphins?
Also, can someone please state which specialty these artery issues relate too?
Is it a heart specialist we should see?
Varicose surgeons arent who we should initially talk too, its got to be another specialist, but who?
I believe that the fact that you feel better during Alcohol consumption is because Alcohol induces P450 (tells your Liver to work faster). However in the long run -as you know- Alcohol creates problems.
It is possible that you will feel even better by consuming Gin . This is so because we have a synergistic effect of Alcohol and Pronthyacinidins from Juniper Berries used to make the distinctive taste of Gin(Hypothesis).
Note that i am not suggesting that you or anyone else should drink Gin.
The complete opposite effect can be experienced by consuming P450 inhibitors such as Grapefruit. This will bring an increase to one's Symptoms and may bring a very intense Crash. Again, i am not suggesting that anyone should try this !