Acne.org Products
here is a study referencing mk7 did not induce any type of hypercoagulation. I'd still like to look more into this though.
Low-dose menaquinone-7 supplementation improved extra-hepatic vitamin K status, but had no effect on thrombin generation in healthy subjects.
CHRONIC FATIGUE SYNDROME: STUDIES ON CLINICAL PRESENTATION,
so this is kind of interesting. Floats around alot of things that have been discussed on here.
Myalgic encephalomyelitis: A highly prevalent debilitating disease Persistent, debilitating fatigue associated with numerous physical and neurocognitive symptoms Disease severity can range from moderate to extremely severe: Prevalence estimates: 0,3 to 0,6%; one million patients in the USA, two million patients in Europe This may just be the tip of the iceberg High socio-economic cost Cost to the society estimated as approximately $16 billion in the USA, 20 billion in Europe
Patients usually present with multiple intestinal symptoms including: Nausea Abdominal pain Poor appetite Abnormal bowel motility Gastric reflux Bloating Inflammation of the gastrointestinal tract Marked alteration of the intestinal microbial flora
Immune alterations resulting from intestinal dysfunction
CHRONIC FATIGUE SYNDROME: STUDIES ON CLINICAL ...
Persistent, debilitatingfatigueassociated with numerous physical and .... Heavy metals interfere directly with energy production. Oxidase.Cu2+. H. S. S. S. S. H.
Here is some more info on k2 safety or thickening the blood.
It is often postulated that excessive vitamin K may result in
overcoagulation, i.e. increased thrombosis risk. However,
vitamin K-dependent proteins have a limited number of Glu
residues capable of g-carboxylation per molecule, beyond
which there can be no further g-carboxylation or excessive
coagulation. Despite this, it is critical to demonstrate that a
high intake of menaquinones does not increase thrombosis
risk. It was shown in rats that thrombosis risk is not increased
at doses up to 250 mg/kg of MK-4(104). In human subjects, the
endogenous thrombin potential, which is the most sensitive
marker to evaluate thrombosis risk in plasma(105), was not
affected by MK-7 intakes as high as 360mg/d for 6 weeks(70).
The only exception to this is observed in individuals on
coumarin-based oral anticoagulants, for whom dietary sup-
plementation with vitamin K can influence the stability of
the international normalised ratio(59,106). MK-7 has the poten-
tial to interfere with oral anticoagulants at doses greater than
50mg/d(13). However, there is little collective experience on
the potential toxicity or adverse events associated with
sustained menaquinone supplementation among individuals
with normal coagulation.
My rant, prob not helpful but anyway...
I remember saying something about the way the artist Prince died last year but here we go again with Chris Cornell - reports suggest he took too much Ativan and this is what lead him to commit suicide.
Why would a doctor prescribe a recovering alcoholic Ativan???
Of course the individual must take some accountability too but I bet my bottom dollar he wasn't given the right info from doctor to begin with...
It pisses me off when doctors can't communicate properly and give good advice....this guys death sounds like it was completely avoidable.
We can relate similar bad practice to Accutane - most of us should never of been put on the drug in the first place if sound advice and proper screening were to of taken place!!
Wake up doctors of the world, wake up....
6 minutes ago, TrueJustice said:Chris Cornell
One of my favorite artists ever. tighter and tighter from down on the upside. Yea the drugs to keep him off the drugs is what might have killed him. Such a loss. Saw him live once, best show ever. He was a rock God, had the coolest friends, a wife and kids, and goes out like that. More then tragic and yea you wonder if he never took those pills...
10 minutes ago, cnb30 said:I wonder if since there's no use of getting better, we could just make ourselves infinitely worse out of curiosity.
What..? People HAVE gotten better. JESUS people.
16 hours ago, guitarman01 said:what your saying has been similar with me. Ive been getting alot of blood test recently, and its like my blood clots so fast i dont even need a bandaid after getting blood drawn. Its a drop or two of blood, then it quickly dries up and thickens.id keep this in mind as well. Natto as the food is very high in k2. Which maybe there could be a balancing effect. There could be more info then just this on the subject as well.
Question: I am a bit confused. I've read that nattokinase can be a good supplement to take for cardio issues as it hasblood thinning properties, and at the same timeread that K-2 can be a good supplement to take for cardio issues, butdoesn't K-2 assist in coagulation? It seems to me that if both of these supplements are taken that they will work against each other?One of the major reasons people take Vitamin K-2 for cardiovascular support is because it supports the formation of Osteocalcin, a protein carrier which helps to transfer calcium into the bone. Nattokinase helps breaks down fibrin, which is the webby structure that forms the basis of clots to help support circulation.
Vitamin K-2 does support the formation of clotting factors in the liver, which under ideal circumstances will simply remain on stand-by until the body has a legitimate need to initiate the clotting process, leading to production of fibrin.
The two could actually be considered as balancing one another. Generally, there is a cycle going on for most substances in the body with the substance being built up or formed and then being broken down. In other words, Nattokinase and Vitamin K-2 have very different effects on the body, but like many other supplements can have some overlapping areas of benefits. They dont exactly work against each other because the clotting factors will allow your blood to clot when needed, but wont force it to clot.
If you have any history of blood clots or anything which might compromise the integrity of the blood vessels and contribute to abnormal clotting, you wouldnt want to take either product without consulting your health care practitioner. If you have a tendency to clotting, K-2 could aggravate this since something is activating the clotting process when it isnt desirable instead of just having the clotting factors sitting around on stand-by. If you take any prescription blood-thinners like Warfarin, Coumadin, Plavix, etc you certainly wouldnt want to take either Nattokinase or K-2 without consulting health care practitioner.
As per usual - love the science, appreciate the research etc and the posting of it, but haven't we all done the Vit K thing? I did it 16 months ago in conjunction with Vit D when it was strongly advised to take together!!
Are we left to believe that only injecting vitamins will work like they do with B12 for example?
My other theory and I've said this a million times, is that gut health is adversely affected and can't process these Vitamins and Minerals correctly, not only that but we also have systemic inflamattion at the same time.
Someone said it years ago on this forum, you've gotta fix inflammation first before you can fix any other tane related problems.
Curcumin, fish oil etc are fine but what else that's stronger??
LDN perhaps.....
It is not just about Vitamin K supplementation. I believe that several pathways must be supported so that Liver function becomes optimal again.
As discussed, i believe that by taking Calcium you are not helping yourself. The same applies for Vitamin D3 if it is taken in supplemental form.
If calcium is let loose and not properly being absorbed it creates problems. Vitamin K takes care of that (does other things as well of course).
So we have to support Liver function in any way we can. I believe that if anyone attempts to take a CYP450 inhibitor such as grapefruit, the symptoms will become much worse. I am not suggesting that you should try this at home!
you can check these genes. It might be good to know this.
Thrombotic Risk Profile, DNA Analysis
https://www.labcorp.com/test-menu/35736/thrombotic-risk-profile-dna-analysis
This assay detects the R506Q (Leiden) mutation in the factor V gene, the G20210A mutation in the factor II (prothrombin) gene, and the C677T and A1298C mutations in the MTHFR gene.
factor is f5, f2
you can find all of this on 23andme. I just checked. I already knew I was heterozygous for c677t and a1298c, but normal for r506q and g20210a
I prefer to use aspirin alternatives like nattokinase, fish oil, garlic, ginger, and turmeric instead. They are useful and safe natural blood thinners.
https://heartmdinstitute.com/health-and-wellness/how-often-can-you-take-aspirin/
So here is a thought. Just for one time purposes you take 2 full strength Aspirin325mg each. Do you feel better? More color in your skin? clearer thoughts? Nice Warm sensation in your head? Im not looking at this for anti-headache. im looking at this for powerful blood thinning properties you might notice pretty quick.
(i would cautionthis for people with gastritisor serious heartburn, maybe try lower dose or safe alternatives first)
If you notice a big difference. This could explain alot. Then we would go from here. id substitute fish with Krill btw.
This could still all tie together with liver/cardiovascular/neurological/Digestive
It could have started with methyl donor loss via loss of PC (choline) or systemic reduction in b12 levels (also methyl donor loss)
that starts to dispose you to some of these conditions.
how can you correct this? maybe a combination of k2 and natural blood thinner? not sure. While continuing to detox the liver. (ie. lecithin)or supply methyl donors like b12.
Just a thought, but id try the aspirin. Becausewhat your feeling or not feeling in your head might be from lack of blood flow.
What they are showing for blood thinners would probably also be the most powerful and safe anti inflammatories. You could maybe include vitamin e in that as well.
It is very interesting this thick blood/flow scenario.
I definitely think it might explain a few things like why I'm out of breath too easily, why I sweat like no bodies business, cold extremities, numbness in limbs etc etc.
Id also def recommend going down the natural path though over trying to introduce another precsiption drug.
Is there any organization/foundation of Post-Accutane Syndrome sufferers? Who do i contact for research if we have cases of individuals that have reversal of symptoms?
Please see here also regarding Lupus, CFS and Vitamin K. I have searched in this forum for Lupus and there are some hits coming up.
On 20 mai 2017 at 9:36 PM, Recreant said:Something else I'd like to add to my list of side effects that I totally forgot about: emotional deadening.
Ever since Accutane I tend to have what people would call a stern, emotionless presence.
Now, it's not that I lack emotions, but I have a lot of trouble expressing them, even when I really try.
The first time I noticed it was when I was at a hairdresser after about 6 months of Accutane. I wasn't really looking at myself in the mirror much at all while having my hair cut because acne had triggered body dysmorphic disorder in me and so staring at myself in a mirror with other people around wasn't something I tended to do. My hairdresser was hot and making a lot of jokes and I was laughing and giggling along - or so I thought. I became a bit confused when she kept asking me if I was feeling okay or was tired after a long day. I didn't know why she was asking me about it until I finally glimpsed myself in the mirror and I had this sort of flat, exasperated expression on my face. And when I would "laugh" at something she'd say, it was more akin to a sad exhalation of air. It was a bit like being in the Twilight Zone. Who was this jackass staring back at me? There was clearly a rift between the emotions I assumed I was conveying and what I really was.
that's a perfect description of many situations and feelings I have experienced too
11 hours ago, mariovitali said:Is there any organization/foundation of Post-Accutane Syndrome sufferers? Who do i contact for research if we have cases of individuals that have reversal of symptoms?
Please see here also regarding Lupus, CFS and Vitamin K. I have searched in this forum for Lupus and there are some hits coming up.
isnt this putting the cart before the horse a little bit? Im sure anyone is capable of answering this question, but I would just say lets cross that bridge when we get there. I'm sure there would be alot of people to tell if we found something concrete.
I have seen there is blood testing for menaquinones, its just not widely available or standardized. Maybe sometime in the future when there is more research and understanding on its importance, it will become a standard test.
Regarding Lupus I am curious if some of us would show some of the antibodies to lupus that might contribute to symptoms but not necessarily have full blown lupus. Here is kind of what im talking about.
There are also associations between antiphospholipid antibodies andheadaches,migraines, andoscillopsia.[5]Some studies have shown the presence of antiphospholipid antibodies in the blood and spinal fluid of patients with psychological symptoms.[6]
Very few patients with primary APS go on to developSLE.
If testing did reveal this to be a autoimmunity issue triggered by accutane, it sounds like there are some people on your forum that might have some good knowledge of this.
There is also this for digestive issues. Some of these tests are the exact tests I just got, being tested by Mayo Clinic.
Serological Profiles Aiding the Diagnosis of Autoimmune Gastrointestinal Dysmotility
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2741093/
Autoimmune gastrointestinal dysmotility is a limited autoimmune dysautonomia occurring idiopathically or in the context of an anatomically remote neoplasm, previously documented or unsuspected. Here we report 24 Mayo Clinic patients in whom the profile of serum autoantibodies aided this diagnosis.
Recorded motility abnormalities included: esophageal dysmotility 8 (6 had achalasia), delayed gastric emptying 12, slow small intestinal transit 7, slow colonic transit 4, and pelvic floor dyssynergia 4. Four patients underwent abdominal surgery; 2 commenced total parenteral nutrition. Plasma membrane cation channel autoantibodies were detected in 23 patients: neuronal voltage-gated calcium channel (5 N-type and 1 P/Q-type), acetylcholine receptor (11 ganglionic-type and 4 muscle-type) and neuronal voltage-gated potassium channel autoantibodies (4). Two patients had anti-neuronal nuclear autoantibody, type 1. Approximately half of the patients had other antibody markers of organ-specific autoimmunity (including skeletal muscle, striational, GAD65, thyroid or gastric parietal cell specificities). Neoplasia was diagnosed in 11 patients (9 recent, 2 remote): lung, breast and endometrial, gastrointestinal and thymoma. Moderate to dramatic improvement in gastrointestinal symptoms was reported following immunotherapy in 4 of 4 patients treated, and following pyridostigmine in 2 of 2 patients treated.
Was just thinking back on my MRA.
One drawback of MRA is that it does not depict small vessels or extremely slow blood flow as well as conventional angiography does. However, with its advantages, MRA is a good examination for many patients.
WHAT SHOULD I EXPECT DURING THE PROCEDURE?
- MRA is a painless and noninvasive procedure in which no incisions or arterial catheters are required. With some MRA techniques, contrast agents are not necessary, so no intravenous lines are needed. With other techniques, a small amount of a gadolinium-based contrast agent is added to highlight the blood vessels and enhance the sharpness of the image. This contrast material is infused through an intravenous line placed in your arm. No other preparation is involved.
- See more at: http://www.asnr.org/patientinfo/procedures/mrangiography.shtml#sthash.fwutECbD.dpuf
@mariovitali
You posted this. Am I missing something here? This is vitamin k dependant. This is vitamin k stimulating.
twovitamin K-dependentproteins, are ligands for the Tyro3/Axl/Merfamily
Increased plasma levels of the soluble Mer tyrosine kinase receptor in systemic lupus erythematosus relate to disease activity and nephritis.
Increased levels of, in particular, sMer and, to some extent, sTyro3, were found in patients with SLE or RA,but not in patients with CLI. Patients with SLE demonstrated the highest sMer levels and there was a strong correlation to higher SLE disease activity score (SLEDAI). In contrast, in patients with RA, the sMer levels did not correlate with the disease activity score (DAS). In SLE, sMer levels were particularly high in those with lupus nephritis, patients who also had decreased C1q levels and increased titers of anti-DNA antibodies. After therapy, the plasma concentrations of sMer decreased in parallel to the decrease in SLEDAI score.
1 hour ago, guitarman01 said:@mariovitali
You posted this. Am I missing something here? This is vitamin k dependant. This is vitamin k stimulating.
twovitamin K-dependentproteins, are ligands for the Tyro3/Axl/MerfamilyIncreased plasma levels of the soluble Mer tyrosine kinase receptor in systemic lupus erythematosus relate to disease activity and nephritis.
Increased levels of, in particular, sMer and, to some extent, sTyro3, were found in patients with SLE or RA,but not in patients with CLI. Patients with SLE demonstrated the highest sMer levels and there was a strong correlation to higher SLE disease activity score (SLEDAI). In contrast, in patients with RA, the sMer levels did not correlate with the disease activity score (DAS). In SLE, sMer levels were particularly high in those with lupus nephritis, patients who also had decreased C1q levels and increased titers of anti-DNA antibodies. After therapy, the plasma concentrations of sMer decreased in parallel to the decrease in SLEDAI score.
Actually it gets interesting when Professor Jonathan Edwards who was responsible for using Rituximab on patients of Lupus, starts saying that the method being used for Research using machine learning will be "Garbage In", "Garbage out"
I specifically ask him if References in the paper are also considered Garbage and he fails to answer this. I believe that this fact is quite interesting.
I recall very vividly that when i crashed with Propecia, i had autoimmune-like symptoms for months including Urticaria ,Joint Pains, dysphagia and dyspepsia.
4 hours ago, guitarman01 said:Was just thinking back on my MRA.
One drawback of MRA is that it does not depict small vessels or extremely slow blood flow as well as conventional angiography does. However, with its advantages, MRA is a good examination for many patients.
WHAT SHOULD I EXPECT DURING THE PROCEDURE?
- MRA is a painless and noninvasive procedure in which no incisions or arterial catheters are required. With some MRA techniques, contrast agents are not necessary, so no intravenous lines are needed. With other techniques, a small amount of a gadolinium-based contrast agent is added to highlight the blood vessels and enhance the sharpness of the image. This contrast material is infused through an intravenous line placed in your arm. No other preparation is involved.
- See more at: http://www.asnr.org/patientinfo/procedures/mrangiography.shtml#sthash.fwutECbD.dpuf
Is a MRA similar to MRI in procedure?
you lie down and go back into machine etc, I got claustrophobic with an MRI and had to get out. They gave me the option next time to be sedated during procedure.
Does this procedure measure brain inflammation? Which is what I need to address first and foremost.
Guys, just want to write a quick sappy post..
Very thankful for the community that we have here. If it weren't for the constant research, love (maybe not all the time lol) and support I truly believe a lot of us wouldn't keep pushing through today. We WILL find a way out. So much respect for all of you.
Just had this blood test as well
http://www.questdiagnostics.com/testcenter/TestDetail.action?ntc=14890
Antiphospholipid Antibody Panel
Hopefully, at least with what i got going on, I'll be able to narrow this down pretty quickly. At least with what's testable.
I mainly got these two tests after reading this paragraph from genetic genie, and doing some research on it. so we will see. This test alone was 900 dollars. luckily fully insurance covered. I hope lol.
Acetylcholine and antiphospholipid autoantibodies are seen in various autoimmune and chronic illnesses. It is well know that with Myasthenia Gravis, patients most commonly have autoantibodies against nicotinic acetylcholine receptor (nAChR).A large number of CFS patients may have acetylcholine receptor antibodiesaccording to a studypublished in theInternational Journal of Molecular Medicine.
Dysautonomia and POTS can also be associated with autoantibodies against acetylcholine receptors. Mayo medical laboratories has a very comprehensiveAutoimmune Dysautonomia Evaluationlab test that tests for autoantibodies against acetylcholine receptors and much more.
Antiphospholipid Syndrome (or Hughes syndrome) is an autoimmune condition that can lead to hypercoagulation and blood clots. Conditions such as Lupus, Sjogrens syndrome, Chronic Fatigue Syndrome, and Fibromyalgia are often associated with antiphospholipid antibodies. Antiphospholipid antibodies can even develop in presence of chronic infections such as Hepatitis C, Syphilis, Chlamydia pneumoniae, EBV, HHV-6, Lyme disease, mycoplasma, Q Fever, and many other infections. Antiphospholipid syndrome can be tested for withLabCorps Thrombotic Risk Profile [Edited link out]
On 5/25/2017 at 7:20 AM, guitarman01 said:Just had this blood test as well
http://www.questdiagnostics.com/testcenter/TestDetail.action?ntc=14890Antiphospholipid Antibody Panel
Hopefully, at least with what i got going on, I'll be able to narrow this down pretty quickly. At least with what's testable.
I mainly got these two tests after reading this paragraph from genetic genie, and doing some research on it. so we will see. This test alone was 900 dollars. luckily fully insurance covered. I hope lol.
Acetylcholine and antiphospholipid autoantibodies are seen in various autoimmune and chronic illnesses. It is well know that with Myasthenia Gravis, patients most commonly have autoantibodies against nicotinic acetylcholine receptor (nAChR).A large number of CFS patients may have acetylcholine receptor antibodiesaccording to a studypublished in theInternational Journal of Molecular Medicine.
Dysautonomia and POTS can also be associated with autoantibodies against acetylcholine receptors. Mayo medical laboratories has a very comprehensiveAutoimmune Dysautonomia Evaluationlab test that tests for autoantibodies against acetylcholine receptors and much more.
Antiphospholipid Syndrome (or Hughes syndrome) is an autoimmune condition that can lead to hypercoagulation and blood clots. Conditions such as Lupus, Sjogrens syndrome, Chronic Fatigue Syndrome, and Fibromyalgia are often associated with antiphospholipid antibodies. Antiphospholipid antibodies can even develop in presence of chronic infections such as Hepatitis C, Syphilis, Chlamydia pneumoniae, EBV, HHV-6, Lyme disease, mycoplasma, Q Fever, and many other infections. Antiphospholipid syndrome can be tested for with[Edited link out]
Keep us updated sir! I think we're getting closer
looking at genes related to lupus, and there are a lot of them. I've flagged bad for quite a few in prometheus. Which some are showing as 50/50 chance basically of inheriting in the general population. But a few of mine are more rare, at least according to Snpedia or this software.
I notice some keywords here possibly relating to vitamin k. I haven't done much research on lupus or categories of it. i'm not sure yet if this could be sort of silent with no skin manifesting symptoms or maybe it's overall a non-issue. I'll look into this a little more. Testing should also help or be definitive.
im homozygous for this snp. 4 percent chance.
| SNP | rs13277113 |
|---|---|
| PubMedID | [PMID 18204098] |
| Condition | Systemic lupus erythematosus |
| Gene | C8orf13, BLK |
| Risk Allele | A |
| pValue | 1.00E-010 |
| OR | 1.39 |
| 95% CI | 1.28-1.51 |