well my et has progressed to mf,platelets normal ,wcc normal, hb slightly low spleen slightly enlarged, main symptom is fatigue. my score is low intermediate so just continue with aspirin and repeat bloods in 3 months.not sure how I feel about it all .
myelofibrosis : well my et has progressed to mf... - MPN Voice
myelofibrosis
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glyndale
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Hi Glynndale,
I'm very sorry to hear about your conversion, but hopeful for you because of all the newer medications becoming available- [especially for MF patients- see my recent posts...].
Please keep us informed of your progress, and we will be here in support.
God bless you, and please keep your spirits up!
Can I mention that the Interferons have been shown to normalize bone marrow, even in MF patients, and have also been shown to reduce/retard/prevent its transformation into AML?
It may be that the aspirin and wait approach is no longer really the way to go.
Has your Heme/Onc discussed more 'assertive' treatment with you?
Best,
PA
Hi Glynndale,
I just came across this, and thought that you might find it helpful:
Myeloproliferative Neoplasm Treatment: What Patients Need to Know
When Should an MPN Patient Retest for Genetic Mutations?
Mar 17, 2021 Naval G. Daver, MD/ Associate Professor
When Should an MPN Patient Retest for Genetic Mutations?
Mar 17, 2021
Naval G. Daver, MDAssociate Professor
Dr. Daver: Hello. My name is Naval Daver, I am a faculty in the Department of Leukemia at the MD Anderson Cancer Center in Houston, Texas. I focus on clinical trials in myeloid malignancies, and it's a pleasure to speak to you today. I'm going to be talking about the optimal testing in the current era for patients with myeloproliferative neoplasms, and what are the time points to consider repeat testing, whether it's molecular cytogenetic to know if there are changes in the status of the disease. So there has been a lot of progress in the understanding of the molecular landscape, as well as the chromosome landscape of myelofibrosis, especially. And we do know a number of mutations now that can be frequently seen in patients with myelofibrosis, including JAK2, MPL, calreticulin. These are what we call the JAK-STAT activating mutations that are very typically seen in about 60% to 70% of the myelofibrosis patients.
When Do Changes to an MPN Patient’s Genetic Profile Typically Occur?
However, now we also know that there are other mutations that can be seen, especially at the time of transformation or progression of myelofibrosis to accelerated phase or blast phase myelofibrosis. So more rapid progressive disease that usually needs to be treated more aggressively. And those mutations that occur when the myelofibrosis is transitioning from the chronic, slow-growing to the aggressive more proliferative accelerated blast phase are mutations like IDH1, IDH2, TP53. And these are very important mutations to look for if there is any concern or clinical signs or symptoms or bone marrow changes that are suspicious for blast or accelerated phase because there are targetable drugs that can target these mutations for IDH1, for IDH2 and even potentially for TP53. So, we usually do bone marrows every one to two years in our primary myelofibrosis patients. We are looking for the traditional JAK-STAT mutations, but also these other mutations IDH1, IDH2, TP53, to see if there's any acquisition or emergence of these mutations that could help us use targeted therapies down the line.
Can Genetic Mutations Have an Impact on Prognosis?
There are other mutations like ASXL1, for example, which has been associated with a relatively adverse outcome and a higher risk of transformation when present. These are not yet mutations that we necessarily act on therapeutically. It's not clear whether we could change the prognostic impact of these mutations with therapies, but these do have prognostic impact. And if I have a younger patient who has primary myelofibrosis and ASXL1 with some splenomegaly and symptoms, I may be a little bit more inclined toward thinking about early intervention such as stem cell transplant. Again, not standard of care, but a lot of us are thinking along these lines because we do know some of these mutations could have an adverse outcome.
So I think again, important to look for those additional mutations, both at diagnosis, and more importantly, at the time of transformation or progression, which could have a therapeutic decision-making, give options for targeted therapies which usually have the best chance of success, and also may push us towards the earlier or more proactive stem cell transplant in certain patients where we know the risk is higher because of certain mutations that they have.
Source Podcast: patientpower.info/myeloprol...
Thank you for your information its very useful,my consultant is reluctant to start anymore treatment apart from aspirin, because I have few symptoms and my bloods aren't too bad,but she is going to discuss my case with other colleagues and we will take it from there,I see her again in 3 months.Thanks again for the info much appreciated.
The discussion here seems to be for primary MF. Not clear whether it also applies to secondary, ie progression from ET.
But there is a big item in here:
IDH1, IDH2, TP53 mutations are likely treatable. I was not aware that any specific mutations were separably treatable.
But ASXL1 mutation has no treatments other than SCT. Another one of frequent concern, SRSF2, is not mentioned here.
Hi Glyndale,
I have to say, that given all the information/evidence which has been present here, the approach that they are advocating seems very short-sighted and lacking awareness of the risks of [and likelihood of] disease progression. It's not what you have now that needs to be treated, it's what you will have 2, 5, 10, and 20 years from now.
Remember that you're the one that has to live with the consequences, so if you have any doubts about your consultant's knowledge base or in what the aim of your therapy should optimally include, seeking a second opinion is highly recommended, and if your current consultant takes issue with that they're demonstrably not putting your needs [or outcome] first.
As you may have read, my initial Heme/Onc MD, who my PCP referred me to only because her group had an office in the local town, had only one thing on her mind- my high-risk status due solely to my advanced old age of 63 at diagnosis, and thought that the only valid treatment option was HU. This was despite the fact that she works out of the University of Rochester Medical Center, which has a very highly-rated medical school and teaching hospital.
I was interested in and asked about getting an IFN instead, but because she had only ever prescribed the highly-side-effect-prone short-acting forms [in the high doses used in the early days of leukemia therapy], she was dead-set against prescribing it.
I then provided her with reams of research findings to the contrary, and in support of both Pegasys and Besremi, but due to her unfamiliarity with them, she still didn't feel comfortable initiating either of them for me- which I admitted was a reasonable response.
At our first visit, when she initially spoke against IFN therapy, she also made it a point to admit her almost complete lack of experience treating PV [or any MPN's], so afterwards, I went to the MPN Forum website, and looked for an MPN specialist in my 'local' area, the closest of which which turned out to be a bit over an hour away [in good weather] at Roswell Park Cancer Center.
I emailed her to ask her if she would consult on my care, and she agreed, in addition, my local Heme/Onc MD also agreed that once my dose titration had been accomplished, she would again accept responsibility for my ongoing care. Thus at present, I am being managed by the Roswell Leukemia Ctr, getting my labs drawn at the U of R, and doing my injections at home.
I included this just to say that you have to be your own advocate in healthcare, and especially with the really rare diseases that our MPN's represent.
Also see: Interferon therapy in myelofibrosis - a systematic review and meta-analysis
which states: "IFN might be an attractive option for selected patients with low-risk MF especially early in the disease course given its safety in pregnancy, the absence of leukemogenic side effects, and potentially less cytopenias compared to ruxolitinib."
Source: ncbi.nlm.nih.gov/pmc/articl...
and
Efficacy and safety of pegylated-interferon α-2a in myelofibrosis: a study by the FIM and GEM French cooperative groups
which states: "In conclusion, Peg-IFNα-2a induced high response rates with acceptable toxicity in a large proportion of patients with primary and secondary myelofibrosis, especially in early phases."
source: pubmed.ncbi.nlm.nih.gov/238...
and: "Weill Cornell Medicine has been at the forefront of using interferons in the treatment of MPNs such as MF. Intriguingly, treatment seems to work best on patients with early stage MF and, in this setting, interferon therapy can even reverse bone marrow fibrosis and lead to normalization of blood cell numbers and reduction of the number of MPN mutant cells in the blood and bone marrow."
silvermpncenter.weill.corne...
and finally: Benefits and pitfalls of pegylated interferon-α2a therapy in patients with myeloproliferative neoplasm-associated myelofibrosis: a French Intergroup of Myeloproliferative neoplasms (FIM) study
States: The median survival of patients with intermediate and high-risk prognostic Lille and dynamic International Prognostic Scoring System scores treated with pegylated interferon was increased in comparison to that of historical cohorts. In addition, overall survival was significantly correlated with the duration of pegylated interferon therapy (70 versus 30 months after 2 years of treatment, P<10−12). JAK2V617F allele burden was decreased by more than 50% in 58.8% of patients and two patients even achieved complete molecular response...
These findings in a large series of patients with myelofibrosis suggest that pegylated interferon therapy may provide a survival benefit for patients with intermediate- or high-risk Lille and dynamic International Prognostic Scoring System scores. It also reduced the JAK2V617F allele burden in most patients. These results further support the use of pegylated interferon in selected patients with myelofibrosis."
Source: haematologica.org/article/v...
I'm hoping that you don't find this too overwhelming, or overbearing, but if you do I apologize.
The only axe I have to grind here is to support self-advocacy, and to support preemptive, proactive therapy, which is intended [and has been proven] to prevent or reduce disease progression and improve not just the duration, but also the quality of life.
Best regards,
PA
hello no I don't find it overwhelming at all it's very useful thank you ,she didn't want me to start on any new treatment at the moment because my bloods and symptoms aren't too bad ,but your right I don't like this watch and wait approach so I'm going to speak to my specalist nurse and take it from there.Thanks for all the info ,much appreciated.
Hi Glyndale,
Thank you for taking it that way- I'm happy to hear that's your thought as well.
You're not going to believe this, but I forgot to add one more posting:
which is the site where I located my MNP specialist at Roswell Park.
If there's ever aught else, I can do, please just ask!
Best always,
PA
ok thank you, best wishes ☺️
Good advice I only managed to get off Hydroxy & onto Interferon by contacting an MPN as my local hospital was totally obsessed with HU even with bad side effects . 👍
Hi Exeter and Glyndale,
I simply don't understand why so many of these 'specialists' haven't updated their treatment practices.
Even in my current practice setting which has only very limited access [and ongoing training] to current medical trends and recommendations, I make it a point to keep current with best practice and advances in evidence-based treatment.
If I can access and understand the clear facts, they certainly could as well.- and it's not like it's some wild and whacky new concept constructed completely out of the clear blue sky- these changes were built on top of previously understood concepts.
Best,
PA
yes my view too. My Drs knowledge of complaint was none existent & had to fight for bloods to get correct one eventually that showed Jak 2 ET. My local Dr would never have found it as kept telling me I was too fit & blood tests fine just slightly above normal platelets 🙈. So glad I pushed else probably would have had a stroke in hymn thinking I was just unfit . No confidence in GPSurgery whatsoever & glad I am now under MPN that I had to hunt & contact from this brilliant website we have here 👍Julia
Hi Exeter,
Pardon my ignorance, but from my copious watching of BBC-created content, doesn't him telling you that you are 'too fit' imply or come across as a somewhat inappropriate comment?
😇
Actually, I'm just kidding- but as you point out, some less competent healthcare providers may inappropriately discount otherwise apparent evidence of disease because of a patient's obviously healthy and physically fit appearance.- which by the way is something we're [supposed to be] trained to avoid.
There is a rule of thumb that in a healthy patient the presence of an abnormal lab finding [or a couple] is most likely spurious and incorrect- however that said, when there is a pattern, persistence, or progression of the abnormalities, a closer look and an open mind are mandatory, and a higher index of suspicion that there is a disease process involved goes along with that.
Another instance of this may be inferred from my MPN specialist's comments upon looking back over about 15 years of my Hct and Hgb results, that I should have been referred for further evaluation some 7-10 years prior to my eventual diagnosis.
To me, this was mostly ironic in retrospect, because if I had been referred and diagnosed back then, I'd have been considered low-risk [under 60 y/o w/o a history of clots], and the recommended treatment would have been pretty much unchanged from what I had already been doing- phlebotomy [for which I was regularly going to the blood bank pre-COVID], daily aspirin- which I was already taking due to my concern about getting a DVT or superficial phlebitis from my varicose veins], and probably the only change would have been more frequent blood tests to monitor my counts.
So, despite the decade of mild to moderate uncertainty about that state of my health, which was caused by the persistent pruritus, shortness of breath on exertion, early fatigue, and slow recovery from exercise- the latter 3 of which I had been sent for work-ups to rule out heart, lung, and neuromuscular diseases, not much else would have changed,, except the struggle to get disease-modifying therapy would have been possibly even worse.
Best,
PA
Ha I am used to stupid comments from professionals. The Dr knows me & as I was Police Officer thinks I am superhuman fit 🙈. Amazingly a young junior Dr doing my MRI for shoulder injury asked me how I worked out I had ET as he wrote about it in University so thought I was lucky to find out . But took a lot of pushing & 6 months to get correct blood checks . Motto is we know our own bodies so I wouldn’t give up & read up on high platelet’s . 👍
hello apparently my consultant was going off the scoring system they use to assess your risk ,as mine was low she s reluctant to start any medication, however I am goin to ask for a specalist opinion.
so sorry to here about your progression. Have you always been on just aspirin
Sorry to hear about the progression to MF. Wishing you all the best as you move forward.
It makes sense that you do not need to rush to do something to deal with the progression due to the low symptom burden; however, suggest that you do need to take action to change the treatment plan. In this situation, it is both symptom control and reducing risk of progression that needs to be the focus of treatment.
PA makes a good suggestion that it is time to seek a second opinion from a MPN Specialist. Most hematologists/Nurse Specialists have little experience with MF and the other MPNs. It is best to consult directly with a MPN Specialist to optimize your care plan. The MPN Forum list is the only international list available. Here it is again for convenience.
Do please let us know how you get on.
Thank you for your advice and the list ☺️
Hi Glyndale,
I was trying to figure out what the current standard of care for MF is and in looking around I found a few new resources:
This is the transcript of a continuing medical education video offering on a professionals-only site:
STATEMENT OF NEED
Myelofibrosis is a rare myeloproliferative neoplasm characterized by the buildup of scar tissue in the bone marrow, leading to decreased erythropoiesis, progressive bone marrow failure, and anemia (Verstovsek et al, 2022). Though allogenic stem cell transplant is potentially curative, comorbidities preclude many patients from receiving this treatment. Therefore, therapeutic goals focus on slowing progression, managing complications, and maintaining quality of life. Currently, the discovery of the JAK-STAT pathway’s role in the pathogenesis of myelofibrosis is transforming the landscape, with novel agents that improve patients’ splenomegaly, systemic symptoms, survival, and overall quality of life (Verstovsek et al, 2022). However, correctly diagnosing and managing this disease using novel therapies and strategies remains challenging for clinicians. In this activity, John Mascarenhas, MD, Professor of Medicine at Mount Sinai Icahn School of Medicine, will update learners on myelofibrosis risk stratification, novel therapies to slow disease progression and reduce symptom burden, and strategies to maintain patient quality of life.
TARGET AUDIENCE
Hematologist/oncologists, nurse practitioners, physician assistants, oncology nurses, and other health care professionals involved in the treatment of patients with patients with myelofibrosis (MF).
Managing Symptom Burden and Optimizing Treatment Outcomes in Myelofibrosis
i3health.com/images/172/173...
It's a pretty comprehensive look at all the available and perhaps some upcoming therapies, and how they should be applied.
It includes this statement: The finding s"...demonstrate a correlation between molecular responses and pathologic changes like bone marrow fibrosis reduction."- which is something about which I believe EPguy [among others of us] has occasionally commented re: the lack of sufficient evidence to support it.
It also discusses prognosis by both driver-mutation status, and symptomology level [mostly at the higher risk end].
Admittedly, there's a lot here to unpack, as they say, but go slow and don't try to read it when you're already tired. [unless you're troubled by insomnia].
Best,
PA
This is probably more applicable to your situation compared with the post above:
Determining Who Has “Early Myelofibrosis” Involves a Broad Look at Patient Factors
August 28, 2020
Patients considered to have early myelofibrosis are a heterogeneous group for whom disease risk, best treatment strategies, and the probability of mortality are best determined individually by looking at patient’s clinical characteristics and molecular markers together.
“The burden of myelofibrosis is variable. Risk in terms of survival is a factor, but not the only factor in treatment,” Ruben Mesa, MD, said in a presentation during the Texas Virtual MPN (Myeloproliferative Neoplasm) Workshop. “It is looking at the entire clinical picture for a patient as well as understanding their wishes [about how aggressive they want to be with the disease] that is important.”
Regarding the term “early myelofibrosis,” Mesa, who is the director of the University of Texas Health San Antonio MD Anderson Cancer Center, said that this term may apply to a case of mild anemia, splenomegaly, or other myelofibrosis symptoms. But, he said that multiple patient factors are involved in determining who it should apply to, such as burden of vascular events, risk of progression, splenomegaly, and baseline health or comorbidities. Generally, he discussed the treatment of patients with low- or intermediate 1–risk disease, as those who typically present with more favorable prognosis.
Assessing Patients
Management of all patients with myelofibrosis should progress through the same steps of evaluating survival and disease burden; developing a treatment plan of either observation, stem cell transplant, or frontline systemic therapy; and creating strategies for eventual disease progression.
Patient-reported symptom assessment tools are valuable and may help calculate symptom burden. Mesa cited using versions of both the MPN-Symptom Assessment Form (SAF) and the MPN-SAF Total Symptom Score (TSS) to look at effects such as fatigue, satiety, and pruritus.
“Just as we think of different prognostic scores, so too can there be different quartiles in terms of the severity and intensity of symptoms,” Mesa said. “These things are not necessarily linked to their risk score, which is predictive of survival,” he said, noting that disease burden and disease risk scores are not interchangeable.
Risk scores, such as the Dynamic International Prognostic Scoring System (DIPSS)–Plus, take constitutional symptoms as well as clinical features like age, degree of cytopenia, and karyotype into account when evaluating patients for prognosis. Using this risk scoring system, one study of 520 patients estimated that the median time spent in the “low-risk” category was 4.9 years (range, 0-26.7). Mesa noted that as patients progressed through intermediate 1–risk to high-risk disease stages, time spent in each category decreased. Therefore, patients considered to have early myelofibrosis, whether it be low- or intermediate 1–risk disease, still had progressive disease.
Molecular phenotypes have also been instrumental in the current era of decision making for treatment of myelofibrosis. Based on an unfavorable molecular marker, patients otherwise considered to have intermediate-risk disease might now have a poorer prognosis and require more aggressive therapy in hopes of extending survival.
“New molecular phenotypes have clearly helped augment and refine prognosis, but they don’t fully give us a sense of disease burden,” said Mesa. Issues can arise in which patients with very high-risk disease don’t have severe symptom burden; conversely, individuals with severe symptoms may actually have lower-risk disease.
“We all know patients are much more complex than just the status of their clone or their molecular phenotype, although that is critically important,” Mesa said.
Patients with intermediate-risk disease are the most heterogeneous group who stand to benefit greatly from information obtained by next-generation sequencing. Results obtains from molecular profiling may better inform a patient’s prognosis, and incorporation of this information may upgrade disease risk and suggest benefit of transplant or clinical trial.
Based on the National Comprehensive Cancer Network (NCCN) guidelines for MPNs, patients should first be assessed using either the DIPSS or DIPSS-plus. Patients who are asymptomatic by the MPN-SAF TSS can be observed or referred for clinical trial. Symptomatic patients can be treated with ruxolitinib (Jakafi), another available systemic agent, or be referred for clinical trial.
For patients considered to have intermediate 1–risk disease by the NCCN guidelines, observation, ruxolitinib, clinical trial, and allogeneic hematopoietic stem cell transplantation are all considered acceptable forms of myelofibrosis management.
Cont:
Systemic Therapy Benefit in Early Disease
The indication for ruxolitinib was based on the COMFORT-I (NCT00952289) and COMFORT-II (NCT00934544) studies,4 both of which examined the use of the JAK2 inhibitor in patients with intermediate or high-risk disease. Mesa said these patients were included in the trial because they represented the greatest need. However, approval based on this evidence should not be interpreted as meaning that ruxolitinib is unsuitable for use in patients with intermediate 1– or low-risk disease.
In fact, data from the phase 2 ROBUST trial that were released after the FDA issued its frontline approval supported the use of ruxolitinib more broadly in patients with myelofibrosis, including 19 patients with intermediate 1–risk disease.5 Similarly, the global, expanded-access phase 3b JUMP trial included the largest cohort to date of patients with intermediate 1–risk myelofibrosis and supported the safety and efficacy of ruxolitinib in this group.
Mesa also added that fedratinib (Inrebic) is approved as frontline therapy for myelofibrosis, but data are lacking to support its use in patients with low-risk disease. “As that becomes available, it can be considered in this group,” he said.
Revisiting the NCCN Guidelines, Mesa reviewed the Evidence Blocks to determine interventions for low-risk disease, including hydroxyurea (Hydrea), interferon, and ruxolitinib. For intermediate 1–risk disease, he said most evidence at this point supports the use of ruxolitinib but he expects that other agents will be added to the list as more data emerge. However, studies of real-world evidence and investigator-initiated trials will likely be needed since trials supporting approval typical involve patients in higher-risk categories.
[Editiorial note- Passing over IFN in favor of Rux here flipped my biscuit !- His bias is explainable, if not excusable: see *** below]
Concluding the discussion, Mesa said understanding why patients progress will be important in the selection of novel therapies for patients with early myelofibrosis. “Earlier patients all have areas in which they might benefit [from therapy], but as is natural, that evolution occurs as we develop more efficacy and safety data for these medications…Once we understand the mechanism of progression and have suitable markers of progression, then we might be in a better position to have progression-free survival be a viable end point for these individuals.”
targetedonc.com/view/determ...
Dr. Ruben Mesa is the director of UT Health San Antonio MD Anderson Cancer Center, one of only four National Cancer Institute-designated cancer centers in Texas
Dr. Mesa’s practice builds on his role as an international expert on myeloproliferative neoplasms (MPNs), a group of bone marrow disorders that often lead to leukemia. He has been involved in MPN research for more than 20 years. He led the development of National Comprehensive Cancer Network’s panel guidelines, the first U.S. guidelines on the diagnosis and treatment of myelofibrosis, polycythemia vera and essential thrombocythemia. Dr. Mesa has been the principal investigator or co-principal investigator of more than 70 clinical trials. He co-led the research team leading to the FDA’s approval of ruxolitinib for polycythemia vera and myelofibrosis. ***
Thank you for the information, much appreciated.
Some notable items in the report. Biggest is the new agent discussed below.
-
"Ruxolitinib has proven to be a very potent anti-inflammatory drug"
CALR indirectly affects MPL while MPL can also be directly mutated, both CALR and MPL therefore being adverse MPL conditions.
For MF CALR-mutated patients, particularly those that have type 1 ... have a median survival of about 17 years, whereas patients who have JAK2 or MPL mutations, approximately 9 years, and patients..(with) triple-negative disease that lacks any driver mutation have a median survival of approximately 3 years
High risk: EZH2, SRSF2, ASXL1, and the IDH1 and 2. IDH1-2 are treatable, while ASXL1 is not (But see below) , as discussed in this thread
healthunlocked.com/mpnvoice...
Rux does not improve marrow nor VAF (I've seen some VAF improvements in other reports, but less than IFN) but it does improve survival.
Rux discontinue has bad prognosis if other than SCT.
Luspatercept drug can help pts on Rux with anemia.
momelotinib (discussed in other threads) is promising for anemia on Rux.
--
A new agent: "In a number of these patients that were treated with navtemadlin (krt-232) ... attained a complete reduction of either driver mutation and/or high molecular–risk mutation, suggesting the ability to deplete the malignant stem cell population, something that JAK inhibitors fail to do" Implication includes reducing ASXL1, this was said to be un-treatable in a different report. Spleen reduction correlated to VAF reduction, VAF correlated to anything is good. "(CD34, present in MF) was dramatically reduced, nearly 90% reduction," "Approximately 30% of patients also attained an improvement in their bone marrow fibrosis grade," But GI toxicity typical of the class if drugs.
MF pts where Rux is not working may want to inquire on this trial.
clinicaltrials.gov/ct2/show...
--
For SCT "it's important to optimize JAK inhibitor treatment to minimize symptoms and reduce spleen burden prior to transplant, right up until transplant"
Your doctor should give more than just aspirin
Sorry to hear of your progression. Stay strong and informed. ❤️❤️❤️
Lots of love and information for you to process. Best of health to you.
Please keep us updated. 🍻
Hi Glyndale,
I know I posted a ton of stuff, but I also wanted to make sure to tell you that one of the most important things to remember is to breathe. I don't say that to imply that you're holding your breath, although we do all know the expression "waiting with bated breath",.
I know from personal experience that when I'm stressed, worried, concerned or whatever you want call the emotions that arise when something in life, [or more particularly health status] changes, it can unconsciously affect my breathing, which in turn affects everything else.
So what I do is to try to remember at least a few times a day to make time to take some really slow deep breaths. There a variety of ways to do this, but no evidence that any one way is better than another, so pick one that feels right to you, and fits into your daily routine.
Here are a couple of resources:
ggia.berkeley.edu/practice/....
realsimple.com/health/mind-...
beaumont.org/docs/default-s....
medicalnewstoday.com/articl....
This is a summary of some deep breathing practices
How does deep breathing relieve stress?
Although many slow breathing techniques are effective in the long term for stress reduction and heart rate reduction, deep breathing methods such work wonder in high-stress situations by calming your autonomic nervous system.
• Many autonomous bodily functions such as blood pressure, body temperature, and heart rate are regulated by this system.
• It is made up of two parts, namely, the sympathetic system, which stimulates bodily activity (fight or flight), and the parasympathetic system, which relaxes your body (rest and digest).
• When you hold your breath, CO2 levels in your blood increase, which increases the cardioinhibitory response (lowering your heart rate).
• This activates the parasympathetic nervous system, resulting in a calming and relaxing effect, or, to put it another way, breathe slowly and deeply to relieve stress.
4 benefits of deep breathing
Deep breathing is an effective method for overcoming stress and improving your body's future response to stress and anxiety.
1. Improves mental well-being:
o Consider learning a deep breathing technique if you've ever considered meditating to reduce stress and improve your mental health.
o Breathing is inextricably linked to cognitive activity such as thinking and reasoning.
o According to many studies, taking slow, mindful breaths helps reduce stress and feelings of depression.
2. Heightens cognitive performance:
o Deep slow breathing clears the mind, allowing for greater focus and concentration.
o Deep, rhythmic breathing exercises have been shown to help even people with attention deficit hyperactivity disorder manage their impulsive behavior.
o Taking slow, controlled breaths helps balance the nervous system, which allows us to clear our minds and increase our attentiveness.
3. Enhances the body’s future reactions to stress:
o Resetting your breath with deep slow breathing will benefit both your mind and body in the long run.
o Researchers discovered that regular deep breathing exercises can activate the genes associated with your body’s energy and insulin levels while decreasing those associated with inflammation and stress.
4. Helps deactivate the fight-or-flight response:
o The sympathetic and parasympathetic nervous systems are two subsystems of the autonomic nervous system.
o When the sympathetic nervous system is activated, the body goes into “fight, flight, or freeze” mode, preparing itself to “fight” for survival by releasing cortisol (a stress hormone) (dilation of the pupils and muting pain perception).
o Panic attacks can occur when the body enters this mode after being triggered- even when the trigger isn’t something harmful or emergent.
o Deep breathing helps the body to return to the parasympathetic or “rest and digest” mode, helping to calm it down in stressful situations.
To practice slow deep breathing
• Set a timer for five minutes.
• Sit with a straight spine on the floor, or in a chair with your feet flat on the floor.
• Close your eyes and inhale for a count of at least four.
• Hold your breath for a count of four to start out, slowly increasing the duration as your body becomes accustomed to the practice.
• Exhale for a count of at least four.
• Hold the exhale for a count of four.
• Repeat until the alarm sounds.
What is tactical breathing?
When under duress, Navy SEALs use this breathing technique to induce a more relaxed state in the body.
Anyone can also use it to control stress.
Tactical breathing is a technique used when you feel the trigger of the fight-or-flight response.
• To do this, place your right hand on your stomach and exhale heavily.
• Then, slowly draw your breath upward from your abdomen to your upper chest by inhaling through your nostrils.
• Exhale slowly, beginning at your chest and working your way down to the air in your abdomen.
• Consider your navel to be in contact with your spine while breathing.
• Once you're comfortable with a full, deep breath, do it again, but this time exhale twice as long as you inhale.
• Breathe to the count of four, pause briefly, and exhale to the count of eight.
• Repeat at least three times.
Deep breathing and tactical breathing are both based on pranayama, an Ayurvedic form of breath work that originated in India and is practiced in yoga. It has extremely ancient roots, with various techniques for calming, bringing in energy, refining focus, and relaxing the nervous system. However, it was recently popularized and brought mainstream by the military.
More importantly, there are sound physiologic reasons why they work, and there is clear evidence that they are able to reduce stress, calm nerves, and improve overall mental and physical wellbeing, when practiced regularly.
Thank you I am stressed at the moment till i get my head round the diagnosis ,need to ask a lot of questions of my consultant, and thank you for all the info ,I will try and breathe 😊
Hi Glyndale,
I think we can all relate to what you're feeling, and know that you are in our thoughts and prayers.
Best,
PA
Thank you.
was your progression confirmed through BMB?
yes it was .
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treated,main symptom is fatigue, slightly enlarged spleen and slight anaemia ( for 3 years)not sure...
Myelofibrosis
I've been taking anagrelide for about 2 years.
At this point, I'm feeling very scared and...
Myelofibrosis
because my allele burden Is going up and my spleen has enlarged a bit. Does anyone have experience...
Myelofibrosis
Myelofibrosis
