The cancer patient as an educated, active resource an coworker in own rehab… ?

(NB this is a very much ongoing working text including risk for dyslexia! – Also, the detailed manual – I briefly discuss below – where the biopsychosocial placebo toolbox will be detailed described – will be published first 2019, when I have sufficient illustrative cases also to present – interested can before publication mail to info@stressmedicin.se)

NB -> Before reading the below please read about my redefinition of placebo at http://biopsychosocialmedicine.com/projects/rd-international-projects-2/placebo-rd/

Summarizing; Working since 1986 with the biopsychosocial medicine manual* “patient as an educated, competent resource and co-worker in own rehab” as one of the corner stones in our clinical stress medicine approach – over the years refined – I, when I surprisingly was diagnosed with very aggressive prostate cancer May 3th this year (2018), thought, why not try to combine this approach with the placebo approach, which I have been informal working with since 1979 when I learned about the Krebozen case, see e,g, http://biopsychosocialmedicine.com/projects/rd-international-projects-2/placebo-rd/the-1957-placebo-case-the-krebozen-story/ – with last two years quite a lot of work. Of course, directly I started myself to frequently make use of the placebo approach (main tool is a new kind of self-hypnosis) together with much of the approach I have worked clinically with so many years with most kind of stress related diseases and mental disorders.

If this integration is productive and practically useful will the coming years show with a planned formal publication probably late 2019. The below is working text while I myself try to increase my understanding of the kind of dysfunctional cell behaviors cancer “is”, how it emerges. Can be prevented and treated biobehavioral as a complement to traditional interventions which I hope will improve in multifaceted systems integrating way ahead.

So, psychophysiology (one other corner stone in our stress medicine approach) refers to “see what you do and do what you see” or “learning while doing while seeing” while my work upstarting at this website and below can be called “learning while thinking while writing while training/practicing/evaluating while hopefully increased understanding” concretized in individual tailoring of the tools enabling patients to be a valuable part of own rehab and not a passive, helpless one. The more detailed scientific, clinical and subjective problems I already have met and will face, will be my way to try to contribute try to, through taking the patient position in general, a constructive broader practical and theoretical perspective on the cancer issues!
*References will come here soon!


The below is based on scientific, clinical and (recent) personal knowledge/experiences!
As I surprisingly, unexpected was diagnosed (2018-05-03) as “having” (probably 1,5 years when I got – my hypothesis – a copper based anemia enabling to activate possible genetic disposition) aggressive prostate cancer (Gleason 9), I turn my focus directly more into detail questions as; “how does cancer dysfunctional  cell behaviors develops and how it can be prevented and treated”. Surprisingly I found so much constructive going son, especially within systems integrating processing as well as in … the importance of diet, not only theoretical but also empirical also based and, not surprisingly increased focus on metabolism and mitochondria behaviors!

I had been on a multifaceted treatment road since my dissertation 1986 and, in my mind also including cancer in officially in my mind since  I first heard about the http://stressmedcenter.com/projekt/om-placebo/placebo-case – a brief comment; The case motivate focus on Limbic (spatial) information processing/elaborations, of which we understand still not very much! As I, since 1983 base my psychological paradigm/thinking on George Kelly´s (personal construct theory, 1955) and e.g. reconstruction conceptualization, today, we may use the somewhat similar, reconsolidation (Karim Nader and many other) but also to some extent on Joseph Wolpe´s (1958) reciprocal inhibition, but also perhaps Karl Jung´s (1906); “Aha, a looking glass into the unconscious!” when he used skin conductance and word processing. As very much processing in our brain concerns older evolutionary parts, we can hardly only through rational thinking catch a glimpse of limbic (mammalian) spatial (“irrational”) processing, which consequences are extreme complex and, which we can consciously observe consequences of (e.g. emotions) as well as, while using integrated biofeedback consciously use strategies when we in real time can see effects on not conscious processes – in data (more about this when the complete manual is presented).           

Back to the Krebozen case, then my focus 1983 was of course on; “how can our Limbic brain, preferably not conscious, in an individual probably (no other explanation so far) completely change fundamental biological behaviors”! During last years I was working with more details further developed the conceptualization inspired by George Kelly´s (still not well understood, excellent Personal Construct Theory (1955) , as I extrapolated into “noncebo-placebo precognitive construct continuum” and its relation to PTSD (post traumatic stress syndrome) as a possible condition for development of severe diseases – that is, not only complex mental problems! A challenging hypothesis – which is really a not quite in mainstream – integrating our 1986 biopsychosocial medicine paradigm conceptualization as well as its implications – the toolbox.

So – as I have been working clinically with a biopsychosocial medicine clinical approach (education the content of a multifaceted toolbox and coaching used for 25 years), I realized that probably with slightly modification the structure and the content can be used for cancer patients too!

Now, the below is a (NB!) draft on a modification of my former biopsychosocial medicine manual after empirical studies possible to be used in different cancer dysfunctions formulated as: “Patient as an educated, competent resource and coworker in own rehabilitation”. When I now go on into the “real” text I will encourage careful, critical (following the Thales principles – see http://stressmedcenter.com/vetenskap only “1” unfortunately still in Swedish – or?) consideration while this is a generalist try to integrated extremely complex biopsychosocial (even cultural) goings on, with the attempt to encourage finding a road (We will either find a way, or make one’ – Hannibal crosses the Alps) where individual can, before becoming patient can prevent and patient who reach patient status, can take the position of a valuable resource in own rehabilitation.

Main consideration is: What is the present workable and practical useful knowledge about down-regulation of programmed cell death? With the corollaries (a) Can we approach cancer behaviors integration both from traditional and behavioral point of departure and (c) can patients make a substantial biobehavioral contribution in their own rehabilitation?

As there are very much substantial information about Apoptopis, I first write my present conclusion which is largely based on the links (and some of their texts) below. Then I encourage you to critical review my practical but still knowledge limited (more than our general limited knowledge in this extremely complex field, which important motivate conscious and carful but into practice, given harm can substantially be excluded!) conclusions. Therefore, I start with the easy part and end with the more complex one!

The content below
1. How can cancer patients constructively contribute beforea7during/after traditional treatments? Below, briefly, a slight modification of the manual “The patient as an educated competent resource in her/his own rehab”

2. Summarizing some information of present knowledge on down-regulation of programmed cell death as well as some different perspective on metabolism of relevance for cancer dysfunctional behaviors.

3. What kind of – so far understood – relations between mitochondria “health” and the development of cell dysfunctions and its practical implication exists?

4. Epigenics and some recent evidence to be considered

  1. How can patients contribute? Below a slight modification of the manual “The patient as an educated competent resource in her/his own rehab”.

First; focus on the gut-brain axis as a general point of departure for biopsychosocial health is now used as a more preferably generalized way to approach lifestyle health and development of unhealth! This has many implications where the metabolism and specifically the mitochondria physiology comes into the picture! Which can be address from many perspectives, in clinical work at best trying to integrate and not just pick out one of them. There are many reasons for this where one is that we all are similar in some sense and not in others, vary in a varying degree between but also within individuals over situations (e.g. effects of postprandial inflammation) and time.

As I myself (and many colleagues, e,g, within www.aapb.org) has work many years clinically with integrated psychophysiological behavioral medicine where dynamic behaviors of the autonomic and metabolic systems are basic systems for examination/assessment (also of patient capacity to influence those systems in real time), interventions by biofeedback assisted biobehavioral tools and documentations), where respiration behaviors is a kind of platform, I do see a possibility to slightly modify our manual (see tittle above), where all the suggested tools are in our toolbox refined last 30 years. Updated English description will be presented at the www.biopsychosocialmedicine.com website (latest July 2018)

But before discussing more practically what patients can do based on education, coaching and self-activities, I will move to an excellent overview, giving some specific focus based on mitochondria perspective!

…. “We tend to think of ourselves as human beings and human beings only: Yet 38 trillion microbes (Sender, Fuchs, & Milo, 2016), distributed into at least 2,172 known species (Hugon et al., 2015), populate each of us in places as supremely personal as our mouth, armpits, gut, genitals—and brain (Branton et al., 2013). It is a sobering thought that we house at least as many foreign as human cells (Sender et al., 2016), and those cells that we consider human stem from archaea and bacteria. With the single exception of red blood cells, which got rid of their nucleus too, each of these “human” cells is itself densely inhabited by direct descendants of bacteria in the form of mitochondria. They have made themselves indispensable and this is good and bad news. On the one hand, mitochondria make our mental health—besides furnishing the energy for the brain to function at all, they enable synaptic plasticity, produce hormones and signaling molecules, dish neurotransmitters out and rein neurotransmitters in. On the other, they also break it—even their proper operation corrodes our brain, while their malfunctioning is associated with cognitive deficits, intellectual disabilities, neurodegenerative disorders, and mental illness. Whether as victims or as perpetrators, mitochondria are right in the middle of virtually all human afflictions. They still look a little like their bacterial forefathers and still retain a bit of independence from us. But because of the deal they struck with archaea 2 billion years ago, their health is now entwined with ours. So, to help get the best out of us as humans, we may actually want to do what is best for our bacteria-like components: exercise, sleep, spend time in the sun, eat well, and meditate.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5761714/

Here I will also add: “BCL-2 expression in solid tumors

BCL-2 may also play a role in nonhematologic tumors, and inappropriate expression has been observed in solid tumors such as prostate, breast, and small cell and non-small cell lung cancers.17-20 In small cell lung cancer, high BCL-2 expression in >90% of patients has been reported.19 Ovarian, neuroblastoma, bladder, colorectal, and some head and neck cancers have all exhibited significant levels of BCL-2 expression.21-25” https://www.biooncology.com/pathways/cancer-tumor-targets/bcl-2/bcl-2-in-cancer.html which also motivate to weight in BCL-2 and how we can influence this!

As well as … The influence of diet on anti-cancer immune responsiveness “Conclusion: The current review highlights the various processes in which nutrient intake could modulate directly or indirectly the immune system and/or the growth of cancer.

Most of the discussion is based on human observation rather than experimental animal models, as the focus of this review was predominantly based on epidemiological grounds. But several experimental models not discussed here extensively substantiate the conclusions.

Yet a gap of knowledge is clear. While the potential mechanisms that may affect immune function and consequently cancer growth and responsiveness to immunotherapy agents have been discovered, very little is known about how they may affect and modulate therapies since parameters linking dietary habits to clinical outcome during immunotherapy are not routinely included.

Here we propose that in the future, detailed information about diet, nutritional status and gut microbiota should be considered in correlative studies during immunotherapy trials identifying parameters that may be relevant to outcome by studying either systemic effects of diet of circulating immune cells, or those that may affect directly the cancer microenvironment. A project is on going to identify the best diets for immunotherapy enhancement against tumours (D.I.E.T project).” https://link.springer.com/article/10.1186/s12967-018-1448-0

Now approaching what we can do as patients:
If we then stop and think/elaborate and move to practical tools; it seems that metabolism is not only the characteristics of life and living organism existence. It does is extremely complex and can be attacked from many kinds of stress, where stress can be defined as strain/challenges on any system which to not return to steady state or do not requires stress related adjustment from compensatory dependent systems. On the other hand, it seems that our biopsychosocial flexibility can cope with extremely much stress. So, if we are too cautious we prevent adjustment to real life and if we go on to hard, we develop dysfunctions?

Considering our complex evolution substantiated in our own brain, perhaps the most complex in the universe, realizing also how we based on millions of years, last few 100.000 have complete change most of our way of living into fast exploding environmental conditions, probably the overall biopsychosocial-cultural  stress get such complex integrated multifaceted dysfunctions in our not very well understood brain-bodily systems that we need to consider “do we really have such flexibility” and critically analyze our real world living at large as well in particular, especially what/how we eat, move, breathe, plan our life, social relate, sleep .. from an evolutionary perspective. The conclusion made by Kramer and Bresshan seems overall a wise perspective not only on mitochondria health, its connection with cancer behaviors but at large with all life style related diseases and mental problems!   

Although much more knowledge development is urgent needed as well as its possible empirical validation (which due to complexity is difficult or even in not few cases, impossible with the present methodology/technology), which can start up ourselves if we try to get some substance out of the exploding ideas on diet, breathing, movements, precognitive and cognitive strategies including hypnosis, personal habits including sleeping quality, social interactions, environmental processes …  at best we can, we with high probability contribute to our own rehab! Below I will discuss this more but first when I am cured, I will describe “my own way”, that is, who I myself development my own tailoring of the toolbox!

But, I can add a graph which shows my PSA at pretreat6ment position below

… more text very soon I hope!

2. Summarizing some information of present knowledge on down-regulation of programmed cell death as well as some different perspective on metabolism of relevance for cancer dysfunctional behaviors. 

First some basics from a few sources:
(a) Evasion of Apoptosis: A Hallmark of Cancer
“Damage to DNA can render a cell useless, or even harmful to an organism. Apoptosis, or programmed cell death, evolved as a rapid and irreversible process to efficiently eliminate dysfunctional cells.1 A hallmark of cancer is the ability of malignant cells to evade apoptosis.2 Cancer cells exhibit many characteristics that would readily trigger apoptosis in healthy cells—for example, they violate cell cycle checkpoints and can withstand exposure to cytotoxic agents.1 Because of these characteristics, cancer cells tend to survive. Apoptosis can be seen as an important barrier to developing cancer; avoiding apoptosis is integral to tumor development and resistance to therapy.3,4”

“Necessity for Cell Death in Multicellular Organisms.
The ability to undergo programmed cell death (Box 46.1) is a built-in latent capacity in most cells of multi-cellular organisms. Cell death is important for embryonic development, maintenance of tissue homeostasis, establishment of immune self-tolerance, killing by immune effector cells, and regulation of cell viability by hormones and growth factors. Both extrinsic signals and internal imbalances can lead cells to kill themselves. Furthermore, many metazoan cells will die if they fail to receive survival signals from other cells. Abnormalities of the cell death program contribute to several important diseases, including cancer, Alzheimer disease, and AIDS. Cell death programs are ancient: much of the current network was present in the last eumetazoan common ancestor (see Fig. 2.8).

Programmed Cell Death Versus Accidental Cell Death: Apoptosis Versus Necrosis
Although cells die in many ways, it is useful to focus on two poles of this spectrum: apoptosis and necrosis. Fig. 46.1 summarizes the major pathways of programmed cell death. (Details are filled in as we progress through the chapter.) Apoptosis, the most widely studied pathway for programmed cell death, is cellular suicide resulting from activation of a dedicated intracellular program. Fig. 46.2 shows a detailed description of the events of apoptosis. At the other end of the spectrum necrosis, also called accidental cell death, occurs when cells sustain a structural or chemical insult that causes the cells to swell and undergo membrane lysis (Fig. 46.3). Examples of such insults include extremes of temperature and physical trauma. Cells can also initiate active programmed necrosis in response to certain stimuli, particularly when induction of apoptosis is inhibited. Programmed necrosis looks morphologically like accidental cell death. A third pathway leading to cell death involves autophagy (see Fig. 23.7). Although usually regarded as a protective response to starvation, autophagy has been implicated in certain examples of cell death, particularly during development.

Necrosis corresponds to what most of us naively imagine cell death would be like. Owing to lack of cellular homeostasis, water rushes into the dying cell, causing it to swell until the plasma and organelle membranes burst. As a result, the cell undergoes a generalized


https://www.biooncology.com/pathways/cancer-tumor-targets/bcl-2/evading-apoptosis.html

(b) What is Apoptosis?
 There are two ways that a cell can die: necrosis and apoptosis. Necrosis occurs when a cell is damaged by an external force, such as poison, a bodily injury, an infection or getting cut off from the blood supply (which might occur during a heart attack or stroke). When cells die from necrosis, it’s a rather messy affair. The death causes inflammation that can cause further distress or injury within the body.

Apoptosis, on the other hand, is relatively civil, even though it may not sound so at first — it’s when a cell commits suicide. How is that better than necrosis? For one thing, the cleanup is much easier. It’s sometimes referred to as programmed cell death, and indeed, the process of apoptosis follows a controlled, predictable routine.

When a cell is compelled to commit suicide (we’ll get to the triggers for apoptosis in just a minute), proteins called caspases go into action. They break down the cellular components needed for survival, and they spur production of enzymes known as DNases, which destroy the DNA in the nucleus of the cell. It’s like roadies breaking down the stage in an arena after a major band has been through town. The cell shrinks and sends out distress signals, which are answered by vacuum cleaners known as macrophages. The macrophages clean away the shrunken cells, leaving no trace, so these cells have no chance to cause the damage that necrotic cells do.

Apoptosis also differs from necrosis in that it’s essential to human development. For example, in the womb, our fingers and toes are connected to one another by a sort of webbing. Apoptosis is what causes that webbing to disappear, leaving us with 10 separate digits. As our brains develop, the body creates millions more cells than it needs; the ones that don’t form synaptic connections undergo apoptosis so that the remaining cells function well. Programmed cell death is also necessary to start the process of menstruation.

That’s not to say that apoptosis is a perfect process. Sometimes, the wrong cells kill themselves off, and sometimes, the ones that should say “auf Wiedersehen” stick around instead. This brings us to our discussion of the triggers of apoptosis. Rather than dying due to injury, cells that go through apoptosis die in response to signals within the body. When cells recognize viruses and gene mutations, they may induce death to prevent the damage from spreading. When cells are under stress, as may happen when free radicals are on the loose or when a person undergoes radiation, apoptosis can occur. But there are also signals within the body that send the message that a cell should continue living. All cells have varying level of sensitivity to the positive and negative triggers, so sometimes the wrong cells live and die.

Scientists are trying to learn how they can modulate apoptosis, so that they can control which cells live and which undergo programmed cell death. Anti-cancer drugs and radiation, for example, work by triggering apoptosis in diseased cells. Many diseases and disorders are linked with the life and death of cells — increased apoptosis is a characteristic of AIDS, Alzheimer’s and Parkinson’s disease, while decreased apoptosis can signal lupus or cancer. Understanding how to regulate apoptosis could be the first step to treating these conditions. https://science.howstuffworks.com/life/cellular-microscopic/apoptosis1.htm

  1. What kind of – so far understood – relations between mitochondria “health” and the development of cell dysfunctions and its practical implication exists? 

More text is coming …

4. Epigenics and some recent evidence to be considered
Especially much work is done on diet and its relation to diseases in general and cancer specifically. Important is to be careful, but also test what is much work on as well as no known destructive effects – as well as, of course not instead of consensus interventions, if not critical of other reasons, e.g. very well R&D work!

Turmeric has long been an important candidate to be included into “patients´ work”. But as usual natur before artificial isolated substances, here of curcumin. Much is written and extremely many studies are done – for now, before giving my scientific/clinical/personal view, I refer to https://www.cancerresearchuk.org/about-cancer/cancer-in-general/treatment/complementary-alternative-therapies/individual-therapies/turmeric + https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2758121/ + more popular website https://articles.mercola.com/sites/articles/archive/2014/03/02/curcumin-benefits.aspx

More is to come …