Re: Behavior and HPA functioning.

[Guest guest]

Depression is a result of hypothalamus/central nervous system injury. It isn't

the cause.

Cheney says

Phase 3:Dynamic Hormone Response Deficits Induced By Hypothalamic Injury

Phase III has a different sound to it. The toxins, in addition to inhibiting

cell function, have invaded the central nervous system and injured deep brain

structures, especially the hypothalamus, resulting in problems with virtually

every hormone in the body. The actual problem is with the loss of " dynamic

hormone response " . This means that hormones that should rise and fall according

to signals or demands from the body do not respond accordingly. The

hypothalamus' major function is to control dynamism. Injuring the hypothalamus

leads to a loss of dynamic response, such that patients can experience great

difficulty in handling the normal stresses and strains of life.

This is biological, and scientifically sound.

For more information on this please see www.cfsunited.com/truth

What these psychoneuroendocardiogastrootolaryngolical theorists are saying is

that by dwelling on my illness, I am making myself ill. But I was already ill,

or I would not be " dwelling " on it.

Mark London <mrl@...> wrote:

HPA hypoactivity is hallmark of CFS and fibromyalgia, and is widely

believed to be a consequence of those conditions, rather than being a

cause. One simple way of testing for HPA functioning is via the

cortisol awakening response test. The following study shows that

self-focused rumination can significantly lower the cortisol

awakening response. CBT attempts to change detrimental behavior

patterns, and self-focused rumination is often one such behavior that

it tries to stop. Thus, can CBT help some people with CFS, by

improving HPA functioning? In any event, here are some quotes from

the study... It's a fun read.

" Decreased cortisol response to awakening is associated with

cognitive vulnerability to depression in a nonclinical sample of

young adults. "

Psychoneuroendocrinology

Volume 32, Issue 2, February 2007, Pages 199-209

Alterations in the hypothalamus–pituitary–adrenal (HPA) axis function

in depression are well documented (Hasler et al., 2004; Antonijevic,

2006). Depression has been linked to altered basal- and stress-

related cortisol responses, and both over- and underactivation of the

HPA axis have been reported, probably depending on subtype and

severity (Stetler and , 2005; Antonijevic, 2006; Oswald et al.,

2006). There is increasing evidence that these alterations are not

merely epiphenomena of the disorder, but may rather be regarded as

endophenotypes, probably playing an important role in causal pathways

of the pathophysiology of depression (Hasler et al., 2004; Oswald et

al., 2006).

With regard to unstimulated HPA-axis activity, the cortisol awakening

response (CAR) has been gaining attention in recent research. The CAR

is a discrete part of the cortisol circadian cycle. In healthy

individuals, it is characterized by a large increase in saliva free

cortisol levels within the first 30 min after awakening (50–60%;

Pruessner et al., 1997; Wuest et al., 2000a; Clow et al., 2004). In

contrast to experimentally stimulated cortisol responses, the CAR

reflects cortisol excretion after a natural stressor (awakening). The

CAR is an easily accessible and reliable means of assessing dynamic

HPA functioning (Pruessner et al., 1997; Rohleder et al., 2004). It

demonstrates moderate to high within-subject stability (Pruessner et

al., 1997; Wuest et al., 2000a; et al., 2001) and—in contrast

to the cortisol profile during the day—appears to be under

substantial genetic control (Wuest et al., 2000b; Bartels et al.,

2003). Furthermore, the CAR seems not to be related to other

parameters of diurnal cortisol secretion or to cortisol responses to

stress, but correlates with the response to standard

adrenocorticotropin stimulation, indicating that it is a marker for

adrenocortical activity (Schmidt-Reinwald et al., 1999; et

al., 2001).

Due to its high intraindividual stability, the CAR may be regarded as

a trait measure of the dynamics of HPA axis activity. In this regard,

it appears ideally suited for investigating possible connections with

psychological vulnerability markers for depression. Investigations of

such kind could contribute important knowledge on the role of

cognitive vulnerability theories within a psychobiological framework

for research on affective disorders (son et al., 2002).

One of the most prominent cognitive vulnerability theories of

depression, the Response Styles Theory by S. Nolen-Hoeksema (2004)

addresses the role of two coping styles, namely perseverative self-

focused rumination versus distraction from negative mood, for the

exacerbation, maintenance, and discontinuation of depressed states.

Ruminative responses are defined as thoughts and behaviours that

comprise passively focusing one's attention on one's dysphoric

symptoms and aspects of the self during low mood and repetitive

thinking about possible causes and consequences of symptoms and

negative self-aspects. Distractive coping is defined as actively

turning one's attention away from one's symptoms on to pleasant or

neutral thoughts and actions (Nolen-Hoeksema, 2004). The theory

postulates that ruminative coping amplifies and prolongs depressed

mood by increasing the likelihood of recalling negative memories, by

interfering with attention and instrumental behaviour, and by

impairing more complex problem solving (cf. Kuehner and Buerger,

2005). There is evidence from observational studies for the proposed

prediction of response styles regarding onset, severity, and duration

of depressed moods (Nolen-Hoeksema, 2000; Kuehner and Weber, 1999).

Furthermore, experimentally induced rumination prolonged depressed

moods, enhanced negatively biased memories, and impaired

interpersonal and complex problem solving, while induced distraction

led to a decline of depressed mood and improved problem solving

(Lyubomirsky et al., 1999; son and Lam, 2004; Joormann and

Siemer, 2004).

The present study investigated associations of basal diurnal cortisol

activity—particularly the CAR—with habitual coping styles in response

to depressed mood and with responsiveness to induced attention

focusing after sad mood induction. In this regard, our study is the

first to connect a measure of dynamic HPA activity to a cognitive

vulnerability marker for depression, the latter assessed both by a

trait measure and by experimental manipulation.

The mood induction procedure used in this study appeared to be

effective. Using a film sequence originally employed by Joormann and

Siemer (2004), levels of mood were lowered significantly from

baseline to post mood induction in the total sample, reflected both

in a decrease of positive and an increase of negative mood.

Participants subsequently induced to ruminate kept their negative

mood whereas participants induced to distract themselves showed a

significant reduction of negative mood along with a significant

increase of positive mood. These results support growing evidence

from the literature showing that actively induced ruminative self-

focused attention prolongs and stabilizes dysphoric mood, while

actively induced distraction attenuates and shortens it (cf.

Lyubomirsky and Tkach, 2004; Nolen-Hoeksema, 2004 for reviews).

Importantly, the present study also revealed that higher levels of

self-focused trait rumination were connected with lower improvement

or worsening of mood after response induction, and these results were

not attributable to interindividual variability in basal levels of

depressive symptoms.

Another key finding of our study was that a low CAR was linked to

high levels of self-focused rumination and to lowered improvement of

mood after induced distraction. This suggests that a decreased CAR is

simultaneously associated with habitual self-related emotional

processing and with a restricted capacity of the individual to lift

negative mood with distractive thoughts. How can this be explained?

There is evidence that depression involves deficient inhibition of

negative information (Goeleven et al., 2006). Research has shown that

depressed individuals show lowered activation in brain regions

responsible for attentional control over emotional interference, such

as the prefrontal cortex and the anterior cingulate (son et al.,

2002; et al., 2004). It has been suggested that impaired

inhibitory function might also be one of the underlying mechanisms of

rumination (Hertel, 1997). For example, self-reported rumination has

been linked to sustained amygdala reactivity to negative words in

depressed individuals (Siegle et al., 2002), with both responses

apparently reflecting difficulties to disengage attention from

negative information. Respectively, in the present response

manipulation task high levels of habitual self-focused emotional

processing appeared to have amplified the negative mood effects of

induced rumination and to have impaired the individual's capacity to

lift mood by switching attention to external cues in the distraction

condition.

In parallel, at the neuroendocrine level, the CAR seems to reflect

the capacity of an organism to focus attention to novel situations or

demands under natural conditions, involving inhibition of task-

irrelevant emotional processing (e.g., kson et al., 2003). It has

been noted that the normal elevation of morning cortisol serves a

variety of functions by mobilizing energy stores, increasing interest

in exploration, and promoting acquisition, attention focusing, and

consolidation in the learning process (Gunnar and Vazquez, 2001).

Similarly, kson et al. (2003) consider moderately enhanced

morning cortisol to reflect a state of heightened attention to the

social environment, which may facilitate the progression of higher

order cognitive mechanisms. Thus, in our opinion, a decreased CAR and

high self-focused rumination appear to share specific vulnerability

qualities involving similar mechanisms. We assume that both hamper

the adaptive shift of attention to external cues during dysphoric

episodes and involve lowered disinhibition of task-irrelevant

negative emotional processing. In this respect, our study revealed

first indications of a possible relationship between a cognitive

vulnerability marker for depression and characteristics of basal

neuroendocrine activity regarding their association with the course

of experimentally induced dysphoric mood.

Within the framework of the present study we are also unable to

determine causal pathways between CAR and self-focused rumination. It

is conceivable that a blunted CAR limits the capacity of an

individual to inhibit interfering negative internal self-evaluating

processes during dysphoric mood. Alternatively, habitual rumination

may promote allostatic load in the individual (cf. McEwen, 2004),

resulting in a long term down-regulation of the stress system as seen

in a number of stress-related conditions (Heim et al., 2000).

Finally, both variables may be influenced by unknown third variables.

This list is intended for patients to share personal experiences with each

other, not to give medical advice. If you are interested in any treatment

discussed here, please consult your doctor.

[Guest guest]

The study doesn't mention CFS. CFS is not depression. Many people with CFS do

not have

depression, and pursuing treatment based on that misdiagnosis can be a harmful

waste of

precious time, energy and money.

Dr. Myhill discusses CFS vs. depression quite clearly:

http://www.drmyhill.co.uk/article.cfm?id=210

>

> HPA hypoactivity is hallmark of CFS and fibromyalgia, and is widely

> believed to be a consequence of those conditions, rather than being a

> cause. One simple way of testing for HPA functioning is via the

> cortisol awakening response test. The following study shows that

> self-focused rumination can significantly lower the cortisol

> awakening response. CBT attempts to change detrimental behavior

> patterns, and self-focused rumination is often one such behavior that

> it tries to stop. Thus, can CBT help some people with CFS, by

> improving HPA functioning? In any event, here are some quotes from

> the study... It's a fun read.

>

> " Decreased cortisol response to awakening is associated with

> cognitive vulnerability to depression in a nonclinical sample of

> young adults. "

>

> Psychoneuroendocrinology

> Volume 32, Issue 2, February 2007, Pages 199-209

[Guest guest]

Hi, Mark.

" Mark London " <mrl@> wrote:

> >

> > HPA hypoactivity is hallmark of CFS and fibromyalgia, and is

widely believed to be a consequence of those conditions, rather than

being a cause.

***This point about HPA derangement in CFS being downstream to

something is likely accurate while this effect being " hallmark " of

this disease is not supported by any data, especially long term CFS.

And it's obviously only transitory where it exists in the super large

self limiting CFS type distinguished by Dubbo(over 98% recover

entirely within two years from onset, so clearly not the CFS reported

about by Hyde, Cheney, , Bell and what most discussion on

lists like this seem to involve).

One simple way of testing for HPA functioning is via thecortisol

awakening response test. The following study shows that

self-focused rumination can significantly lower the cortisol

awakening response. CBT attempts to change detrimental behavior

patterns, and self-focused rumination is often one such behavior that

it tries to stop. Thus, can CBT help some people with CFS, by

improving HPA functioning?

***There is no data supporting CFS recovery as behaviorly connected or

impeded by certain behaviors such as " self-focused rumination " , which

also, btw, is not included in any of the known case definitions as a

symptom of this disease. But if what is meant by it is that someone

with CFS daily observes the intense symptoms of this disease

unavoidably at the forefront of their experience then I suggest it is

a very normal response to intense symptoms from any cause, painful,

pleasurable or otherwise.

***It's clearly a normal response to many conditions that eventually

get sent into remission with treatments that required no attention or

concern for dealing with it. Be careful of any publication titled or

using the phrase " Psychoneuroendocrinology " .

***It's telling of the publishers likely bias for psychologizing

poorly understood diseases and is not supported by mainstream science.

***

[Guest guest]

> ***This point about HPA derangement in CFS being downstream to

> something is likely accurate while this effect being " hallmark " of

> this disease is not supported by any data.

See this study:

http://www.ncbi.nlm.nih.gov/pubmed/18160468

" Women with CFS exhibited significantly attenuated morning cortisol

profiles compared with well women. "

The average duration of illness was 7.54 years.

For men the difference was not significance. However, no other study

has shown a similar gender difference with response to HPA functioning,

and there were only 17 men vs 58 women. Plus, compliance could be a

problem, as this was a home based study. It's possible a larger lab

based study would show a difference for men also. Indeed, in a

previous study that also showed lowered ACR in CFS, women actually had

a slightly higher ACR response than men:

http://www.ncbi.nlm.nih.gov/pubmed/14754825?dopt=Abstract

This study didn't say how long the people had CFS for.

- Mark

[Guest guest]

> The study doesn't mention CFS. CFS is not depression. Many people

with CFS do not have

> depression, and pursuing treatment based on that misdiagnosis can

be a harmful waste of

> precious time, energy and money.

These study subjects weren't depressed either. HPA hypoactivity is

well known to occur without being depressed. Any treatment that can

improve HPA functioning, might be capable of helping someone with HPA

hypoactivity.

A treatment like CBT isn't just depression. It can be useful for a

wide range of conditions, even with people with severe physical

handicaps, and severe conditions such as cancer. Techniques like CBT

don't get to the root cause of these other conditions either, but

they may still help some people.

Keep in mind, that chronic fatigue in many conditions, have multiple

causes. No single cause has been found for the severe fatigue which

occurs in HCV, MS, and lupus, for example. That's true, even in the

case of HCV, where it's known that an infection is the cause of the

condition. You can't necessarily write off a treatment, just because

it isn't getting to the " root " cause of the disease. It may be only

treating the cause of " secondary " fatigue, but it may still be useful.

Perhaps CBT isn't enough by itself to help a condition like CFS, but

a combination of different mind techniques might help, or when

combined with drugs. I would compare it to the use of low dosages of

drugs, at doses that aren't useful by themselves, but which have a

potentiating effect when combined with other drugs.

Btw, do you believe that CFS is a brain disorder, i.e. a problem with

central fatigue (vs peripheral disease)? Mind techniques can help

brain disorders. Take the example of major brain daamage due to a

stroke. In that case, part of the brain actually dies off. That's

why a person loses motor functioning. However, it's possible, using

the correct mind techniques, that one can slowly train other parts of

the brain to recover the lost functioning. Have you read about

neural plasticity? What's to say, therefore, that proper mind

techniques aren't capable of offsetting some of the damage from CFS?

- Mark

[Guest guest]

Hi, Mark.

An observation of a fact does not inherently tell us anything about

it's relevance to identifying or producing a condition. Confoundingly

to researchers who pay attention, there are numerous commonly found

abnormalities in PWCs, including many with HPA axis derangement, that

although observations of fact do not in themselves constitute data for

these being " hallmarks " of the condition.

Other than using what's in the current accepted case definitions to

say this, such characterization as fact is not possible for noted CFS

abnormalities such as those found in the HPA axis, the RnaseL system

and other things that have been argued to be central to CFS pathology.

Even the NIH considers CFS to be a condition of unknown origin and

they still have many subsets to yet get clear about to determine what

is hallmark for each, possibly unrelated diseases.

<mrl@...> wrote:

>

>

> > ***This point about HPA derangement in CFS being downstream to

> > something is likely accurate while this effect being " hallmark " of

> > this disease is not supported by any data.

>

> See this study:

>

> http://www.ncbi.nlm.nih.gov/pubmed/18160468

>

> " Women with CFS exhibited significantly attenuated morning cortisol

> profiles compared with well women. "

>

> The average duration of illness was 7.54 years.

>

> For men the difference was not significance. However, no other study

> has shown a similar gender difference with response to HPA functioning,

> and there were only 17 men vs 58 women. Plus, compliance could be a

> problem, as this was a home based study. It's possible a larger lab

> based study would show a difference for men also. Indeed, in a

> previous study that also showed lowered ACR in CFS, women actually had

> a slightly higher ACR response than men:

>

> http://www.ncbi.nlm.nih.gov/pubmed/14754825?dopt=Abstract

>

> This study didn't say how long the people had CFS for.

>

> - Mark

>

[Guest guest]

Yes, I believe CFS is a brain disorder. My current belief is that it is a

disorder of

everything, due to failure of cellular energy metabolism in the mitochondria.

With limited resources and in survival mode, one needs to prioritize. I

prioritize attempts

to improve cellular energy production (NADH, COQ10, Vitamin B3, Glutahione,

D-Ribose,

caffeine, etc.). When I previously prioritized psychologists, CBT, mind

approaches, my life

got worse.

Again, Dr. Myhill seems to have a clue:

http://www.drmyhill.co.uk/articles.cfm?subject=Fatigue

For me at this time, CBT, psychologists, mind techniques (beyond the likely

excessive

mind excercise required to work a bit, pay some bills and maintain some minimal

kind of

life) are harmful wastes of time. This deserves repeating, as those approaches

are so

dominant in the medical mainstream right now that to consider anything else is

seen as

subversive and crazy.

If you have " proper mind techniques " to suggest, please do. One might consider

them, if

they happen to stumble upon a surplus of time, energy and money.

> > The study doesn't mention CFS. CFS is not depression. Many people

> with CFS do not have

> > depression, and pursuing treatment based on that misdiagnosis can

> be a harmful waste of

> > precious time, energy and money.

>

> These study subjects weren't depressed either. HPA hypoactivity is

> well known to occur without being depressed. Any treatment that can

> improve HPA functioning, might be capable of helping someone with HPA

> hypoactivity.

>

> A treatment like CBT isn't just depression. It can be useful for a

> wide range of conditions, even with people with severe physical

> handicaps, and severe conditions such as cancer. Techniques like CBT

> don't get to the root cause of these other conditions either, but

> they may still help some people.

>

> Keep in mind, that chronic fatigue in many conditions, have multiple

> causes. No single cause has been found for the severe fatigue which

> occurs in HCV, MS, and lupus, for example. That's true, even in the

> case of HCV, where it's known that an infection is the cause of the

> condition. You can't necessarily write off a treatment, just because

> it isn't getting to the " root " cause of the disease. It may be only

> treating the cause of " secondary " fatigue, but it may still be useful.

>

> Perhaps CBT isn't enough by itself to help a condition like CFS, but

> a combination of different mind techniques might help, or when

> combined with drugs. I would compare it to the use of low dosages of

> drugs, at doses that aren't useful by themselves, but which have a

> potentiating effect when combined with other drugs.

>

> Btw, do you believe that CFS is a brain disorder, i.e. a problem with

> central fatigue (vs peripheral disease)? Mind techniques can help

> brain disorders. Take the example of major brain daamage due to a

> stroke. In that case, part of the brain actually dies off. That's

> why a person loses motor functioning. However, it's possible, using

> the correct mind techniques, that one can slowly train other parts of

> the brain to recover the lost functioning. Have you read about

> neural plasticity? What's to say, therefore, that proper mind

> techniques aren't capable of offsetting some of the damage from CFS?

>

> - Mark

>