neuroscience; what exactly are our memory problems

[leaves]

I try to figure out where in the brain my memory problems are located.
I am good analytically but i have problems
-recognizing faces
-remember numbers/ dates or "non-connected events or items"
-process information
-word recall
-remember what I read / working memory
-anticipating
-orientation/spatial memory

so this seems all hippocampus. So probably the NMDA receptors are messed up in some way? thoughts?

 

[Wonko]

What memory problems? I dont remember anything about memory problems.

(sorry, will try and resist harder next time)

I'm not sure how I'd seperate out memory only issues with processing issues, yes I have specific memory issues but, as far as I am aware, most of the time its inability to think thats the issue.

 

[Nielk]

I try to figure out where in the brain my memory problems are located.
I am good analytically but i have problems
-recognizing faces
-remember numbers/ dates or "non-connected events or items"
-process information
-word recall
-remember what I read / working memory
-anticipating
-orientation/spatial memory

so this seems all hippocampus. So probably the NMDA receptors are messed up in some way? thoughts?

Hi Leaves,

Besides the symptoms you mentioned, I also have an attention problem not unlike ADD which I didn't have before.
Also, and it might be the same problem. It's very hard for me to focus. For exam[ple, if someone is talking to me, I can't have any other distraction like backround noise otherwise I'm totally lost.

I did not have any of the neurological problems before I got sick.

 

[alex3619]

Partial Episodic Amnesia?

Hi leaves, this is a timing coincidence. Late last year I was going to write a blog on memory but didn't get around to it. Just yesterday I started again, but I think I will say something here. I don't know if I will ever finish the blog, it is a deep and complex topic and I lack the resources to do it justice, but I will keep plugging away at it from time to time.

Last year I noticed a pattern in many long term patients (including me). We look around us, scan the environment, analyze it, and run over that analysis in our memory. This is similar to strategies some students use - it assists conversion of memory to a type of memory called semantic memory, the memory of ideas. Why is this important?

My observation is about a very specific type of memory: episodic memory.

Do you know what a dog is? That is semantic memory, abstract and central to understanding the world. Its what students use to pass exams.

When I think back, I can remember a childhood dog of mine, affectionately nicknamed Stupid because he did lots of silly things. I know I had a dog with that name, I know where I was living at the time, I know how he died - but I don't recall playing with the dog, seeing the dog, or anything similar. Specific memory of events is extremely hard to me to recall - and its not just a dog, its everything: family, friends, school, work. Some things do stick out, but not many. Specific memory like this is called episodic memory.

Yet I have no trouble recognizing people when I see them, discussing events with people often promotes recall, I think the memories are there I just can't get hold of them. A tentative title for my blog is "Memory Cat and Mouse", where my memory plays out like a Tom and Jerry cartoon: but my mind is the cat, not the mouse, and the mouse always gets to run away.

The upshot of this is that, aside from deep feelings which seem intact, my memory is like something I read in a private journal: words and ideas. I remember that I went to a birthday dinner for a friend of mine, but not the dinner itself except for one or two half second flashes. Because I run things over and over in my head, analyzing every way I can think of, I connect events to other memories, create a web of ideas that I will remember. These are my journal entries. Using these I can fake real memories, and do so regularly. Most people never notice; some do notice that something is wrong, particularly close friends, but they have never really figured it out.

When I was with two other long term patients, discussing this theory I had of my own memory issue, they confessed they have the same issues. All three of us had been sick longer than ten years, and two of us had profound circadian sleep dysregulation.

ME or CFS may have very specific long term memory deficits. Most of the research being done on cognitive deficits in ME and CFS is for patients who have not been sick as long or are only moderately disabled. The question I want answered is how many severe patients who have been sick for decades have these kinds of problems? Does it get worse? Do any memory or dementia treatments work to reverse it? I don't have answers to these questions, I just hope that as treatments for ME and CFS finally roll out we will find these problems go away.

Bye
Alex

 

[taniaaust1]

When I was with two other long term patients, discussing this theory I had of my own memory issue, they confessed they have the same issues. All three of us had been sick longer than ten years, and two of us had profound circadian sleep dysregulation.

ME or CFS may have very specific long term memory deficits. Most of the research being done on cognitive deficits in ME and CFS is for patients who have not been sick as long or are only moderately disabled. The question I want answered is how many severe patients who have been sick for decades have these kinds of problems? Does it get worse? Do any memory or dementia treatments work to reverse it? I don't have answers to these questions, I just hope that as treatments for ME and CFS finally roll out we will find these problems go away.

Bye
Alex

I believe they dont necessarily get worst and that they can get better.. based on my own experience of it.

Ive been having an incredible experience of late (since I started on molybdenum and selenium) of regaining memories of my childhood. In the last month ive suddenly remembered some toys of my toddler years, not just what they were and my childhood name for them but also what they looked like... its weird having memories long lost (even before the ME) come back.

This is kind of incredible for someone who dont remember anything much at all from the time before she was 13-14yrs old (interestingly that is about the time I got severe EBV but I didnt get ME then but 11 years later). I had no picture memories at all before then.. just facts.

Currently once or twice a week.. Im suddenly regaining lost memories from over 30 years ago..
I can only assume I had that deficiency of molybdenum as a child and hence caused me to loose all my memories. (I wonder if various long term deficiencies we didnt know we had could also be playing a part into our susceptability to getting ME in the first place?)
.............

As far as ME memory loss goes (rather then my childhood memory loss before ME time) .. that started to improve before the supplements as my ME has improved. I dont now days forget what a "toaster" looks like or forget how to cook toast.. and I nowdays dont forget what my own relatives look like... I have some facial recognition back (thou i still cant remember strangers I meet faces).

 

[Enid]

I found a very similiar pattern tania - from not even recognising say a plug in the sink or recalling my own name without long thought, I now (range of supplements over years) remember faces, past events, do limited multitasking etc. The situation can and does improve. A little bit of encouraging thinking processes eg difficult crosswords seems to help too.

 

[richvank]

I try to figure out where in the brain my memory problems are located.
I am good analytically but i have problems
-recognizing faces
-remember numbers/ dates or "non-connected events or items"
-process information
-word recall
-remember what I read / working memory
-anticipating
-orientation/spatial memory

so this seems all hippocampus. So probably the NMDA receptors are messed up in some way? thoughts?

Hi, leaves.

I think you are correct in focusing on the hippocampus in ME/CFS. See the abstracts below.

As you may know, the hippocampus also plays a role in controlling the HPA axis, and that is dyfunctional in ME/CFS, also. There has been research that indicates that long-term stress, causing high cortisol levels, can damage the hippocampus over time, and that after this occurs, the HPA axis does not respond normally to stress.

I think the hippocampus is a good place to look for problems in ME/CFS.

Best regards,

Rich

Br J Radiol. 2000 Nov;73(875):1206-8.
Proton magnetic resonance spectroscopy and morphometry of the hippocampus in chronic fatigue syndrome.
Brooks JC, Roberts N, Whitehouse G, Majeed T.
Source

Magnetic Resonance and Image Analysis Research Centre, University of Liverpool, Pembroke Place, Liverpool L69 3BX, UK.
Abstract

Seven patients with chronic fatigue syndrome (CFS) were matched with ten healthy control subjects of similar age. Hippocampal volume, obtained from magnetic resonance images using an unbiased method, showed no difference between the two groups, whereas proton magnetic resonance spectroscopy showed a significantly reduced concentration of N-acetylaspartate in the right hippocampus of CFS patients (p = 0.005).

PMID:
11144799


Biol Psychiatry. 2005 Feb 1;57(3):239-46.
Brain 5-HT1A receptor binding in chronic fatigue syndrome measured using positron emission tomography and [11C]WAY-100635.
Cleare AJ, Messa C, Rabiner EA, Grasby PM.
Source

Section of Neurobiology of Mood Disorders, Division of Psychological Medicine, Institute of Psychiatry and Guy-s, King-s and St. Thomas- School of Medicine, London, United Kingdom. a.cleare@iop.kcl.ac.uk
Abstract
BACKGROUND:

Research from neuroendocrine challenge and other indirect studies has suggested increased central 5-HT function in chronic fatigue syndrome (CFS) and increased 5-HT1A receptor sensitivity. We assessed brain 5-HT1A receptor binding potential directly using the specific radioligand [11C]WAY-100635 and positron emission tomography (PET).
METHODS:

We selected 10 patients from a tertiary referral clinic who fulfilled the CDC consensus criteria for CFS. To assemble a homogenous group and avoid confounding effects, we enrolled only subjects who were completely medication-free and did not have current comorbid psychiatric illness. We also scanned 10 healthy control subjects.
RESULTS:

There was a widespread reduction in 5-HT1A receptor binding potential in CFS relative to control subjects. This was particularly marked in the hippocampus bilaterally, where a 23% reduction was observed.
CONCLUSIONS:

There is evidence of decreased 5-HT1A receptor number or affinity in CFS. This may be a primary feature of CFS, related to the underlying pathophysiology, or a finding secondary to other processes, such as previous depression, other biological changes or the behavioral consequences of CFS.

PMID:
15691524

 

[leaves]

Thanks Rich that is very interesting.
Do you have any idea on how to improve hippocampus function? Any meds or supplements?

Hi, leaves.

I think you are correct in focusing on the hippocampus in ME/CFS. See the abstracts below.

As you may know, the hippocampus also plays a role in controlling the HPA axis, and that is dyfunctional in ME/CFS, also. There has been research that indicates that long-term stress, causing high cortisol levels, can damage the hippocampus over time, and that after this occurs, the HPA axis does not respond normally to stress.

I think the hippocampus is a good place to look for problems in ME/CFS.

Best regards,

Rich

Br J Radiol. 2000 Nov;73(875):1206-8.
Proton magnetic resonance spectroscopy and morphometry of the hippocampus in chronic fatigue syndrome.
Brooks JC, Roberts N, Whitehouse G, Majeed T.
Source

Magnetic Resonance and Image Analysis Research Centre, University of Liverpool, Pembroke Place, Liverpool L69 3BX, UK.
Abstract

Seven patients with chronic fatigue syndrome (CFS) were matched with ten healthy control subjects of similar age. Hippocampal volume, obtained from magnetic resonance images using an unbiased method, showed no difference between the two groups, whereas proton magnetic resonance spectroscopy showed a significantly reduced concentration of N-acetylaspartate in the right hippocampus of CFS patients (p = 0.005).

PMID:
11144799


Biol Psychiatry. 2005 Feb 1;57(3):239-46.
Brain 5-HT1A receptor binding in chronic fatigue syndrome measured using positron emission tomography and [11C]WAY-100635.
Cleare AJ, Messa C, Rabiner EA, Grasby PM.
Source

Section of Neurobiology of Mood Disorders, Division of Psychological Medicine, Institute of Psychiatry and Guy-s, King-s and St. Thomas- School of Medicine, London, United Kingdom. a.cleare@iop.kcl.ac.uk
Abstract
BACKGROUND:

Research from neuroendocrine challenge and other indirect studies has suggested increased central 5-HT function in chronic fatigue syndrome (CFS) and increased 5-HT1A receptor sensitivity. We assessed brain 5-HT1A receptor binding potential directly using the specific radioligand [11C]WAY-100635 and positron emission tomography (PET).
METHODS:

We selected 10 patients from a tertiary referral clinic who fulfilled the CDC consensus criteria for CFS. To assemble a homogenous group and avoid confounding effects, we enrolled only subjects who were completely medication-free and did not have current comorbid psychiatric illness. We also scanned 10 healthy control subjects.
RESULTS:

There was a widespread reduction in 5-HT1A receptor binding potential in CFS relative to control subjects. This was particularly marked in the hippocampus bilaterally, where a 23% reduction was observed.
CONCLUSIONS:

There is evidence of decreased 5-HT1A receptor number or affinity in CFS. This may be a primary feature of CFS, related to the underlying pathophysiology, or a finding secondary to other processes, such as previous depression, other biological changes or the behavioral consequences of CFS.

PMID:
15691524

 

[kaffiend]

I try to figure out where in the brain my memory problems are located.
I am good analytically but i have problems
-recognizing faces
-remember numbers/ dates or "non-connected events or items"
-process information
-word recall
-remember what I read / working memory
-anticipating
-orientation/spatial memory

so this seems all hippocampus. So probably the NMDA receptors are messed up in some way? thoughts?

It doesn't necessarily implicate the hippocampus. The hippocampus in humans is believed to be involved in encoding new memories and retrieving old ones from widely distributed networks. Memory is a vague term and covers a variety of cognitive processes. The hippocampus is shown to be active in declarative memory (i.e., facts about the world) and episodic memory (i.e., personal memory about events in time). These are deficits seen in Alzheimer's.

My own neuropsych deficits fall into problems with short-term memory and processing speed. Short-term memory covers things you've just read or seen that have to be "maintained" briefly. This would also include internally generated events; for example, I find that I lose track of immediate goals. By that I mean, as I start to do something, I completely forget what it was. It can become so severe that writing a do-to list is pointless, as I forget what I'm trying to list as I'm writing it. I also have problems with procedural memory (over-learned motor behaviors such as typing or tying your shoes). Also, anything involving choice conflict becomes difficult, such as which button to press for accepting a debit charge at the grocery store, etc. Deficits such as these are classically defined as "frontal." The SPECT, MRI and perfusion studies done in CFS/ME patients show profound metabolic/perfusion reductions in lateral frontal and medial frontal structures, as well as brainstem, which contains the cell bodies projecting to frontal regions.

www.lumosity.com is good program for measuring (and improving) cognitive processing along a variety of dimensions. Under the "assessments" tab is a series of validated neuropsych tests. Processing speed will probably show the largest deficit. My reaction times on bad days are 25-30% slower.

If there is involvement of the hippocampus, I think it would be due to disruption of the HPA axis - hippocampus expresses receptors for glucocorticoids and mineralcorticoids. Binding of these receptors controls a number of downstream processes (genomic effects) that are way above my pay grade.

 

[leaves]

Oh my.. thats all pretty complex. so I guess you cant suggest a magic pill ? ;-)

It doesn't necessarily implicate the hippocampus. The hippocampus in humans is believed to be involved in encoding new memories and retrieving old ones from widely distributed networks. Memory is a vague term and covers a variety of cognitive processes. The hippocampus is shown to be active in declarative memory (i.e., facts about the world) and episodic memory (i.e., personal memory about events in time). These are deficits seen in Alzheimer's.

My own neuropsych deficits fall into problems with short-term memory and processing speed. Short-term memory covers things you've just read or seen that have to be "maintained" briefly. This would also include internally generated events; for example, I find that I lose track of immediate goals. By that I mean, as I start to do something, I completely forget what it was. It can become so severe that writing a do-to list is pointless, as I forget what I'm trying to list as I'm writing it. I also have problems with procedural memory (over-learned motor behaviors such as typing or tying your shoes). Also, anything involving choice conflict becomes difficult, such as which button to press for accepting a debit charge at the grocery store, etc. Deficits such as these are classically defined as "frontal." The SPECT, MRI and perfusion studies done in CFS/ME patients show profound metabolic/perfusion reductions in lateral frontal and medial frontal structures, as well as brainstem, which contains the cell bodies projecting to frontal regions.

www.lumosity.com is good program for measuring (and improving) cognitive processing along a variety of dimensions. Under the "assessments" tab is a series of validated neuropsych tests. Processing speed will probably show the largest deficit. My reaction times on bad days are 25-30% slower.

If there is involvement of the hippocampus, I think it would be due to disruption of the HPA axis - hippocampus expresses receptors for glucocorticoids and mineralcorticoids. Binding of these receptors controls a number of downstream processes (genomic effects) that are way above my pay grade.

 

[alex3619]

Hi kaffiend, most of us have problems with short term memory, working memory (what we are actually thinking about) and procedural memory (like tying shoelaces). The cognitive deficits in ME and CFS are very broad, I only mentioned the episodic memory issues because it is frequently not discussed. Slow processing speed is a classic finding in us, and is often severe enough to support disability claims by itself.

I am not convinced we actually have slow processing speed though. The time it takes us to process is slow, yes, but I think that it is more likely to be from our having to compensate for deficits. Because some of our brain is functionally suboptimal, I think we recruit and integrate capacity from other parts of the brain, and this will make things slower as a matter of course. There have been several studies (don't recall details offhand) in which brain recruitment on fmri was higher than normal, regions being recruited that should not be, iirc. Maybe someone who has read such research recently can comment further.

The thing about declarative memory in my experience, is that the semantic component is usually fine (unless you forget what a coffee cup is or something, a story I hear from time to time) but we have more problems with word recall - we either can't remember the right word or use something similar. I think this is a variable binding problem. The stimulus is so weak that words associated with the correct word sometimes get activated instead. So when I mean to say library, I say bookshop. Sometimes it is not a similar meaning though, but a similar sounding word that is used. (I used to be a neural network researcher, or at least was attempting to be.)

I think this crosses over to the real world. The other night I went to the fridge to grab something, and came back with something else - a bad of rice. This is also a variable binding problem, and indicates working memory deficits, and probably altered consciousness.

So I think that the cognitive deficits are all over the brain, though possibly affecting some parts worse than others, but I am very interested in the brain stem lesions. Even if the deficit is global and not focal, it would still affect some mental processes more than others.

The thing about adapting to brain problems though is that I suspect those with long term illness will have different usage of their brain to new patients. It would be interesting to compare the two groups, but I can't see that ever happening in a formal study when our funding is so pathetic.

Bye
Alex

 

[kaffiend]

I am not convinced we actually have slow processing speed though. The time it takes us to process is slow, yes, but I think that it is more likely to be from our having to compensate for deficits.

I also have transient problems with word finding. I find myself doing "circumlocutions" which is to say things about the word I'm trying to find, while being unable to produce the actual word. In aphasia, it's called anomia and sometimes occurs within strange categories (tools and animals) but problems with names, proper nouns, dates, and more generally, supra-ordinate terms within a category are common. But there's clear, focal anatomical damage there and the compensatory recruitment is due to chronic loss of function.

Processing speed is definitely an imprecise term. Compensatory recruitment is seen in recovery after strokes, but I think an inflammatory process is actually limiting conduction speed and communication in CFS. The following is from a book chapter:

David W. McCandless Editor
Metabolic Encephalopathy (2009)


Post Infectious Encephalomyelitis
Altered mental status is a pre-requisite for the diagnosis of acute disseminated encephalomyelitis (ADEM), often a consequence of non-CNS infection or immunization (Tenembaum et al., 2007) The disorder is the subject of a complete chapter in this book, so this discussion will be limited to the mechanisms of brain injury as it pertains to encephalopathies mediated by brain inflammation. There is excellent evidence to suggest that the brain injury is primarily immune mediated and there- fore inflammatory in nature. Antigenic similarities between the viral antigens(or vaccine) and the brain result in injury to the brain in the course of a normal immune response of the host to the pathogen. This phenomenon, known as molecular mimicry, constitutes the basis of this disorder (Menge et al., 2007; Quaranta et al., 2006; Gout, 2001). For the most part the injury appears to be a leukoencephalitis affecting the periventricular as well as the subcortical white matter of the brain. Axonal rather than myelin injury appears to be the basis of morbidity following inflammatory demyelination. The mechanism of axonal injury is unknown but there is some evidence to suggest that it is in part caused by the phenomenon of virtual hypoxia (Stys, 2004, 2005). According to this concept, injury to the mitochondria occurs probably from nitric oxide produced by inflammatory cells. Experimental studies that exposed axons to concentrations of nitric oxide seen at sites of inflam- mation (~ 4 ?M) were capable of causing axonal conduction block (Smith et al., 2001; Kapoor et al., 1999; Redford et al., 1997) When conduction was carried out at 50100 Hz, the conduction block outlasted the period of exposure to nitric oxide, indicating a permanent rather than transient injury. Examination of these axons identified marked edema with disorganization of myelin indicative of depolariza- tion injury. It appeared that the axons depolarized to the stimuli but were incapable of repolarization, which is an energy dependant state. The Na+ ions that entered the axons during depolarization could not exit the axon because the Na+ K+ ATPase pump requires ATP to function and in the absence of mitochondrial function there was depletion of the limited ATP available through glycolysis. The accumulation of Na+ leads to accumulation of water and edema of the axons. This situation leads to exchange of one Ca2+ for two NA+, through the Na+Ca+ exchanger and this leads to intra axonal accumulation of free Ca2+. Transport of Ca2+ to the axoplasmic reticulum is also an energy-dependent function and therefore does not occur in the state of limited ATP supply. The accumulation of Ca2+ then leads to activation of a variety of proteases with eventual irreversible injury to the axon. These observations suggested that blockade of Na+ channels in a demyelinated animal could pre- serve axonal function. Indeed this was the case when mice with experimental autoimmune encephalomyelitis were treated with flecainide, a sodium channel blocker; preservation of axons was demonstrated in a dose-dependent manner (Bechtold et al., 2004; Kapoor et al., 2003).

 

[richvank]

Thanks Rich that is very interesting.
Do you have any idea on how to improve hippocampus function? Any meds or supplements?

Hi, leaves.

No, sorry, I don't know anything specific. The best I can suggest is to correct the oxidative stress by treating to lift the partial methylation cycle block, and then supplementing with DHA (as from fish oil). I don't know the nature of the damage to the hippocampus, but if oxidative stress has damaged lipids that make up the cell membranes and the myelin, this might help.

Rich

 

[justy]

A very interesting discussion and im afraid one i no longer have the brain power to engage in as well asi would like.
I have many of the problems mentioned above, especailly word recall and also the inability to physically say the word once i have remembered it, recently this has moved onto me saying the wrong but similar word many times a day.
I also have problems with very short term memory such as forgetting what i am writing about whilst writing or going upsatirs and then not knowing why, often these days i never can remember and have to give up.
I also have a problem with remembering things that have happened recently, every week my mum asks me if i had a nice weekend and i can never remember what i did,who i saw etc, there is just a huge void in the place where the memory should be, also i seem to have lost all track of time. Yesterday we where talking at home about things we had done over the past few years and i cant really remember the order of things anymore -but i do have a good long term memory -scarily similar to the elderly with dementia -i dont know what i had for dinner but can recall long involved stories from my teenage years.

Dr Myhills thoery on this is that it is completely reversible by supporting the mitochondria (Co Q10, magnesium, d ribose etc) as well as pacing as she feels it is a defect in mitochondrial ebergy production that is causing thses symptoms. As far as i understand it the brain has a high need for ATP and cant recycle it like other systems in the body can (sorry thats very oversimplified)
Vitamin D3 is also very very useful for brain function -mine works better if i take 2,000iu a day.

http://www.drmyhill.co.uk/wiki/Category:Neurological_problems

http://www.drmyhill.co.uk/wiki/Brain_fog_-_poor_memory,_difficulty_thinking_clearly_etc

http://www.drmyhill.co.uk/drmyhill/images/a/a7/ATP_as_a_neurotransmittor_Sci_Amer_2009.pdf

Justy.

 

[Sallysblooms]

Rich, what about getting the neurotransmitters tested and balanced. Also, hormone balancing. Those things, Carniclear, supplements for n.transmitters, getting seratonin up to a good level with supplements, Lipo C, Lipo GSH and others have all done a great job. I guess we are all different, but I do know what helped me. I never give up and my doctors have helped so much. For me at least, balancing things I needed was what helped. Many doctors do not understand how illness and many meds deplete our reserves. We have to replenish them.

 

[richvank]

Rich, what about getting the neurotransmitters tested and balanced. Also, hormone balancing. Those things, Carniclear, supplements for n.transmitters, getting seratonin up to a good level with supplements, Lipo C, Lipo GSH and others have all done a great job. I guess we are all different, but I do know what helped me. I never give up and my doctors have helped so much. For me at least, balancing things I needed was what helped. Many doctors do not understand how illness and many meds deplete our reserves. We have to replenish them.

Hi, Sally.

I agree that these are good things to do. Maybe some of them will help the hippocampus, I don't know. I would like to better understand if and how the hippocampus is damaged. My understanding from the literature is that the hippocampus has the highest concentration of glucocorticoid receptors. When a person is under long-term stress, cortisol initially goes high and stays high. Apparently the sustained high levels of cortisol damage the hippocampus. I'm guessing that oxidative stress is involved.

As we know, when a person moves into the higher stages of what has been called "adrenal fatigue," the cortisol level goes too low. This may reflect accumulated damage to the hippocampus. I hope to be able to look into what this damage might consist of. and what can be done about it.

Incidentally, Sally, you might find the book by Mia Lundin interesting. It has a very catchy title: "Female Brain Gone Insane." She is a nurse practitioner in Santa Barbara, CA. She does bioidentical reproductive hormones treatment, neurotransmitter treatment using amino acids, and then treats thyroid with natural thyroid, and also supports the HPA axis. I think the last part is the most difficult.

Best regards,

Rich

 

[Sallysblooms]

Yes, I had the cortisol checked also. It was lower in the afternoon. I take a small amount at noon as my doctor suggested. That has been great. That and thyroid also. SO many things needed to be addressed. It would really be handy if more doctors would be educated in these things! That book sounds good, just like me. I do those things. I just had my twice yearly blood testing with Dzugan Method. My doctor always gets others too. Lots of vials, lots of information!