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later Health items

Health items from before 2009:

Backs and Bricks   Dyslexia 1   Dyslexia 2   Dyslexia 3   Dyslexia 4   Dyslexia 5   Weight 1   Weight 2   Weight 3   Alzheimers 1   Alzheimers 2   Alzheimers 3   Celiac Disease   Nutritionism   More exercise

Backs and Bricks

Here is an idea that no one takes seriously as far as I know. THE SPINE DOES NOT WORK LIKE A PILE OF BRICKS WITH LITTLE PILLOWS BETWEEN THE BRICKS.
I read a book about Buckminster Fuller's ideas once, a long time ago. One of the items was a mast. I think he called it a DiMaxion Mast. It was held up by tension rather than compression. There were a number of solid pieces, one above the other but they were not actually touching. Each piece was like an old fashion jack that kids used to play jacks with, or like a cross shape where two opposite arms of the cross were bent upward and the other two arms bent downward. Each piece was placed in the pile so that its up arms were between the down arms of the peice above and its down arms were between the up arms of the peice below. Now a cable or string is put around the mast between each pair of peices. This cable is attached to the four arms between each pair of pieces, (the up arms from the lower one and the down arms from the upper one). Now the cable is tightened and this aligns the ends of the arms so that they are all in a plane, and that separates the two pieces. The mast is held up by the tension on those cables. Each piece is sort of resting in a hammock provided by the up arms of the piece beneath it. Finally 4 cables run length-wise through each set of arms up the mast from bottom to top and they are tensioned. This makes the mast stay vertical.
One day many years later, I was looking at a model of the spine. And hey, for a lot of the spine each vertbra has two downward projections and two upward ones. There are little muscles and connective tissue banding around the spine and some long muscles going up and down. I thought, that looks like Fuller's mast.
Full of excitement about this idea, I told my doctor the next time I was there. I got no reaction. But I thought, that's doctors-and-backs. The next time I exposed the idea was at a session on looking after your back being given by a physiotherapist. At one point she said, "think of the back as a pile of bricks". So after the session I took her up on that. I asked, "if the back is a pile of bricks, how can I just stand here and stretch myself a little taller?" Well she says I do that with my lungs and abdominal muscles. Which is true. So I hold my nose and keep a hand on my stomach to make sure I'm not tightening and I still think I can stretch taller, but she thinks I am fooling myself. She had no more time for such silly ideas. "Believe me", she says, "it works like a pile of bricks."
For my own peace of mind I tried stetching after I had abdominal surgery. I was sure I could tell if I used my abdominal muscles because they were so tender. I held my nose. I lined my eye up on a point along the window frame. I stetched and I was taller because I could see the shift in the background against the frame. I also noticed that people could stretch their necks. I am convinced that the back is not like a pile of bricks but is an active and reactive system of muscles holding the vertebra in various states of posture and tone. Believe me, it is not like a pile of bricks.

Dyslexia 1 A lot has been learned about dyslexia since I last had a look. Unlike the theories a few years back, the current contenders seem to fit much better with my experience.
Researchers are going after the genes responsible and have found at least four. All the genes probably have not been found yet, but the ones found so far all point to a similar cause for the condition. I was excited when I told Harry about this and he said I might as well be talking gibberish - so this time I will start in a different place.
When the brain is forming in the embryo, the cells that are going to become neurons migrate from a central place where they have multiplied and accumulated to the outside layer of the cerebrium, to form the neocortex. They do this by climbing up a scaffolding formed by cells of another type, glia cells. The scaffolding already contains axons from the parts of the brain that have grown earlier. Each radiating line of glia scaffolding will form one column module of the neocortex, a group of neurons that cooperate to process a particular type of information. For example, one module might end up registering whether there is a movement to the left in a little spot of the visual field or whether a given spot is red. When these modules are being assembled, waves of neurons migrate up the glias and past the previous wave to settle on the outside. Then another wave pasts them. Once the cells of a module have all arrived in the cortex, they change to the different types of neurons needed in a working module. The module, as a whole, sort of remembers where it came from, what it passed on the way, where it is and what outside axons run through it. Some of its cells grow axons to specific places in the rest of the brain and then the module is ready to take on its job. Imagine billions of cells with trillions of connections organizing themselves with a number of adhesives, chemical tags, attractants etc. in an extremely complex process. A slightly weak adhesive for example would create a finally structure that was not quite right.
Well, all this, so I can say that three of the genes that cause dyslexia are involved in this migration process. One of these is only active if inherited from a father. The fourth is involved in the guidance of axon growth, a similar process to migration.  It may control an axon's crossing of the midline of the brain and therefore the connections between the left and right hemisphere. Therefore, dyslexia is a result of an architectural or wiring fault during the brain's development. There are other conditions that are now being associated with inherited faults in neuron migration: schizophrenia, autism, epilepsy, some mental retardation, attention deficit syndrome and a number of oddly specific conditions like dyslexia. Of course, the same disruption can occur from poisons and other environmental factors if they occur at just the right time, perhaps fetal alcohol syndrome.
What is implied by this fault in brain architecture?
1. These genes are very old and occur in all vertebrates (the axon growth one even occurs in invertebrates). They have been conserved although many millions of years. Therefore they have nothing to do with language, as such. There is likely to be some generalized functional fault between the errors in migration and the inability to learn written language, a way that the structural fault causes a particular functional fault. That is for next month.
2. It seems unlikely that the architectural abnormalities can ever be 'cured'. The brain would always have the same faults. So overcoming the learning problem involves finding ways to bypass the faults and learn in a different way. That is how I feel about my learning - the brick wall is still there but I have found ways around, over and under it. The plasticity of the brain may allow some structural compensations to develop.
3. The migration fault would exist in people whether they learned to write a dyslexia-unfriendly language like English, a written language with clean phonetics, or never attempted written language at all. The severity of the condition would depend on the language, the teaching, the individual's other strengths and weaknesses as well as the severity of the architectural fault in the brain.
4. For dyslexia to be at 10% or so in the population, there may be (or have been) an advantage to extremely mild cases or to the offending genes when they occur without causing the condition. (As with sickle cell anemia and resistance to malaria). Another time for this.
While I was nosing about, I had a look at the left-handedness gene too, and found at least one gene has been firmly identified as a lefty gene. There is not a consensus on whether there is any tie between left-handedness and dyslexia.

Dyslexia 2
It seems to me that there is more than one kind of dyslexia. Especially there is a difference between those dyslexics that have poor short-term memory, poor mathematics skills and are poor organizers of their lives and those dyslexics that are the opposite with good memories, mathematical skills and are good organizers. As a good memory and the ability of organize are such a help to dyslexics, it is not too surprising that those dyslexics that can hone these abilities do so. This creates even more of a difference between the two types of dyslexia.
The symptoms that I have found in the literature are:
1. Dyslexics have phonological problems. They do not naturally identify the component sounds in a syllable and the idea that this is possible does not occur to them. They have difficulty in connecting sounds with letters. This may be on top of the phonological problem or a result of it. (true of me)
2. Reading is slow and hesitant with many misread words. Writing has erratic spelling, often phonetic, and there is a tendency to reverse letters, as b for d or was for saw. (true of me)
3. Dyslexics may have difficulty with memory, organizing thoughts and sequencing actions. There may be difficulties with mathematics. (not true of me- but I have a problem when saying numbers out loud of saying the wrong number and not realizing it, I did have problems when young with learning sequences like making a knot, and I cannot hold a string of letters longer than about 4 in my mind without writing them down. On the other hand I have an extremely good memory with organized thoughts and fairly good mathematical skills.) 
4. The condition is often not apparent before a child attempts to read and write. (true of me)
5. Dyslexics may confuse directional words such as up/down, in/out and left/right. They may have a poor sense of direction. (true of me except that I have a good sense of direction - I have great difficulty with left and right and mirror images do not appear to be really different in any important way.)
6. Young dyslexics may enjoy being read to but show no interest or curiosity in the letters or printed words. (true of me)
7. Young dyslexics may have problems learned to count, days of the week, months of the year, the alphabet, times tables and other sequences.(not true of me)
8. Dyslexics may start to talk later than expected. (not true of me)
9. Young dyslexics may have problems learning nursery rhymes and rhyming words. (not true of me)
10. Dyslexic children may jumble phrases, use substitute words or be unable to remember words of common objects. (not generally true of me, although I have a little tendency in this direction which is getting worse as I age)
11. Dyslexics may appear clumsy. They may have difficulty in clapping a simple rhythm. (true of me)
12. Dyslexics can have difficulty reading long words, places, times and dates. (partly true of me - times and dates are OK but proper names for people and places just don't register when reading unless I know them well.)
13. It is common for dyslexics to have good days and bad days for reading and writing. (true of me)
14. Dyslexics are often unable to concentrate and are day-dreamers. (was true of me until I learned to concentrate at about 7 or 8 and then I was able to concentrate better than most but I still can be unaware of events that others take in.)
15. Dyslexics tend to think more in images and less in words than many others. (true of me)
16. Dylexics are often prone to motion sickness. (true of me although it has got better with age)
17. Dyslexics usually can to master reading and writing as children or as adults. They are helped by learning phonetics. (true of me)
18. Adult dyslexics have poor reaction times. (true of me)
19. In autopsy, dyslexics show at least two abnormalities. Normally the left temporal lobe (an important language area) is larger than the right temporal lobe. In dyslexics they tend to be more symmetrical. In dyslexics the magocellular layers of the lateral geniculate nucleus have fewer large neurons than in non-dyslexics. The same is true of the medial geniculate nucleus. These are the pathways that can process very short duration changes in visual and auditory signals.

20. Of the treatments/aids for dylexics, the most universally effective is training in phonetics. ( From my experience I think that young dyslexics at least and maybe older ones to cannot, by themselves, deduce the phonetic rules of a language and need to get a start at the process before they can advance. I needed some phonetic rules to identify component sounds and therefore could not use the sounds to figure out the phonetic rules.)

Dyslexia 3
What sort of disability accounts for the set of symptoms in Dyslexia 2?
There are a number of theories but two are very interesting to me. One theory (Gaab) brings together many of these symptoms with an inability to processing quickly-changing sights and sounds. Again we have to start in a different place or we will have gibberish.
The signal from the eyes goes through the optic nerve to the left and right lateral geniculate nucleus of the thalamus and from there to the visual cortex at the back of the skull. Signals move from one part of the visual cortex to another and also feedback goes to the part of the thalamus that the signal originally came from. It is like a map of the retina exists in the thalamus and several other maps of the retina exist on the surface of the visual cortex. Signals stream in both directions between the different maps. The important thing here is that there is a fast and a slow processing layer in the thalamus map. The fast is called the magnocellular pathway. The slow, with more precision but less speed, is called the parvocellular pathway. Dyslexics have a less well populated magnocellular layer and therefore are less able to perceive quickly changing visual events. The same is true of the medial geniculate nucleus which receives signals from the ears, passes them to the auditory cortex and receives feedback from the auditory cortex. It is the same type of system but in this case it is the ear's cochlea membrane that is mapped in the thalamus and several times in the cortex. And again the problem is the underdevelopment of the fast channel. As well as this anatomical evidence, the weakness of a magnocellular pathway can be shown experimentally in dyslexics in both the visual and auditory systems. Non-dyslexics easily differentiate sounds and lights that are more than about 150 milliseconds apart, dyslexics need 350 or more milliseconds. Speech sounds change over tens of milliseconds, out of the range of the slow system. As a metaphor, it is like the dyslexic has twice the 'blur' in sound and vision. This difference in the resolution of sounds is probably the source of phonological problems. It may also contribute to slow reading by not allowing the letters to be seen clearly if the eyes move too fast. It may contribute to motion sickness and to poor reaction times. Dyslexics improve with training on progressive faster and faster sound changes.
This theory rings true to me.
Another theory (Shaywitz) deals with a lack of coordination in timing between visual and auditory processing.  Much of the brain's functioning depends on the communication between areas of the brain being accurately timed, simultaneously in some cases and sequentially in others. The inferior frontal gyrus of the cerebral frontal lobe is particularly important to language - it is more than Broca's area but for simplicity I will call it that. In the left hemisphere it is larger than in the right, except in dyslexics where the two sides are near equal. As with the rest of the cerebrum, an area on one side has a lot of nerve connection with the corresponding area on the other side. In the left Broca's area phonological processing is done, both to produce and perceive speech. It also controls the timing of language processes. The right 'Brocas' does similar processing of written phonological symbols.
When trying to sound out words, dyslexics show a pattern of more communication between the two areas then do normal people. Also there is a lot more metabolic energy being consumed by the dyslexics meaning a lot more short-term memory use. After special phonetic training, the pattern appeared more normal - less simultaneous activity of the two 'Broca's' and less overloading of memory. It is believed that the improvement is in the timing of communication between the two 'Broca's'.
Dyslexics use between 4 and 5 times as much energy and brain area to sound out written words as non-dyslexics use. This seems to me to be something like the 'wall' feeling, when no matter how hard I try, nothing happens. For example, I remember when I was a teenager and a very poor but somewhat phonetic speller, there were times when I went blank, before I learned to relax and doing something completely different for a while. It was little words that got me. 'Yet', for example, I knew I knew how to spell it but I could not find any sound or letter to start to build around. The word was like a fog that could not be grasped. Sometimes when reading there would be a word, I knew it's meaning and I knew it was part of my working vocabulary but I just couldn't get a handle on what was the first sound to say. I would have to close my eyes and relax, think of the meaning of the word and then try to say it.
When I first encountered 'threshing' in early computers, where the machine stops doing anything useful but has maximum activity, I thought 'I know that tiring brick wall'. Old computers literally sounded and shook like a threshing machine in this condition. The computer had been asked to do too many things simultaneously with limited resources and it could not do any of them because of interference from the other tasks.
So I now tentatively understand:
1. I cannot process quickly changing sounds because of  - a structural fault in the brain - caused by a fault in neuron migration in my embryo - which did not produce enough of some vital chemical - because of a genetic condition.
2. Language sounds are crowded in at about 10 per second  - so my brain did not naturally identify the sounds as separate component sounds - and therefore could not connect them with corresponding letters - therefore did not get the hang of the connection between sound and letters.
3. I had to be given a hint through contact with phonetics of the existence and basic nature of the link between letters and sounds and between sounds and whole words.
4. Attempting to make the connection in the normal way resulted in a 'threshing-like state' - so I then had to develop in my own ways of mastering reading and spelling - by finding other pathways in my brain. These both improved my ability to hear the individual sounds and conversely allowed me to do without individual sounds and deal with larger sound/print units - also making the attempt to hear the differences in sounds, that phonetics pointed to, helped to find novel ways to notice the differences.
But in my whole life I have never felt that there as any problem with my verbal communication. I was a fair speaker and listener, even maybe a very good one.

Dyslexia 4
There are some bits and pieces left to discuss:
Males are more at risk
There is a funny thing about some of the conditions that are now being linked genetically with faults in neuron migration during development: Schizophrenia, Autism, Attention deficit hyperactivity disorder and Dyslexia all have higher percentages of males with the conditions then females. Also men have more striking lateralization of the brain and therefore are less able to regain speech after a stroke in the left hemisphere, while women find it easier to shift their language processing to the right hemisphere. Little boys are later developing their language skills than little girls. I could not find accurate figures for gender differences in Asperger's Syndrome because of the lack of consensus on what it is. Those that have a tight definition have small or no gender differences but those that have definitions corresponding to 'nerd's disease' have a higher male incidence. This is not surprising as it is more men who have nerdy interests (math, engineering, IT etc.). Maybe testosterone has an effect on the development of some areas of the brain that exacerbates these conditions or maybe the X chromosome has genes that offer protection.
Lefties may be more at risk
Some studies have left-handed people with more dyslexia and some studies have no effect for handedness. Of course they all differ in the group they study, their definitions and their corrections. I am assuming that there is a very small and highly specific connection. Left-handed people differ in the lateralization of their brains. Most people (about 96%) including presumably all right-handed people have their language centers in the left hemisphere. Of left-handed people about 70% similarly have their language centers in the left hemisphere. The majority of the rest of left-handed people have a mirror image with their language centers in the right hemisphere. A small number of left-handed people have various placements of language centers that split the language group between the two hemispheres. It may be that one of these sub-sets of left-handers is more prone to dyslexia.
So far there is no indication of any genetic connection between handedness and dyslexia, although the tendency to both is inherited. The severity of dyslexia may be affected by the distribution of language centers. It is hard to image that it would not be.
Those taught without phonetics are at risk
Basically there are three educational theories about the teaching of reading (but currently teachers tend to use a mixture of techniques). Over the years there has been almost outright war between the camps:
1. phonics - words recognized by decoding them letter by letter,
2. holistic word recognition - words are recognized by learning their shape,
3. whole language - words are recognized by their context.
All of the methods work with at least some children but it seems none are best for all children. Some students are bored by phonics and turn off, some never get a creative urge to write without the whole language approach, and dyslexics need the phonetics to get started. After reading is mastered apparently all the ways of recognizing words are used in reading and their contribution to reading speed is additive, not redundant (66% from the phonics, 16% from the shape of words, 22% from meaning in context).
I was taught with absolutely no phonics during my first two years at school (at the height of the whole word fad) and very little phonics at any time later in school. I learned the bits that I did learn in elementary school from one teacher and my family at home. My first encounter with phonetics (with my family) near the end of my second year in school was a frightening revelation that started me learning to read. But now that I do read, I think my percentages, if I had to guess, would be 10% phonics, 40% shape and 50% context.
It does make me angry to think of any children being deprived of any teaching method because of dogmatic educational theories. Dyslexia is not the only learning problem. Educational fads are also found in mathematics, music etc. probably hurt of some of the students.
English speakers are at risk
Some people have the idea that dyslexia only occurs in languages that are not phonetically spelt. It seems this is not true but the severity of the condition is worst in a language such as English which is not very phonetic.
English has 1120 ways of writing its 40 sounds (both a sound can have more then one representation and also a group of letters can represent more than one sound). Italian has 33 ways of writing its 25 sounds (no group of letters can stand for more than one sound). The neurological nature of dyslexia is the same in the two languages but there is twice the incidence of dyslexia in the USA as in Italy. This seems to be because the severity is worse in English and therefore it is more likely to be detected and the person labeled as dyslexic.
I assume that hieroglyphic languages would not show up dyslexia and that languages using a syllabic representation would have even less severe effect in dyslexic individuals then would a perfect phonetic language.
Why no effect on the oral language
To most people the written language seems just a simple extension of the spoken one. So to them dyslexia is a little baffling. For example, if you know the meaning of a word and you know that you use it in speech and it is there written in front of you, why can't you read it aloud. But actually there is not that much processing in common between oral and written language. Only the act of pronouncing a written word or of spelling a heard word really uses both systems.
I have often thought that there must be some advantages to left-handedness or it would have a much lower prevalence. And the thought crossed my mind about dyslexia but the more obvious reason that dyslexia has a high prevalence is that it is a very new disadvantage. There has not been time to eliminate it from the population.
Human language has evolved slowly over a couple of million years and has probably had very close to its current form for 100 thousand years or so. This is plenty of time to integrate verbal language into the structure of the brain and stabilize its genetics. On the other hand, written language is about 5 thousand years old and for the first part of that time it was not phonetic at all but rather 'pictures' of ideas. It is only in the last few centuries that there has been anything like general literacy. Taking the world as a whole, literacy is still fairly patchy. There has been practically no time for an evolutionary process to integrate written language skills into the language facilities of the brain. For example, it takes about 50,000 years for populations that move from tropics to high latitude or vice versa to achieve the right amount of pigment in their skins. Written language may be 'sort of stuck on willy nilly' to oral language and therefore prone to genetic problems.
Verbal language doesn't have to be taught; children are able to learn language if they are with people who speak, without any instruction. Normal children have mastered all the basic elements of their mother tongue by age three. We have to wait until children are older and then spent a few years of formal instruction to give children written language skills. It seems that the skill is not easy for any children, but many seemingly normal children have very great difficulty learning to read and write. 

Dyslexia 5
Some more bits and pieces:
Early diagnosis
It may soon be possible to diagnosis the inability to discriminate very quick sound changes (the assumed cause of most dyslexia) in young children, long before school age. So in the future we can probably see training to overcome the dyslexia problem started well before it is needed for language learning.
Brain abnormalities
Recent research (Walsh) shows disorganized and meandering nerve fibers affect reading skills.
Periventricular nodular heterotopia is a genetic disease which has nodules of gray matter deep in the brain in the white matter areas. Usually gray matter is confined to the surface of the brain and white matter to the interior. They have reading problems. "In PNH patients, unlike in normal readers, white matter fibers took circuitous routes around the misplaced gray matter, and in some cases, didn't organize into uniform bundles, which could leave regions of gray matter poorly connected. Importantly, the more disorganized the PNH patients' white matter, the less fluent their reading."
Other scientists have found white matter disorganization in ordinary dyslexics. The researchers (Chang) have put forward a theory that reading depends on white matter organization. "When we read, we need to take in information visually, hook it up with our inner dictionary of what letters and words mean, and when we're reading aloud, connect that with the region that gives us our ability to speak. For smooth, automatic reading, the white matter is there to connect different regions of gray matter and allow them to function seamlessly. When reading fluency is the primary problem, it may be that the areas of the brain that are important for reading are not connected efficiently,"
There is another type
It seems that another pattern of dyslexia exists. There are children who can read and do not have difficulty recognizing individual sounds within words but are nevertheless poor spellers. They are usually strongly right-handed and they appear to have special problems with homophonic words ("to here but not sea"). There are indications that the problem is visual and perhaps involves inter-hemisphere communication.
A little test
At the site
here there is a test of how fast you can read letters. I took the test and it does seem that I am not very quick at it. Harry did the test and was at the other end of the scale. There was one set of characters that I could not see clearly at the top end (300msec). Harry did not see the effect of disappearing letters even at the bottom end (20msec). I guess I really do not have the fast perception mode.

Weight 1
I find that my weight is higher than my bathroom scales will go! My attempts to lose weight are not working - panic stations. For the whole of my life - barring exceptional situations - my weight has slowly crept up. It has dropped when I have been very ill on a couple of occasions. I had anorexia for a short period when I was a teenager and lost a lot of weight because I ate nothing but sunflower seeds most days. One day Mom said I looked like I had some incurable tropical disease and I was not going to live by myself anymore; I was going to live at my aunt's. It was caught early and I started eating proper meals. Twice I have done the Atkins diet and lost lots of weight and another time I lost some but then stopped because it was inconvenient to continue. All the rest of the time, I have gained slowly, except when I took a jump in weight after I quit smoking. I eat more, I eat less, I have more exercise, I have less, but I gain weight at a slow even pace. Only very extreme circumstances reverse or accelerate the pace.
When people say that I real should do something about my weight, I am not offended. They are just showing their concern for me. But when people, especially friends, say that there is no problem losing weight, just eat a little less, I become hurt and angry. Eating a little less has not worked for me in 68 years. I am too arthritic to want to exercise more. I had read that the Atkins diet was not healthy and it was the only one that had ever worked. It seemed that I was in a hole. My weight made exercise painful but I was not getting the exercise needed to lose weight without extreme dieting and the diet that worked was unhealthy. Because I react to gluten, I had already cut out all things made with flour from my diet. I eat very little sugar as a rule. There was getting to be very little to avoid. Great! Then I read an article about how fat people deserved to be hated and discriminated against because they were unwell and ugly and it was all their fault. "How does anybody increase their body mass to 16 stone (220 lbs) 'by accident'? These kinds of weight entail industrious and committed eating. It's eating as a career. It involves the consumption, python-like, of about six whole rotisserie chickens a day washed down with 16 pints of double cream, half a cow and probably the entire produce of Ireland's potato farms, deep-fried and with a coating of beer batter." I'm used to that kind of sympathy!
I have 'hit the books' so to speak. I know a bit of biology and so I thought I should be able to find what is happening and a way out, if there is one. After looking at close to a hundred science reports I think I understand what is happening and I am going back on the Atkins diet along with a few other things.
I am writing a little series on this in my web page - this is the first part. I may not have all the relevant science but I am sure I have enough to understand the general picture accurately even if some details are missing or wrong.
Metabolic Syndrome
What I think I have is called metabolic syndrome. Being overweight is just a symptom of something much more dangerous; the condition leads to diabetes, cardiac problems and other serious problems. I want to avoid this progression.
Metabolic syndrome is also called Syndrome X or Insulin resistance. It is a grouping of abnormal fat metabolism, insulin resistance, high blood pressure and tissue inflammation. Various medical bodies have differing definitions but they are all very similar. There is a list of symptoms of which the patient must have at least a certain number to meet the definition. Then there are other lists of conditions that are somewhat confirming.  The bodies also have similar lists of conditions that have a higher risk for people with metabolic syndrome.
Symptom list:
Abdominal obesity; a high waist circumference (I have this)
High serum triglycerides (? 15 or so years ago this was OK)
Low serum HDL cholesterol ( ?15 or so years ago this was OK)
High blood pressure (I have this)
High fasting blood glucose and/or high post meal blood glucose/high blood insulin (? 10 years ago fasting glucose was OK but non-fasting glucose has always been a little higher than normal - it has not been measured for a very long time)
Confirming conditions:
General obesity (I have this)
Fatty liver (?)
Albumin in the urine (?)
Sleep apnea (mild if at all)
Polycystic ovary syndrome (no)
Cognitive decline in elderly (not since taking high blood pressure medicine but worrying before that)
Prothrombotic state/ abnormalities in blood flow and coagulation (?)
Proinflammatory state/ markers of inflammation (arthritis seems to be inflammation)
Old age more at risk (yes)
Hispanic or Asian more at risk  (no)
Family history of type 2 diabetes, cardiovascular disease or hypertension more at risk (brother had all)
Sedentary lifestyle more at risk  (yes)
Cardiovascular disease (?)
High LDL cholesterol (?)
Cholesterol gallstones (yes)
Acanthosis nigricans (no)
Gestational diabetes (no)
Increased risk of developing:
Type 2 Diabetes
Heart disease
Liver disease
Kidney failure
There is a surprising logic to why these seemingly different types of symptoms and associations are grouped together. That is the subject of Part 2.

Weight 2
Insulin Resistance, Obesity and Inflammation - the vicious circle
The most important aspect of Metabolic Syndrome is Insulin Resistance. Insulin is a hormone secreted by the pancreas that stimulates muscle and liver cells to absorb glucose from the blood and store in as glycogen or use it for energy. After a meal the level of insulin raises in the blood until the extra glucose in the blood has been lower by the muscle and liver. When the muscle and later the liver cells stop responding to insulin several things happen:

-  the levels of insulin in the blood become abnormally high because the glucose level remains high for longer. High insulin can cause harm.
the levels of glucose in the blood remain high for longer. High glucose can cause harm.
- liver cells respond to the high glucose by converting glucose to fats so that levels of blood fat rise. High blood fats, especially LDL, can cause harm.
fat is removed from the blood and stored in fat cells, muscles and in organs such as the liver. Increased fat storage, especially in the organs, can cause harm.
the abnormal glucose and fat metabolism can produce periods of very low energy and of hunger as a result. Lack of exercise and over eating can result.
So insulin resistance increases weight gain and leads to obesity. But it is not that simple because being overweight is one of the things that increases the resistance to insulin. We can look at it one way and see that insulin resistance is the cause of obesity and we can look at it the other way and see that obesity is the cause of insulin resistance:

obesity causes inflammation. Inflammation can cause general harm.
cytokines are released by inflammatory macrophages. These are what cause insulin resistance in muscle. They also affect liver cells and fat cells in a similar way.
Fat stored in the liver is especially dangerous and causes more disruption of liver functions leading to increased resistance to insulin.
The only way out of this terrible spiral is to eat a low carbohydrate diet and to exercise. A low carbohydrate diet means that there is much less glucose in the blood after a meal. (Starches and sugars are converted into simple sugars, mostly glucose, in order to be absorbed into the body). Less glucose stimulates less insulin production. Less glucose means less is converted to circulating fat (triglyceride, saturated fatty acids, cholesterol, LDL). A 'high carb' diet results in more fat in the blood after a meal than a 'high fat' diet. 'Very low fat' diets (but not just 'low fat' diets) cause an increase in blood fats. This is counter intuitive; you would think you would cut fats in order to have less fat in the blood but, no, it is important to cut carbohydrates rather than fat. Less circulating fat means there is less fat for fat cells to store away.
Exercise has the result that the fat that is circulating in the blood is taken up by muscle cells and oxidized for energy. The muscles end up taking in more fat than they need and store the excess as IMTG (intramuscular triglyceride). Again this lowers the fat available for fat cells to store away and also makes the muscle cells slightly less resistant to insulin. It is not a question of getting fit, it is just exercise that is needed. Even Tai Chi, which is hardly strenuous, is of some benefit. If the exercise is shortly after the meal it is more beneficial.
It is not hard to see how metabolic syndrome gets worse and involves more organs (heart, liver etc.). And it is not hard to see how it is hard to reverse metabolic syndrome. But how does it start in the first place. This seems to be a genetic thing. There are a lot of genes controlling various aspects of metabolism that can give someone a tendency to fall into the spiral. One theory has it that fat accumulation is favoured by genes selected for adapting to a cold climate in the stone age - very little heating and a sometimes lack of food. Fat can be oxidized in a way that is not connected with muscle contractions but simply creates heat. Those genes for cold adaptation do not work well in good warm housing and clothing, abundant rich food and less need for strenuous work.
A particular study shows just how much of a genetically thin person someone can be. "Sims put thin people on a forced-eating diet. Sims wanted to know whether people 'would have a hard time gaining weight. In his first experiment with college students, Sims found that these subjects found it all but impossible to gain much weight; no matter how much they tried to eat, they just could not become obese. Sims reasoned that perhaps the students raised their activity levels and were burning off more calories. He thought of the perfect subjects, people who really have no chance to cheat and burn off calories: prisoners. The study volunteers in prison did indeed gain weight. But producing obesity turned out to be much harder than Sims had anticipated. The men increased their weight by 20 to 25 percent, but it took four to six months for them to do this, eating as much as they could every day. Some ended up eating 10,000 calorie a day, an amount so incredible that it would be hard to believe, were it not for the fact that the researcher study had attendants present at each meal who dutifully recorded everything the men ate. In this and other similar experiments, Sims showed that men gained weight at different rates, that metabolism rates change, and together these play a central role in the biological differences between naturally fat versus thin people. The implications were clear. There is a reason that fat people can't stay thin after they diet and that thin people can't stay fat when they force themselves to gain weight. The body's metabolism speeds up or slows down to keep weight within a narrow range."
It is also the case that people are genetically more or less prone to inflammation and therefore more or less likely to fall into metabolic syndrome. Inflammation is part of the immune response, protecting the body from pathogens. But it can attack the body's own cells causing various autoimmune conditions. The longer the metabolic syndrome lasts, the more likely there will be a progression to diabetes, heart disease, liver disease or kidney disease.
There are a few pieces of advice about diet that are helpful:

low carbohydrate reduces triglyceride, saturated fatty acids, cholesterol, cytokines, chemokines, adhesion molecules, glucose and insulin in the blood. This response to carbohydrate is almost a definition of metabolic syndrome.
the carbohydrates that are most dangerous are those with a high glycemic index (meaning they are digested and absorbed faster than other carbohydrates giving more of a glucose peak in the blood). Examples of high glycemic index foods are unrefined sugars, white breads, unrefined corn products, potatoes. Low glycemic carbohydrates are found in whole grain breads, brown rice and non-starchy vegetables.
artifically made  'trans fats' are bad for us. Some naturally occurring trans fats are good for us. Trans vaccinic acid is found in dairy and meat products. It reduces total cholesterol and LDL. It also reduces the production of chylomicrons.  (particles of fat that form in the small intestine following a meal, travel through the lymph and get dumped into the blood stream at the thoracic duct). This is the raw dietary fat before it has been processed by liver, fat cells or muscle. Presumably less chylomicrons means less fat actually absorbed from the gut.
red wine contains resveratrol which activates SIRT1 enzyme and therefore is likely to increase insulin sensitivity. Low doses have an effect and so moderate consumption is beneficial.
dark chocolate especially only lightly sweetened and containing plant sterols as well as flavanols lowers cholesterol, LDL and blood pressure. This has not been shown for sweet milk chocolate.
carbonated drinks, both diet and containing sugar, are not good for metabolic syndrome or for weight loss. Fruit juice and milk are good.
oil from fish (polyunsaturated) is better than from olive and nut (monounsaturated) and they are both better than saturated fat.

Weight 3
Here are a few of the more interesting bit and bobs from the literature.
Fat tissue produces hormones
We tend to think of fat as inactive. But fat (adopose tissue) is now recognized as an endocrine gland at the heart of a complex network influencing energy regulation, glucose and lipid metabolism, blood pressure, immune response and reproduction. Virtually all known adipose secreted proteins are dysregulated when the fat mass is markedly altered, either increased in the obese state or decreased in lipoatrophy.

Leptin is a hormone produced by fat tissue that regulates appetite and metabolism. The gene of the leptin receptor is one that shows clear differences in cold adapted populations. The 'cold' version of the receptor gene is associated with increased respiratory quotient (using oxygen and releasing carbon dioxide) which would allow more heat production. This version is also linked to lower body mass index, less abdominal fat and lower blood pressure and so is protective against metabolic syndrome. Mice that have been bred to lack the leptin hormone are extremely obese. Lower body fat produces lower leptin levels. When working properly this system should be able to sense the bodies amount of fat and adjust its intake, use and storage appropriately. There are a number of receptors as leptin affects a number of different organs including the brain. Cells can become resistant to leptin; especially in obese people there are high levels of leptin but it is not effective.
Adiponectin hormone is produced only by fat cells but opposite to what would be expected, the level circulating in the blood is inversely correlated with body fat and therefore reduced in obesity. It lowers glucose production and stimulates cells to use fats. It suppresses the conditions leading to type2 diabetes, obesity, fatty liver and antherosclerosis. It reduces protein loss into urine, reduces oxidative stress and inflammation.
Resistin is produced by fat cells but also by other tissues. There is a scientific disagreement about whether resistin is the link between obesity and insulin resistance. It is clear that there is a connection. Levels in the blood rise with waistline fat accumulation and it promotes inflammation. Insulin inhibits the production of resistin. 
- Several Cytokines are produced by fat cells. Cytokines are messenger molecules between cells. One of many cytokines from fat cells is interleukin-6, an inflammatory IL. A deficit of IL-6 increases insulin resistance, leptin resistance and obesity. IL-6 production is stimulated by exercise.
Adipsin is acts like a thermostat for fat production. Reduction in adipsin can result in obesity.
ASP (acylation-stimulating protein) increases the production of insulin when blood glucose is high but does not have any effect on insulin resistance.
Angiotensinogen is produced by the liver and fat cells. Normally it is modified by renin in the kidneys to produce angiotensin-1 and then by ACE in the lungs to produce angiotensin-2. Angiotensin-2 produces constriction of blood vessels and high blood pressure but it also has effects on blood clotting, the adrenal gland, the brain and the kidneys.
PAI-1 plasminogen activator inhibitor is produced by the lining of blood vessels and by fat tissue. It inhibits the breakdown of blood clots such as those in thrombosis.
Some steroid hormones
Circadian rhythms
There are articles in the literature that link disruptions of circadian rhythms with metabolic syndrome. Aging, jet lag, steep disorders, and shift work may all have effects on weight gain.  Seasonal changes also seem to be implicated.
The two big effects of appetite are leptin and ghrelin.
Leptin binds to the 'appetite centre' in the hypothalamus and suppresses appetite. As leptin is produced by fat tissue this should be a good feedback system. However, leptin resistance can develop (like insulin resistance). Ghrelin is produced by an empty stomach and stimulates appetite. Ghrelin production is also increased by lack of sleep and leptin production is decreased during sleep. There are a number of less well studied appetite influences.
Appetite is a real problem for many obese people. Food intake is not voluntary in the long term. You can hold your breath voluntarily for a short period of time and then you gasp for air. You can not take in liquid voluntarily for a medium period of time and then you must drink. You can not take in food voluntarily but not for ever. Hunger is one of the most powerful biological signals from an ancient brain area. It cannot be fought with just will power in some people.

Alzheimer's 1

Grandmother Wight had Alzheimer's disease. That is one of the reasons that my memories of her differed from my Mother's and those of others, older than me. I only just manage to remember her before the Alzheimer's. When I was 16-17 she had all the signs of the disease and was with Aunt Marjorie and Uncle Walter. I remember her most clearly from that time as I lived in the house. When I was 12-13, I lived with Grandma and Grandpa in Yellowgrass. As far as I know, no one thought she was ill then, just getting old. But in hindsight, the disease had already started. She puttered around in a distracted sort of way, accomplished very little and said very little. This was not the woman who was a marvel of efficiency and know-how. She was not how my mother, aunts and older cousins remember her. I lived with my grandparents when I was 7-8 and she was active then. It took about 10 years for her to go from her normal self to being hospitalized with dementia and more years to die.
The time in Regina with Marjorie and Walter was disturbing. Grandma called me May and thought I was my mother. She walked through the house and picked up little things (pens, keys, books and the like). She carefully wrapped each item she found in kleenex and put it somewhere (a drawer, behind a picture, under a pillow etc.). We were forever looking for things she had 'put away'. The most heartbreaking thing was that she would sit with a little pillow and rock it. She though she was looked after her dead daughter Marion. She rocked Marion at night for a number of years before Marion finally died and she was reliving that time of her life. Uncle Calvin's wife at the time bought a very realistic and life-sized doll for her. Grandma rocked it. The problem was that every once in a while she seemed to realize that she was looked after a doll and not a baby. This would throw her into a terrible rage and she would hurl and doll across the room and then shout about her disgrace for a while. This didn't happen with the little pillow - I suppose because she was not forced to think she had been playing with it. I tried to hide the doll when this happened but soon she would be looking for Marion and worry about where she was. I would have to give her the doll.
(a sidelight: Oh how I hated that doll. When Grandma died many things were returned to the people who had given them and so the doll was given back to Olla and she immediately gave it to me 'to remember Grandma by'. All my dealings with Olla to that point had been very unsatisfactory and so I simply thanked her, waited until she was gone and put the doll in the garbage. I have never regretted throwing the doll away and I still avoid contact with dolls that look as realistic as that one.)
Many years later, my Mother started to be forgetful. She died of cancer before her cognitive impairment got very bad. But it did have the hallmarks of Alzheimer's rather than just old age. She was not aware of the extent of her memory loss and told me several times that her husband, Melvin, was telling lies about her. It hurt her deeply. He was not, of course, but I could not convince her of it. She did not realize she forgot and that she was doing the things Melvin said she was doing. She was beginning to lose some of her intellectual ability too. We played games: scrabble, the 5 letter game, tile rummy. Her ability to play these games took a sharp fall but again she did not realize the extent. She became interested in fewer things and was showing depression. Melvin had to start doing the cooking and laundry because she made mistakes with the stove and washing machine. She did not wander but that was because she had limited mobility. I have no doubt that my Mother had the first stages of Alzheimer's.
So when my memory failed me a bit, I decided to look into Alzheimer research. My memory improved when my blood pressure was treated, but it was still a little scare.
Alzheimer's Description
Alzheimer's is a dementia usually found in older people. It starts with memory loss, difficulty in forming new memories and poor learning. Later people suffer confusion, anger, loss of older memories and skills, and difficulty with language. Finally people loss bodily functions and die. The whole course of the disease takes many years. It is difficult to diagnose in its early stages and can only be definitively seen in an autopsy. Current treatments are usually fairly ineffective. There is no cure.
The burden on care-givers and relatives/friends of patents is terrible and the cost of care is very high. Alzheimer's is an important disease for medicine to tackle, both because of its effect on individual sufferers, their relatives and friends, and the health care system finances. So there is a great deal of current research aimed at understanding the disease and finding preventions, treatments and cures.
Physically the disease shows accumulations (plaques) of beta-amyloid, fibrillary tangles within neurons, death of neurons and shrinkage of grey matter. These can be seen in autopsy. There are two types of Alzheimer's: a rarer, early onset type that runs in families; and a commoner type that occurs in old age is a not as clearly inherited. There are similarities between Alzheimer's and other forms of dementia: Parkinson's, vascular dementia, Creutzfeldt-Jakob disease (human mad cow disease) and other rarer dementias. 
There have been a number of theories about the causes and development of Alzheimer's. The favourites today vary in many details but have the following general picture in common.
1. A small bit of protein (a peptide) is produced badly (genetically wrong, in too high an amount, cut wrong, or folded wrong). During this faulty process a toxin (maybe the peptide) affects neurons.
In more detail - A large protein, amyloid precursor protein, sticks through the cell membranes of neurons. It seems to be an important molecule but its function is not known. The part of this molecule that sticks outside the cell membrane is cut off by the beta secretase enzyme leaving the rest still sitting through the membrane. Gamma secretase splits the remaining molecule from within the membrane to produce a beta-amyloid peptide free outside the cell. Again the reason for this processing is not known. Beta-amyloid is soluble and can be from 39 to 43 amino acids long. The type that is 42 units long can undergo a refolding and can form small aggregates, then insoluble fibrils and finally the fibrils can aggregate into plaques. Some parts of this process (such as a component of secretases has been conserved unchanged through both animal and plant evolution) are extremely important but of unknown function. Amyloid plaques are found in other diseases such as Creutzfeldt-Jakob and in normal senile brains, so the plaques themselves do not dictate the nature of Alzheimer's but they are a defining part of the condition. A form of beta-amyloid (not the newly produced or the final plaques but some form between - a soluble adhesion of very few molecules, perhaps three) is definitely the trigger for the start of memory loss. It has been shown that beta-amyloid blocks the function of a key signaling receptor, the nicotinic acetylcholine receptor in the hippocampus, the seat of memory, motivation and emotion in the brain.
2. The faulty peptide molecules stick together to form fibers and then plaques. The plaques appear to start an inflammation.
In more detail - Surrounding neurons in the brain are other cells that outnumber them about 10 to 1, the glia cells. These are important in guiding the development of neurons, supporting and feeding them, insulating their electrical fields, repairing them and also acting as the brain's immune system. There is a barrier between the brain's fluids and the blood (the blood-brain barrier) and so the normal immune system does not operate in the brain. Microglia and astrocytes are attracted to plaques. They do not destroy the plaques but appear to be part of an inflammation response and attempts to protect and repair the neurons.
3. The toxin, inflammation or some other process disrupts the transport mechanism within neuron axons leaving 'tangles'.
In more detail - Cell have a sort of skeleton made of microtubules. In the long axons of nerve cells the microtubules transport chemicals between the cell body and the synapses at the very end of the axons. The protein tau is associated with microtubules and acts like railway ties between pairs of microtubules. Tau is regulated by having phosphate added or subtracted from its structure. In Alzheimer's (and Creutzfeldt-Jakob, Parkinson's and other dementias) tau is hyperphosphorylated and the microtubule structure collapses. Neurofibrillary tangles form within the neurons. Without a cytoskeleton, neurons cannot function as nerve signal processors.
4. Affected neurons die. Neurons in the hippocampus are the first to be affected.
In more detail - Cells can either die in a pre-programmed tidy type of suicide, apoptosis; or they can be murdered in a very messy manner, necrosis. In this case neurons die by apoptosis. Some event (damage they sustain or some signal they receive) causes them to wind-up all their cellular processes and shrivel up. Neuron death in a series of regions starting with the hippocampus would account for the series of symptoms that follow simply memory loss and mild cognitive impairment: loss of intelligence, personality and bodily control. Other dementias have different patterns of neuron death.
Also - Some genes, iron, lead, infections, free radicals etc. may be involved but they are not part of the agreed picture yet. Calcium signaling is definitely implicated as an important part of the story but it is not clear how. Cholesterol signaling has been implicated.
Without an understanding of how memories are formed, conserved and removed, it is difficult to understand a disease of memory.

Alzheimer's 2
Existing medicines not very effective

1. The oldest hypothesis is the "cholinergic hypothesis" that Alzheimer's begins as a deficiency in the production of the neurotransmitter acetylcholine. Early medicines were acetylcholinesterase inhibitors (galantamine, donepezil, rivastigmine) and this was a little helpful with symptoms but did not halt, reverse or cure the disease. The hypothesis is no longer being pursued.
2. Excessive glutamate, another neurotransmitter, can overstimulate the brain and lead to cell death. A receptor antagonist, memantine, is sometimes used to stop this problem and can help somewhat in the later stages of Alzheimer's.
3. Anti-psychotics are used to manage behavior but not for the disease.
4. The drugs often given for incontinence can make Alzheimer's symptoms worst.
Possible treatments on the way
A hundred or so possible medicines are being investigated. With so much activity and so many leads, there may soon be effective medicines. It is not clear yet which theories are going to be fruitful.
1. The enzyme gamma-secretase that makes the fateful cut cannot be inhibiting because it is involved in cutting other important proteins. Ways are being looked for to interfere with the production of beta-amyloid without touching gamma-secretase.
a) Inhibiting beta-secretase and therefore blocking the cutting of APP might work. A drug to do this is in trials.
b) Gamma-secretase modulators (GSM) reduce the amount of long sticky beta-amyloid and increase the amount of short non-sticky instead. They work in three ways at the same time: inhibit production of long beta-amyloid, block aggregation of beta-amyloid, and increase production of shorter beta-amyloid which also inhibits aggregation. GSM does not act on the enzyme but on the protein itself to give it a different structure and thereby change the point of the enzyme's cut. One GSM being tested is tarenflurbil or r-flurbiprofen.
c) There are groups looking for a way to affect the production of BACE1 or A-secretase in the belief that it is the faulty cutting by this enzyme (found to be increased in Alzheimer's) that is the key to reducing the faulty beta-amyloid rather than gamma-secretase.
2. It appears that the plaques of beta-amyloid are not important to the disease but that beta-amyloid in smaller aggregates is. So drugs are sought to prevent aggregates and even clear them.
a) A small molecule called DAPH attaches itself to amyloid fibers and stops their growth.
b) Transthyretin (TTR) protein is naturally produced by diminishes as people get older. TTR transports vitamin A and thyroid hormone and can bind to beta-amyloid to stop toxicity and plaque formation. The search is for way to increase TTR production in aging.
c) The omega-3 fatty acid, docosahexaenoic acid (DHA), from fish oil increases the production of a protein LR11, which is low in Alzheimer's. LR11 prevents plaque formation. It is effective in animals and human tissue culture. Humans do not make DHA although it is the most abundant essential fatty acid in brain tissue. All DHA comes from diet.
d) Vaccines or stimulation of immune system to recognize and attack beta-amyloid or plaques has been tried. Trials on the first vaccine were stopped as it made the patients more ill through inflammation in the brain. Another vaccine has been shown to reduce plaques but it did not improve symptoms, showing that the plaques are not themselves dangerous but an earlier from of beta-amyloid. A third vaccine has also failed. Some vaccine ideas have not yet been tested. A vaccine based on the potato virus might work because it is not human tissue but resembles beta amyloid. Another packages some beta amyloid that would trigger the immune response with interleukin-4 to stop inflammation.
e) PBT2 (derived from clioquinol) counteracts the production and build-up of beta amyloid. It seems to interrupt the interaction between metal ions and beta amyloid and return levels of zinc and copper in the brain to normal levels. Early trails are promising.
3. An extract of grape seed is being tested for controlling beta-amyloid production. The major compounds in the extract are catechin and epicatechin found in wine, tea, chocolate, and some fruits and vegetables.
4. It has been found that a molecule p75 neurotrophin receptor is necessary for beta-amyloid to cause nerve cell death. Blockers of p75 are being tested in animals.
5. The tau tangles may be the source of many symptoms in Alzheimer's although it is not a primary cause. Tau effecting drugs are being pursued to provide good treatment rather than cure.
a) Agents that can inhibit or reverse the tau tangles include an extract of cinnamon.
b) Thiazoline is an enzyme inhibitor that effectively tricks the brains own enzymes into installing a sugar on to tau in place of phosphates.
c) AL-108 is under test. A protein ADNP is made by glia cells to protect neurons under threat. It is too large to pass the blood-brain barrier but a small part of it (NAP) appears to be protective. It appears to stop the death of cells due to the destruction of microtubule transport by tau dysfunction.
d) Pin1 (prolyl isomerare) promotes the removal of phosphates from tau and detangles the protein. It also inhibits the production of toxic beta-amyloid. Pin1 activity is inhibited in Alzheimer's by stress and other conditions. Pin1 has the opposite effect in frontotemporal dementia whose primary cause is a tau mutation.
e) The drug Rember gave an 80% difference in the rate of mental decline in trails. It is methylthioninium chloride or methyline blue which has been used in various ways in medicine since the 19th century. It was tested because in dissolves tau tangle filaments in a test tube. In the brain it blocks the toxic effects of aggregated tau. It has completed phase II trial. It slows or even stops cognitive decline, increases blood flow and halts the spread of tangles.
6. Reducing inflammation might help slow Alzheimer's.
a) A number of non-steroidal anti-inflammatory drugs (NSAIDs) are being tested. Ibuprofen has shown promise. Some but not all studies have shown naproxen and aspirin to be equally effective.
b) The drug etanercept used to treat inflammation and arthritis has been tested on Alzheimer's with good preliminary results. Etanercept administered by a unique perispinal method reduces elevated TNF-alpha. TNF-alpha is an important part of the brain's immune system. There have been was tests with good results by without the controls needed in proper trails.
c) A new anti-inflammatory drug called CN1-1493 is in testing. It may be more effective than ibuprofen against Alzheimer's.
d) Dimebon was a Russia allergy medication that is no longer in use. It appears to help Alzheimer's patients with memory, thinking and behaviour. It will enter trails soon.
7. Enkephalins are part of the endogenous opiod system which modulates learning and memory. They are produced by cells in the brain areas affected by Alzheimer's and are released with neurotransmitters like glutamate at synapses. The precursor of enkephalins is increased in early stages of Alzheimer's. It is not known if it is a cause or compensation, but compounds that blocked opoid receptors reduced cognitive damage. Ways to limit enkephalin production and signaling are being looked for.
8. Oxidative stress from free radical is thought by many to be involved in the damage.
a) There were clinical trials of Vitamin E to see if antioxidants and free radical scavengers were beneficial but the results were disappointing. The hypothesis was that free radicals were causing blood vessel damage. Other drugs limiting vascular damage are being looked at. Vitamin E does seem to prolong life in Alzheimer's patients without improving the symptoms.
b) Mitochondria, the energy producing organelles in cells, become less efficient with age. This leads to less ATP energy produced, less oxygen used, more free radicals released. This accounts for an energy deficit in the Alzheimer brain. It was thought that estrogen protects against Alzheimer's by protecting mitochondria, but recent studies show that estrogen is not effective against Alzheimer's. Other drugs that protect mitochondria are being sought.
c) Oxidative stress from the accumulation of iron in the brain may be a trigger for Alzheimer's. CSF can contain reactive and non-reactive iron. Reactive iron rises from normal with mild impairment and then falls abruptly with the start of Alzheimer's; total iron stays level. Iron may be sequestered in amyloid plaques. This is being studied in hope of understanding the role of iron so that it could be treated.
9. It seems that cholesterol is somehow involved in Alzheimer's.
a) The cholesterol lowering drug, lovastatin can also reduce nerve cell death in Alzheimer's. The statin stimulates nerve cells to produce a receptor molecule for tumor necrosis factor-alpha. TNF-alpha has a strong beneficial effect on nerve cells.
b) A link between cholesterol lowering statins and dementia is not settled. Some studies show improvement with statin medication and some the opposite. Glial progenitor cells (stem cells of the brain) can become the various types of glia cells. The progenitor cells use the cholesterol-signaling pathway in development. Some statins spur progenitor cells to become oligodendrocytes rather than astrocytes. This would give fewer progenitor cells and an imbalance in the glia cells produced. This may be true of some diabetic medications too.
c) Apolipoprotein E (ApoE) is a cholesterol transport protein and also a regulator of brain beta-amyloid levels. It is likely that regulation of ApoE activity with influence beta-amyloid deposition and clearance. The genetic form of ApoE affects its ability and so does the number of lipid molecules it carries. Activation of liver receptors (LXRs) enhances the ability of ApoE to degrade beta-amyloid.
d) High cholesterol can damage the blood-brain barrier and caffeine can provide protection from this damage (equivalent of one cup coffee a day). The barrier is weakened in Alzheimer's which may be why high cholesterol is a risk factor.
10. Endocytosis is one way in which a cell takes in chemicals. The cell membrane is sucked in to make a bubble enclosing some of the liquid that was outside the cell. It is pinched off and becomes part of the inside of the cell. Shutting down endocytosis in Alzheimer mice dropped the levels of beta-amyloid dramatically. Most of the endocytosis that was stopped was that involved in normal nerve cell communication at the synapses. The endocytosis is essential to nerve function. So the search is for drugs that can stop the membrane binding the precursor to beta-amyloid production, APP, so that it is not taken in during endocytosis.
11. Culling of memories goes on in the brain and some researchers believe this is hyper-activated in Alzheimer's. There is a biochemical 'switch' associated with the cleavage of amyloid precursor protein by capases. In Alzheimer's the 'switch' gets stuck in the breaking memories mode. It is not the beta-amyloid that is at fault by the process it is intended to regulate. The researchers are looking for a way to affect the down stream processes.
12. There is some indication that ginkgo biloba extract may be protective.
13.  A cocktail of nutrients that increase dendritic spines and synapses is in the trial. The idea is to help neurons recover function when damaged. The cocktail contains the following. Omega-3 fatty acids are not produced in the body but are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Choline can be synthesized in the body and obtained through the diet; it is found in meats, nuts and eggs. Uridine cannot be obtained from food sources, but is a component of human breast milk and can be produced in the body.
14. There is a lot of work concentrating on calcium regulation. Recent indications that dysfunction of a calcium channel for calcium to enter neurons is the earliest event in the development of Alzheimer's. Researchers will be looking for way to compensate for this calcium signaling fault. Calcium is important to brain growth, learning and memory. It is involved in cell death too. One drug lead is to inhibit an enzyme called calcineurin to control calcium overload which can damage cells.
15. Proteins called calpains are involved in memory formation. Two drugs that inhibit calpains improve Alzheimer mice. There are indications that the drugs restore signaling between cells in the hippocampus.
16. Calorie restriction increases proteins known as sirtuins which seem to be responsible for reduction of Alzheimer's symptoms in mice. SIRT1 is a sirtuin being studied.
17. One group has taken skin cells from patients, cultured them, genetically engineered them to make human nerve growth factor and injected them into areas of the brain where cells were dying due to Alzheimer's. There was improvement but time will tell if it lasts.
Better diagnosis is ahead
There is also work underway to make diagnosis easier, more accurate and possible earlier in the disease's course. Currently diagnosis relies on reviewing medical histories, administering physical exams, and taking into account the results of a battery of neuropsychological assessments that measure cognitive performance. After death a definitive diagnosis can be made at autopsy.
1. Until now accumulation of beta-amyloid was only found on autopsy. A project has demonstrated that a neuro-imaging scan called PiB PET can be used to identify amyloid and therefore individuals who may develop Alzheimer's disease up to 18 months earlier than all currently available diagnostics. Using positron emission tomography (PET) and a radiotracer known as Pittsburgh Compound-B (PiB) that is capable of binding to plaques found in the brains of AD patients. Unfortunately plaques are found in patients with other dementias and simple old age. But by showing which areas of the brain are affected, this procedure may be able to differentiate between conditions.
2. Redox-active iron levels in the CSF increased with the degree of cognitive impairment from normal to MCI subjects, while AD patients showed an abrupt decrease to levels close to zero. However, no difference in the total CSF iron was found between the different groups. This discovery offers the possibility to monitor iron levels in the CSF in relation with cognitive impairment and perhaps be used as part of a battery of biomarkers for an early diagnosis of these disorders.
3. A company using the proteomics method has patented several blood proteins associated with neurodegenerative disease and a test that measures a suite of 59 protein biomarkers. They say the test can distinguish between Parkinson's, Alzheimer's, and Lou Gehrig's. The test is being tested. Another group is trying to identify markers in blood and spinal fluid that can be used to show the early 'silent' stage of Alzheimer's and to track the progress of the disease. They hope for a screening test that can be used in massive programs like mammograms in example.
4. Fluorodeoxyglucose positron emission tomography (FDG-PET) measures blood glucose metabolism in the cerebral cortex. Less glucose uptake means less active cells. Using this technique shrinkage in various parts of the brain can be calculated. This may help in diagnosis of Alzheimer's. Comparing the change in various areas of the brain allow different dementia to be differentiated. In Alzheimer's disease, nerve cell death and tissue loss cause all areas of the brain, especially the hippocampus region, to shrink. MRI with high spatial resolution allows radiologists to visualize subtle anatomic changes in the brain that signal atrophy, or shrinkage. But the standard practice for measuring brain tissue volume with MRI, called segmentation, is a complicated, lengthy process. Using sophisticated computer programs the accuracy of this method is improved dramatically.
5. Work is going on to detect alterations in the optical properties of the brain using near-infrared light which passes through the skull and brain without harm. How the light is scattered can identify the amount of plaques.
6. Preliminary studies indicate that Alzheimer's appears to involve the formation of strongly magnetic iron compounds. These compounds have a strong MRI signal and may by a way to diagnose Alzheimer's. 
7. A technique called functional magnetic resonance imaging (fMRI) examines the patterns of brain activity. Networks can be found with this technique and Alzheimer's patients had fewer functional hubs in their networks. A compensating increase in connectivity in the frontal lobes in Alzheimer's was seen. Increase accuracy of diagnosis is likely to develop with this method.
8. "Combining a megapowerful magnet, multiple detectors, and carefully tweaked contrast, a new MRI technique developed at the National Institutes of Health (NIH) provides an unprecedented look at the fine structure of the brain. Using an MRI machine equipped with a magnet more than twice as powerful as one in an ordinary device, the researchers created a way to measure the magnetic field changes caused by tissue properties to optimize contrast in the image. Picking up on such differences may help researchers look more deeply into the brain's subdivisions, allowing them to map it in greater detail… It may also bring about advances in diagnosing diseases like Alzheimer's and multiple sclerosis, both of which involve abnormal iron accumulation in the brain."
9. The size of the brain's fluid-filled cavities, ventricles, becomes larger with cognitive impairment and Alzheimer's. MRI scans can measure changes in brain ventricle size and with recent computer programs to measure the ventricles quickly and accurately, the method could be used to follow the progression of the disease.

Alzheimer's 3
Risk factors
Because Alzheimer's may exist for some time before symptoms are noticed, it is difficult to know which things that seem to come with Alzheimer's are causes and which are consequences.
1. Genetics:
There are two types of Alzheimer's. (a) The early onset familial type is explained by mutations in three genes (amyloid precursor protein gene and two presenilins genes, all of which result in increased beta-amyloid with 42 units. (b) Late onset sporadic Alzheimer's also has genetic risk factors. Half of patients have a particular allele of the apolipoprotein E gene (APOE). There are other genes that affect risk.
Four genes that control tau have been found to not be risk factors for Alzheimer's but to be risk factors for earlier symptoms of the disease if the person does get Alzheimer's.
Another gene that has been implicated as a risk factor is the TRPC4AP gene. It is believed to regulate calcium and calcium dysregulation can result in inflammation, nerve call death and
possibly plaque production. A mutation of a gene, CALHM1, for a calcium receptor may be a risk factor.
2. Age:
The strongest risk factor is age. In the US, 5% of people 65-74 have Alzheimer's, 20% of people 75-84, and 50% of people 85 and older. Incidence is lower in some other countries but is still higher in old age.
3. Gender:
Women are more prone to Alzheimer's. The general picture is different as well. "Men with mild cognitive impairment were more likely to be overweight, diabetic, and to have had a stroke. Men who had had a stroke were almost three times as likely to progress to Alzheimer's. Women with mild cognitive impairment were more likely to be in poorer general health, disabled, suffering from insomnia and to have a poor support network."
4. Diet:
A bad diet seems to be a risk factor. There may be advantages to a Mediterranean diet (bread, cereals, olive oil, fish, and red wine). There may be advantages to vitamin B, C, and folic acid. Lack of omega 3 fatty acids is definitely is risk factor. Cur cumin in curry appears to have some protective effect. 
5. Brain size and use:
There seem to be a risk from low levels of social interaction and intellectual activities. This may be simply a question of the early stages of Alzheimer's being hidden and therefore an effect not a cause. There is also an association with small brain size especially smaller hippocampus. It may be that neuron death takes longer to affect a brain with more neurons to start with.
6. High blood pressure:
Hypertension appears to damage the blood vessels in the brain. It can also cause a type of mild impairment (reversible) that is not related to Alzheimer's. Hypertension may also be associated with Alzheimer's.
7. High cholesterol:
High levels of cholesterol seem to be a risk factor. High cholesterol in a person's 40s increases the risk of Alzheimer's in old age.
8. Diabetes:
This seems to be due to high glucose levels and damage to blood vessels in the brain. Diabetes in mid-life increases the risk of Alzheimer's later.
9. Depression:
Depression was thought to be an early symptom of Alzheimer's but is now thought to be a risk factor that predates the condition. Perhaps the brain is less resiliant to damage when depressed. Perhaps the hippocampus becomes smaller. Perhaps anticholinergic drugs are a risk. The risk is greater in women.
10. Stroke:
Stroke as a risk factor applies mostly to men. After a stroke the amount of beta-amyloid produced increases.
11. Infection:
This may or may not be a risk factor. There is some evidence for spirochetes, Chlamydia pneumoniae and Herpes simplex virus type 1. The route may be chronic inflammation.
12. Short arms and legs/ early nutrition:
People with shorter arms and legs are more likely to get Alzheimer's and this is thought to be because of poor nutrition in the first two years of life.
13. Anesthesia with desflurane and low oxygen levels combined (not either alone) is a risk factor.
14. Heavy drinking and heavy smoking:
These do not increase the risk of Alzheimer's but lowers the age of onset.
15. Perhaps some metals:
16. Lack of exercise
The Problem of Grief
The hardest thing for the loved ones of Alzheimer victims is that they are often caring for the person for a long before they are taken into professional care in a home or hospital. It is almost unbearable for many.
1. The disease robs the care-giver of the support and companionship they once had from the patient.
2. There is no hope of improvement or even of things not getting worst.
3. There are often financial problems.
4. There is very little time for the caregiver to relax from their responsibility.
5. Much of the work is physically hard.
6. The sufferers become very difficult to handle and upset or even attack their caregivers. They are often confused, angered, depressed. They say and do hurtful things.
7. The biggest problem is losing someone and grieving for them for years before they actually die. This is called 'anticipatory grief' and 'ambiguous loss'.
8. Others do not understand the difficulties, caregivers can be isolated and sometimes they are blamed for not providing enough care.

Celiac Disease
It seems I have celiac disease. After years of trying to find what would stop my diarrhea I have discovered that avoiding gluten is the answer. So I am one of those many people who have seen a number of doctors, had many tests and medicines, followed lots of advice. These helped some but really not a great deal. I had undiagnosed celiac, probably for 30 or more years. A year or so after I heard that an adult cousin had celiac and I got used to the idea that adults could have it, it suddenly occurred to me that …oh, maybe me. I looked to see if it had an inherited tendency and it does. Further that tendency is shared with other autoimmune diseases like type 1 diabetes. My father and uncle had type1 diabetes, my mother rheumatoid arthritis; two cousins have celiac as children and one at least as an adult. I stopped eating gluten and started improving.
Put very simply, celiac is an allergic reaction to gluten (from wheat, rye and barley - possibly oats) that damages the small intestine so that it causes malnutrition and diarrhea. That is just the simply story. The symptoms are extremely varied and the cause is a little more complicated than a simple allergy. There is only one treatment - avoid eating any gluten.
Here are the symptoms:

        recurring abdominal bloating and pain
        chronic diarrhea or sometimes constipation
        pale, foul-smelling, or fatty stool
        weight loss/weight gain
        unexplained anemia (a low count of red blood cells causing fatigue)
        bone or joint pain
        osteoporosis, osteopenia
        behavioral changes
        tingling numbness in the legs (from nerve damage)
        muscle cramps
        missed menstrual periods (often because of excessive weight loss)
        infertility, recurrent miscarriage
        delayed growth in children
        failure to thrive in infants
        pale sores inside the mouth, called aphthous ulcers
        tooth discoloration or loss of enamel
        itchy skin rash called dermatitis herpetiformis

Here is a summary of the disease:
1. It is an inherited disease.
In more detail: Celiac runs in families. Celiac individuals have a specific tissue type that recognizes wheat proteins. The HLADQ tissue type gene is part of a system which presents antigens to white blood cells and distinguishes between self and non-self molecules. Celiacs have the variants DQ2 and DQ8. The receptors formed by these genes bind gliadin peptides from wheat very tightly and therefore are more likely to activate T lymphocytes. But not all the people with this tissue type get celiac. The ones who do also lack a protective DNA sequence in the region of interleukin-2 and -21. These cytokine proteins are produced by white blood cells to control inflammation. The missing DNA sequence probably leads to different amounts of the cytokines being produced. Four of the nine known gene regions implicated in celiac are also implicated in type 1 diabetes. Risk of celiac is higher in those with auto-immune diseases. It is a package that sounds familiar to me - relatives with type 1 diabetes, celiac, auto-immune disease. Celiac is more common in Northern European people then others. Recent studies have shown that close relatives of celiacs have a 1 in 22 chance of having celiac disease, for those not closely related to a celiac the chance is 1 in 133.
2. In adults, at least, there is often an environmental trigger to the onset of the disease.
In more detail: A trigger is often the case in auto-immune disease. Some infection (such as rotavirus or human intestinal adenovirus), stress or damage starts the attack by the immune system on the body's own cells. Smoking is somewhat protective and so quitting smoking may be a trigger. Baby's who get celiac disease usually need no trigger other than gluten itself.
3. A component of gluten, gliadin, resembles proteins in the intestinal lining. Immune attacks on gliadin also attack the intestine.
In more detail: Gluten is a protein in wheat; a similar protein is found in all grains but only wheat (normal, spelt, triticale, kamut), rye, and barley cause celiac. Gluten is not fully digested in humans. It is partially broken down and the fragments cause the harm in celiac - gliadin is the harmful component of wheat gluten, hordein in barley, secalin in rye. An enzyme, tissue transglutaminase, modifies the gliadin and it then resembles protein in intestinal tissue. This starts an inflammation that destroys the villi and microvilli in the lining of the small intestine which are responsible for much the absorption of food. This results in pain, diarrhea and malnutrition. The decreased surface area of the intestine do to the loss of microvilli leads to a decreased production of lactase and therefore the symptoms of lactose intolerance may add to those of inflammation. Gliadin also stimulates membrane cells, enterocytes, to allow larger molecules around the sealant between cells. The two way leakage  allows liquid to enter the intestine through the intestinal walls and allows large proteins and other molecules that have not been broken down yet by digestion to enter the body. Gliadin entering the body can cause inflammation elsewhere.
4. Celiac symptoms are varied because it attacks a number of organs as well as the bowels.
In more detail:
Different symptoms can show at different times. It has been estimated that it takes about 10 years for a patient to be correctly diagnosed. They are often diagnosed with other conditions first.
Classic intestinal symptoms are do to damage to the intestine. Some symptoms are caused by malnutrition. Other symptoms are due to the triggering of inflammation in other areas of the body. Some conditions may be the result of shared genetic risk rather than being related to gluten.
5. The condition can be diagnosed but is often missed.
In more detail:
It is thought that most cases go undiagnosed, often because it is assumed that other diseases cause the symptoms or because symptoms are mild in some people. Diagnosis can be made by blood tests (for IgA antibodies against reticulin, gliadin, endomysium, tissue transglutaminase), HLA tissue type testing, endoscopic examination for villi in the duodenum, biopsy of intestine and by a gluten free diet followed by a gluten challenge. There has been debate on proposals to screen everyone with certain conditions for celiac in some countries. In the UK, NICE recommends to doctors that they should screen for celiac in newly diagnosed cases of chronic fatigue syndrome and irritable bowel syndrome and say it is justified in cases of type1 diabetes, iron-deficiency anemia, Down's syndrome, Turner's syndrome, lupus, Crohn's disease, and autoimmune thyroid disease.
6. There is no treatment except to avoid eating gluten.
In more detail
Avoiding gluten is easier said then done. An amount of gluten that is harmless has not been agreed and varies from person to person. US 'gluten-free' labeling is not regulated and can mean anything. Other, regulated, labeling for gluten probably allows too much and will be changed in future.
Traces of gluten are found in foods that would not be expected to contain gluten. Celiac are often advised to cook from scratch. Hidden sources of gluten include additives such as modified starch, preservatives, stabilizers, thickeners, and texture enhancers. Gluten may also enter other foods as contaminates in factories manufacturing many products. Oats is often contaminated with gluten. It can even be found in some medicines.
Even with strict avoidance of gluten, it takes time for the body to heal (as much as 6 months in children or 2 years in adults) and some symptoms may persist, especially if the condition has been present for a long time before diagnosis.
Having had celiac often leaves people with other sensitivities (milk products, mold-based cheeses, mushrooms, yeast and yeast products). One lingering sensitivity can be particularly problematic - sensitivity to xanthan which may be used as a binder in gluten-free products.
7. Dermatitis Herpetoformis is a complication in some celiacs.
In more detail
This also called Dulring's disease and is sometimes called 'celiac disease of the skin' as opposed to 'celiac disease of the gut'. The symptoms are small papules or vesicles on the skin, red bumps and blisters. These are intensely itchy and burning or stinging. The blisters come in bouts and may take from 7 to 10 days to lose their itching. They then crust over. They are rarely inflamed and don't contain pus. The only real treatment for the condition is a gluten-free diet. Dapsone is used to control severe symptoms but has unfortunate side effects. People can have the skin condition without the intestinal condition and vice versa.

The diet.
Celiacs can eat plain meat and fish, eggs, legumes and other sources of protein. They do have to avoid breading, flouring, gravy and sauces which contain gluten. They can eat all fruits and vegetables. For carbohydrates, there is rice, corn, potatoes and more rare foods like millet, buckwheat, flax, arrowroot, soy, sorghum, nuts and so on. Again prepared foods are a problem. Potatoes are OK but prepared fries often have a flour coating, so do many potato chips and corn and tortilla chips. Oats is safe except that it is often contaminated with other grains. Watch out for candy, cold cuts, hot dogs, salami, sausage, soy sauce, self-basting turkey, imitation fish or meat, and on and on with processed foods. Processed foods are likely to have some gluten.
And, of course, avoid at all costs anything made of flour (bread, cake, cookies, pastry etc), pasta, semolina/couscous, porriage/most cereals.

I really do not have too much faith in some areas of modern medicine: back pain and nutrition. Recently I ran across a reference to an article from 2005 by John Allen Paulos on health research, Why Medical Studies are Often Wrong. He is a professor of mathematics and interested in statistics.
A study of papers from major journals between 1990 and 2003 by J. Ioannidis showed that a third were contradicted or significantly weakened by later work.
Hormone replacement does not protect against heart disease; vitamin E does not protect against cardiac problems. And on… Single studies can not be trusted. They may be statistically flawed in some way. Studies as they are presented in the popular media may mislead us even if the originals are reliable. Unfortunately researchers may not be impartial and may even be supported by a drug company and pressure group. I think that the type of information that is most prone to being unreasonably hyped by the press is nutrition studies.
In the past I have fallen for some nutrition myths. One was vitamin C in large doses - if I felt off colour I would take a lot of vitamin C for a couple of days. But some fads I didn't touch. I remember when fancy margarines came out with their poly-unsaturated fats and they were supposed to be so much more healthy than butter. Well, I just could not believe that something that came out of a chemical factory was healthier than something that came out of a dairy. I cut way back on the butter but I didn't replace it with margarine, so I have not been taking in trans-fats from any margarines all these years.
Then there were eggs. Would an egg do any harm? (Which reminds me of a story about Harry's mother: Harry heard about pies at school and what a special treat they were so he bugged his mother to bake pies. Harry's mother was a very experienced and good cook but in a Ukrainian cuisine that did not include pastry. She got a recipe from somewhere and started to make a pie. The crust had only flour, water and lard. What was that for food? Where was the nutrition - could an egg do any harm? It was a spectacular failure.) One day eggs became unhealthy because of their cholesterol. We must not eat anything high in cholesterol. I could not believe that cholesterol, something that the body could make for itself and that was important for metabolism, was not regulated. If we ate more then we would make less and if we ate less then we would make more. Something would be setting the level of cholesterol in our bodies and it would not be how much we ate. I have not stopped eating those eggs, full of so many healthy things.
The phrase - 'you are what you eat' - has caused a lot of misunderstanding. By and large, the body can make what it needs from what it gets. It can make carbohydrates from fats and fats from carbohydrates and so on. What it cannot make and so you must supply in your diet is minerals, vitamins, essential fatty acids and essential amino acids. If you eat a well balanced and varied diet than you will get these essentials (or you can get them from pills). And, of course, you want to avoid the things that are poisonous. Then you would aim to get enough calories but not way too many. Finally if you have some medical problem, you may have to eat more of some things and less or none of others. Metabolism is complex and controlled by feedback loops (some still being discovered) and we are very definitely not what we eat.
The writer Jonah Lehrer says about 'Nutritionism', "There are many good reasons to eat sardines, beets, turmeric, etc. But don't eat them because of some correlation in a medical study. There's a good chance, after all, that such a correlation will turn out to be dead wrong."

More Exercise
It seems clear to me that I do not get enough exercise.
Recent reports have conclusions like:
1. Exercise reduces blood pressure, cholesterol, diabetes and depression.
2. It improves blood flow and nerve cell growth in parts of the brain associated with memory. It improves both memory and cognition in elderly people.
3. It reduces calorie intake - suppression of appetite by increased brain-derived neurotrophic factor. Apparently this effect does not apply in obese women, those that are resistant to the hormone leptin. They must diet and exercise in order to lose weight.
4. The bain works better when using lactate rather than glucose. Lactate is the by-product of strenuous exercise which can be cleared by the brain.
5. Genetic susceptibility (by FTO gene) to obesity is blunted by a very active life.
6. Older people lose less muscle mass if they do low-intensity exercise and take nutrient supplements. When older people diet without exercising they lose valuable muscle mass.
7. Lifestyle, more than heredity, contributes to insulin resistance in obese people. Physical inactivity contributes (alon with genetics) to defects in mitochondrial oxidative phosphorylation.
8. Exercise helps trim the faty liver that complicates diabetes, heart disease and liver failure.
9. Older people decrease risk of disability aramatically with a walking exercise program.
10. Age-related changes to circulation in the brain are reduced by exercise - resulting in better blood flow and more small blood vessels.
Current recommendations prescribe 30 minutes of moderate physical activity on most days of the week, for a total of 150 minutes per week. However, a growing consensus suggests that more exercise may be needed to enhance long-term weight loss. I have to lose weight but it seems that I should do it with exercise rather than just diet alone. But how to get exercise? What I have to figure out is how to be active without my joints getting painful and the pain stopping the exercise for a few days until I have recovered. If I lose some weight I should have less trouble with my joints but that will be a long time in the future. In hindsight, I should have watched my weight when I quit smoking, but I thought I could deal with it later. So I have to slowly work up to more than 30 minutes a day of real exercise.