Archive for September 2007
It’s hard to find statistics on how many people have asperger’s diagnoses. According to the BBC (and please feel free to ignore the horrible and depressing descriptions of autism and asperger’s that they use), the number of people ranges between 0.01% (one in a thousand) to 3.6% (one in twenty eight). A lot of sites quote the 1:10 female to male statistic, other sites quote 1:6.
Most of the aspies I’ve met online are female aspies who have self-diagnosed in adulthood. The male aspies I’ve met seem to be more extreme, probably because the male brain is less suited to social skills in the first place. I personally think that most of the genes may occur in a 1:1 ratio, but that being female acts to mask some of the more extreme differences of asperger’s. The only gene I know of that is sex linked is monoamine oxidase. Males only have one copy, so if they get an inefficient version they become more vulnerable to amines. A female has two copies of the gene, so statistically they have more protection against amines.
In my family, there is a definite trend for eccentric women as well as eccentric men – both grandmothers in particular! I had a particularly crotchety and unsociable great aunt, Aunt Kath, on my father’s side who my mother really disliked (my mother dislikes most of the aspies in the family). Aunt Kath, I’m told, liked me but disliked all the other grandchildren. Perhaps I was less alien to her.
I’ve been thinking about when I was at secondary school. The school had well over a thousand pupils – perhaps 180-200 in each year. In my year there were four girls I considered ‘like me’. They were like me for slightly different reasons than each other. One was very quiet and studious and tagged along with the privileged girls. She went on to get a masters degree – I think the only person from my year to do so that I know of apart from me. The other two were my friends. I didn’t meet them until I was about fifteen – I was a loner for most of my time at secondary school. There was a neurotypical girl (we’ll call her R.) who seemed to collect eccentrics and went to unusual measures to be my friend. Her two other friends were M. and A.
M. was so quiet that she never spoke of her own accord, and when you addressed her directly her response would be monosyllabic. I don’t recall her having a problem with eye contact. I don’t recall her appearing shy or embarrassed, but she always seemed to have a funny Mona Lisa smile on her face that made me think she was probably enjoying a secret joke at everyone else’s expense. In hindsight, I think she was probably just very embarrassed, but also quite amused by our other friend, A. who was very noisy.
A. reminded me of my sister a bit because she was noisy. She was very opinionated and talkative, and definitely had a case of ‘little professor syndrome’. She would lecture you on any subject under the sun given half a chance. I used to describe her personality as a mixture of C-3PO and Mary Poppins. She held some very eccentric ideas about the world and I once had an argument with her because she thought that radio waves could be blown around by the wind. Whilst I was maths blind, she was extremely good at maths and physics, and went on to study as an engineer at university. She had two other sisters, one who was totally NT and the other was older and a bit wild. A. also had middle-child syndrome. She was my best friend for several years until we went our separate ways to university. She often took things very literally, and she seemed blind to the fact that R. was always mocking her. No one ever ‘got’ her jokes, and she complained that people were always misinterpreting her.
So that’s four girls in my year of 200 pupils who had the potential to score very highly – or one in fifty. I have no idea how many boys would score highly. I don’t remember much about the boys at secondary school. I don’t remember their names, and I didn’t interact with them. Seriously.
The first boys I met who were in any way ‘like me’ were on my masters degree. I think most of the people on my masters degree were quite eccentric and had social interaction issues in one way or another. I expect people on a masters course make up a very small, select segment of society. I guess most of the neurotypicals had been weeded out by that stage! Several of them seemed to be incapable of talking about anything but sex. Others didn’t talk much at all, or were very, very sensitive. One was a (really lovely) schizophrenic – who would not have had her creative talent if not for her schizophrenia. I’m big on neurodiversity.
I happen to think there’s an undiagnosed syndrome in existence – let’s call it auteur syndrome for want of a better name. It’s not neurotypical, and it comes with creative talent, whether it be writing, acting, painting, music, or something else. It might manifest as a kind of creative asperger’s syndrome, or it might manifest like my maternal cousins and my sister – as popularity and sociability combined with creative flare. It seems to go hand in hand with obsessions, bipolar disorder and ADHD. People like this get very frustrated in ordinary office jobs and have to do something a bit unusual with their lives – like being chefs, actresses, comedians or rock stars. I think it must be a dopamine thing. Aspies often have people like this in their family – brothers or sisters or cousins.
When I first started meeting computer programmers through temping work after university I was surprised to discover how much I had in common with them in terms of personality. I should have guessed then I suppose! My other half, a programmer, was the first person I met who I felt was really like me. He scores high-normal, and there are only five IQ points between us. I use him as a social crutch. He’s also the smarter one. Just.
Wow. Donna Williams’ family history sounds just like mine!
I was born into a very challenged and challenging household of unusual, eccentric, personalities. Various combinations of mood, anxiety, compulsive disorders, addiction, rage, dyslexia, ADHD, Asperger’s, autism, suicide, Crohn’s, Colitis, Coeliac, Diabetes, eczema, asthma, croup, hives and allergy rashes all run in various side of my family, going back generations on my father’s side.
Not all people with autism have my physical, sensory-perceptual, language processing, neurological integration or co-morbid mood, anxiety or compulsive disorders. Most of these issues run on one or both sides of my family. I feel that what I inherited was the combined impact of the challenges of both my parent’s sides of the family and that under certain environmental conditions, these things expressed themselves in early infancy, causing the developmental breakdown that presented as a ‘psychotic infant’, disturbed child, autistic adult. Autism; it ain’t all physical
I was going to say I can’t think of a case of suicide – but I can – my dad’s cousin was a millionaire who lived in a stately hall in Bakewell, and he killed himself.
No Crohn’s/colitis/coeliac as far as I know – just plenty of garden-variety IBS. Also some kidney stones and gallstones.
Like me, Williams seems to have inherited most of her autie personality from her father. My father is a boffin, crazy inventor, tinkerer, collector, and all-round know-it-all.
I even have something in my family history that Williams doesn’t – my maternal grandfather’s sister had intractable epilepsy and was locked up in a sanitarium until she died.
I would have loved to have met my great grandfather Beau Pré. He was an African missionary – a very angry man by most accounts – an alcoholic, who died in the African jungle of an asthma attack.
I am so repeating myself here. Do you think if I keep saying “IT’S GENETIC” some of the chelators and the gut bacteria folks and the vitamin deficiency zealots will eventually stop and listen?
Or am I talking to a brick wall here?
Michael Eades and Anthony Colpo have been involved in what can politely be described as a ‘debate’ recently. Less politely it might be described as Eades trying his best to remain calm and professional whilst Colpo lashes out with personal insults like a rabid attack-dog. I enjoy both of their outputs – as long as they both stay off the subject of politics – though I worry about Colpo sometimes, if the man is THAT angry ALL the time, there must be something very wrong.
Eades has put up a post citing science in favour of the metabolic advantage. He quotes from a recent study on mice who were put on a ketogenic diet and lost more weight than controls due to changes in gene expression that caused them to burn at a hotter rate. The results of the study didn’t break the laws of thermodynamics.
On the other hand we have Colpo saying “Calories in equal calories out, there is no metabolic advantage.” Because that’s one of the main premises of his weight loss book, I haven’t bought it, as I’ve a more complex understanding of metabolism.
I honestly don’t know what these two are fighting about. It’s apparent that a ketogenic diet (usually but not always) makes one burn more calories than a carbohydrate-based diet because it increases metabolism and heat expulsion, at the very least in the short term. This theory has been around since at least the 1950’s. This doesn’t break the calories in = calories out rule, it never has. I think there are genetic exceptions to this too. Some people fair better with more carbohydrates in their diet, or less protein or more protein. I tend to favour ‘cycling’ between low and moderate carbohydrate content and not eating too much protein in order to maintain weight loss over an extended period – and eating very low chemical and opioid free.
Anyway, I’m not posting this to get into a tired old debate about the metabolic advantage. I’m here to fill in this blank:
What if underlying levels of fatness or genetics or _____ (we’ll fill in the blank later) cause us to eat more and burn less? Eades
With something like this:
What if underlying levels of fatness or genetics or increased insulin output caused by salicylates, amines, glutamates, additives and other food chemicals cause us to eat more and burn less?
Because that’s the way it went for me. I spent several years struggling with frighteningly rapid weight gain caused by food chemicals until I found the failsafe diet. I was very successful at controlling this weight gain though. This is because I have a will of iron – I may not be Posh Spice in terms of discipline, but I’m not Kirstie Alley either! Every three months or so I had to resort to a ketogenic diet in order to lose the weight I’d gained on the Atkins maintenance diet. I really didn’t eat that much – and believe me, I calculated my calorie intake very truthfully in FitDay. In fact, eating lots of fat and calories had the perverse effect of making me lose several pounds. I was extremely sensitive to relatively small amounts of carbohydrate though.
These days I eat a lot more carbohydrate and I don’t gain any weight at all. I only gain weight when I’ve cheated on failsafe – most usually by visiting a restaurant and eating meat or fish that is too old and aminey/glutamatey. Vacuum packed meat at home does the same thing to me. Physically I may not even feel bad (in fact I often feel happy-high), but I certainly feel it on my backside after a couple of days!
Whether you are underweight or overweight, if you struggle to control your weight on a normal diet, consider lowering your food chemical intake.
More on this debate here. The comments section gets quite nasty!
Chris has come up with the goods again and has sent me another great news story! At last some sanity appears to have returned to the vegetable antioxidant researchers:
CORVALLIS, Ore. – Flavonoids, a group of compounds found in fruits and vegetables that had been thought to be nutritionally important for their antioxidant activity, actually have little or no value in that role, according to an analysis by scientists in the Linus Pauling Institute at Oregon State University.
However, these same compounds may indeed benefit human health, but for reasons that are quite different – the body sees them as foreign compounds, researchers say, and through different mechanisms, they could play a role in preventing cancer or heart disease.
Based on this new view of how flavonoids work, a relatively modest intake of them – the amount you might find in a healthy diet with five to nine servings of fruits and vegetables – is sufficient. Large doses taken via dietary supplements might do no additional good; an apple a day may still be the best bet.
A research survey, and updated analysis of how flavonoids work and function in the human body, were recently published in Free Radical Biology and Medicine, a professional journal.
“What we now know is that flavonoids are highly metabolized, which alters their chemical structure and diminishes their ability to function as an antioxidant,” said Balz Frei, professor and director of the Linus Pauling Institute. “The body sees them as foreign compounds and modifies them for rapid excretion in the urine and bile.”
Flavonoids are polyphenolic compounds with some common characteristics that are widely found in fruits and vegetables and often give them their color – they make lemons yellow and certain apples red. They are also found in some other foods, such as coffee, tea, wine, beer and chocolate, and studies in recent years had indicated that they had strong antioxidant activity – and because of that, they might be important to biological function and health.
“If you measure the activity of flavonoids in a test tube, they are indeed strong antioxidants,” Frei said. “Based on laboratory tests of their ability to scavenge free radicals, it appears they have 3-5 times more antioxidant capacity than vitamins C or E. But with flavonoids in particular, what goes on in a test tube is not what’s happening in the human body.”
Research has now proven that flavonoids are poorly absorbed by the body, usually less than five percent, and most of what does get absorbed into the blood stream is rapidly metabolized in the intestines and liver and excreted from the body. By contrast, vitamin C is absorbed 100 percent by the body up to a certain level. And vitamin C accumulates in cells where it is 1,000 to 3,000 times more active as an antioxidant than flavonoids.
The large increase in total antioxidant capacity of blood observed after the consumption of flavonoid-rich foods is not caused by the flavonoids themselves, Frei said, but most likely is the result of increased uric acid levels.
But just because flavonoids have been found to be ineffectual as antioxidants in the human body does not mean they are without value, Frei said. They appear to strongly influence cell signaling pathways and gene expression, with relevance to both cancer and heart disease.
“We can now follow the activity of flavonoids in the body, and one thing that is clear is that the body sees them as foreign compounds and is trying to get rid of them,” Frei said. “But this process of gearing up to get rid of unwanted compounds is inducing so-called Phase II enzymes that also help eliminate mutagens and carcinogens, and therefore may be of value in cancer prevention.
“Flavonoids could also induce mechanisms that help kill cancer cells and inhibit tumor invasion,” Frei added.
It also appears that flavonoids increase the activation of existing nitric oxide synthase, which has the effect of keeping blood vessels healthy and relaxed, preventing inflammation, and lowering blood pressure – all key goals in prevention of heart disease.
Both of these protective mechanisms could be long-lasting compared to antioxidants, which are more readily used up during their free radical scavenging activity and require constant replenishment through diet, scientists say.
However, Frei said, it’s also true that such mechanisms require only relatively small amounts of flavonoids to trigger them – conceptually, it’s a little like a vaccine in which only a very small amount of an offending substance is required to trigger a much larger metabolic response. Because of this, there would be no benefit – and possibly some risk – to taking dietary supplements that might inject large amounts of substances the body essentially sees as undesirable foreign compounds.
Numerous studies in the United States and Europe have documented a relationship between adequate dietary intake of flavonoid-rich foods, mostly fruits and vegetables, and protection against heart disease, cancer and neurodegenerative disease, Frei said. Studies force new view on biology of flavonoids
I don’t mean to sound smug (actually I do), but I was saying this a year ago based on what I had learned about chemical detoxification: polyphenols are the emperor’s new clothes in terms of antioxidant capacity, and that the body wants to get rid of them as fast as it can!
Now that the antioxidant theory is falling apart, researchers are trying to justify the last ten year’s worth of bad advice (eat lots of fruit and vegetables for the antioxidants), by trying to find more complex reasons to self-fulfill their dubious hypothesis that vegetables “are good for you”.
The first assertion is that they increase the antioxidant capacity of the blood by increasing uric acid levels. High uric acid levels are how you give yourself gout – people with gout have inefficient enzymes that causes uric acid to build up in the blood and crystalise in the joints, particularly the toe and finger joints.
In humans, about half of the total antioxidant capacity of plasma comes from uric acid. This is a particular adaption of higher primates, who have lost their uricase enzyme in response to having previously lost their vitamin C enzyme. Uric acid.
There is however, more than one way to skin a cat. Uric acid is formed from purines, heterocyclic aromatic compounds that are formed around a nitrogen base. They have the particularly special quality that they form a part of our DNA and RNA and have biological functions in molecules like ATP and coenzyme A. A diet of red meat and shellfish is high in purines. People who eat meat tend to have higher uric acid levels than people who do not eat meat. Perhaps the most stereotypical way to give yourself gout is to eat a diet of liver and red wine. In other words – why eat vegetables when eating red meat will achieve the same effect of raising your uric acid levels through an inbuilt, natural capacity?
The second assertion is that a diet of fruit and vegetables ‘may help’ induce Phase II detoxification enzymes in the liver. Remember that they have not proven that dietary flavonoids actually help anything overall – they merely have some tenuous population studies that show that people who eat fruit and vegetables as opposed to junk foods (sugar, additives, MSG, trans fats), seem to be healthier. Which they would be, wouldn’t they? If you give one rat a full dose of arsenic, and another rat half a dose of arsenic, the second rat is going to appear to be healthier, isn’t it?
The situation with phase II detox enzymes is actually very complicated. Some specific flavonoids induce certain phase II enzymes through drug-like mechanisms, whilst other specific flavonoids inhibit certain phase II enzymes through other drug-like mechanisms. Flavonoids are not all the same by a long shot, and by randomly eating fruits and vegetables, you are playing the flavonoid lottery. Last year I came across an article that stated the only reason that resveratrol from red wine stayed in the body for any time at all was that some of the other bioflavonoids in red wine totally nuked a bunch of phase I and phase II detox enzymes. In other words, red wine kills the liver.
Beyond this, the only reason you need to induce phase II detox enzymes beyond normal capacity in the first place is because 1) you are up to your liver’s maximum capacity already due to putting so many flavonoids in your system, and 2) you are putting carcinogenic compounds into your system in the first place! Those carcinogens are some of the flavonoids and phenols found in fruits and vegetables! Phenols – found in fruit and vegetables – are one big free radical on a stick.
The last defense of flavonoids comes from the point that they induce nitric oxide synthase. Again, this is a case of very specific flavonoids having this very specific effect, and randomly eating fruit and vegetables is playing a lottery, as some flavonoids (for example soybean flavonoids) have the opposite effect of suppressing nitric oxide synthase. Nitric oxide keeps your arteries wide and flexible. This is all very well for people who have chronically high blood pressure (which can indeed be food chemical induced as well as genetic). But people with fibromyalgia have too much nitric oxide, their blood pressure is usually on the low side, and it’s the excess of nitric oxide that triggers a significant part of the spiralling feedback loop of inflammation, exhaustion and ill health. Considering how many people with fibromyalgia that I know who eat lots of ‘healthy’ fruit and vegetables, it’s hardly surprising…
This is an interesting essay refuting Amand’s guaifenesin protocol for fibromyalgia. The paper goes into a detailed exploration of the similarities between salicylate intolerance and fibromyalgia, and offers alternative explanations for why the guaifenesin protocol works. It’s not 100% accurate on a few things but still points in the right direction.
One thing I didn’t know is that salicylates block the excretion of uric acid. Might they therefore be responsible for some cases of gout? No wonder I sometimes, rarely, get aches in my toes or finger joints. I suppose throwing folate at this is going to cause more purines to be produced and make the situation worse.
Coming down off methyl donors is hell.
When I used to drink caffeine I felt the same way. Sometimes caffeine hits me like speed. Withdrawal gives me the shakes, brain fog, headaches and back pain. I feel like my head is full of wool. Memory completely shot. Misspellings. Malapropisms. Inability to speak sentences, get words out. This is what it feels like to be a nonverbal autistic. Like my brain is one big stutter.
Once in the brain, the principal mode of action of caffeine is as an antagonist of adenosine receptors found in the brain. The caffeine molecule is structurally similar to adenosine, and binds to adenosine receptors on the surface of cells without activating them (an “antagonist” mechanism of action). Therefore, caffeine acts as a competitive inhibitor. The reduction in adenosine activity results in increased activity of the neurotransmitter dopamine, largely accounting for the stimulatory effects of caffeine. Caffeine can also increase levels of epinephrine/adrenaline, possibly via a different mechanism. Acute usage of caffeine also increases levels of serotonin, causing positive changes in mood. Caffeine Mechanisms of Action
On top of inhibiting adenosine, caffeine – trimethylxanthine – is a methyl donor. The liver detoxifies caffeine by stripping off the methyl groups and using them for other tasks. During the first pass through the liver, one methyl group is stripped away, and this has the effect of changing the shape of the caffeine into dimethylxanthine so it becomes physiologically more active. This is why caffeine usually hits you about an hour or two after you’ve drunk it.
The half-life of caffeine—the time required for the body to eliminate one-half of the total amount of caffeine consumed at a given time—varies widely among individuals according to such factors as age, liver function, pregnancy, some concurrent medications, and the level of enzymes in the liver needed for caffeine metabolism. In healthy adults, caffeine’s half-life is approximately 3–4 hours. In women taking oral contraceptives this is increased to 5–10 hours, and in pregnant women the half-life is roughly 9–11 hours. Caffeine can accumulate in individuals with severe liver disease when its half-life can increase to 96 hours. Caffeine Metabolism
I wonder what the half-life of salicylate is in my body?
Funny story. I went to the supermarket earlier and I decided to buy some pesticide. Much as I would love to be totally organic, I have a small yucca that is infested with black fly and I can’t seem to shift them just by physical removal.
I am coming down off methyl donors and inevitably I have brain fog today.
I sprayed the pesticide on my yucca. I held my breath, but I got a good whiff of the stuff anyway. It smelled like moth balls. Within seconds of smelling this stuff my brain fog cleared. I looked to see what the active ingredient was: bifenthrin. What’s in it?
Shame the effect only lasted ten minutes.
Just what has happened to Courtney Love?
The singer is a shadow of her former attractive self, and appears to be afflicted with a skin condition which has left her mouth looking sore and scabby.
The widow of dead rocker Kurt Cobain arrived at the Groucho Club in London sans make-up unwittingly revealing her scabbed mouth and spotty skin. […]
Despite the major weightloss, a reported 44-pounds, it appears that her methods may be exacting a heavy toll on her once attractive looks as Love looks far from healthy.
Her straw-coloured hair is almost a perfect match for her deathly pallor, and the low-riding jeans, and cropped shirt she’s wearing do little to flatter her size zero figure.
Love, credits her new figure to visits to a clinic for “colonics and fasting” several times a year and eating a daily diet of two meal replacement shakes and “fish and macrobiotic food.”
Love explained: “Some people think it’s about weight loss, but it’s about detoxing.” Daily Mail: WHAT has happened to Courtney Love’s lips?
Enough with the irony already! Courtney Love detoxes from drugs and wreaks her skin with a macrobiotic diet. Love, as well as developing bad skin, appears to be suffering from a pot belly.