Archive for May 2008
I watched a channel 4 documentary on the Elizabeth Fritzl case a couple of days ago. In case you have been living in a hole yourself, this is the case of the poor woman who was imprisoned and abused by her father for more than twenty years in a dark, airless cellar in Austria.
The only picture I could find of Elisabeth (which I have now lost again) is that of a woman with a blanket thrown over her head, being accompanied by police officers. Her legs are bare and have the lilac quality of skin that has absolutely no pigmentation.
Elisabeth’s freedom only came about when Kerstin Fritzl, Elisabeth’s oldest child, was bought to hospital unconscious by Josef Fritzl, with a note from her mother. She later suffered seizures and was found to be suffering from multiple organ failure.
Doctors had no idea what was wrong with her and a media appeal was launched asking her mother to come forward as she may be able to provide answers as to the cause of Kerstin’s illness. Police suspected severe neglect and abuse.
Days later Elisabeth appeared with her father at the hospital where Kerstin was being treated. At first Elisabeth evaded police questions, but then promised to tell the truth if the police promised she would never have to see her father again.
With the revelation that Kerstin had spent 18 years locked in an underground cellar with her mother and two siblings, it must have become obvious to the doctors that she was suffering from dramatic vitamin D deficiency. This information is largely absent from internet news accounts of the case, but it was revealed by the channel 4 documentary to be the cause of Kerstin’s illness. Kerstin currently remains in an induced coma – presumably to manage status epilepticus or unbearable pain – though reports are promising that her health is recovering. Apparently her kidneys have started working again.
What is amazing to me is that her mother, Elisabeth (42), and siblings, Stefan (19), and Felix (5), did not end up in the same state. Elisabeth has survived for twenty four years without any sunlight whatsoever. There have been a number of reports in the British press that suggest the Fritzl family’s teeth are badly decayed and that they “speak in animal noises” and walk strangely (ricketts?), but this has been denied by police officers and doctors close to the case, though all are said to be deficient in vitamin D, anaemic, and have poor posture and poor immune systems. Why did Kerstin get so sick above and beyond her peers? Perhaps her genetics make her more vulnerable to vitamin D deficiency. Perhaps she did not eat something protective that her family members ate – like dairy products, mushrooms, or blood sausage (blood is a very rich source of vitamin D). Perhaps she contracted an infection, perhaps a kidney infection (vitamin D is largely regulated and recycled by the kidneys), that led to her crisis.
Natascha Kampusch, fellow Austrian, who was imprisoned at the age of ten for over eight years in a cellar under similar circumstances appears not to have suffered from any bone structure abnormalities. In fact she has a remarkably attractive face with a well-formed, broad jaw line. As does her captor, Wolfgang Priklopil.
Far from speaking in animal noises, the Fritzl children are said to be eloquent, polite, well-behaved and very intelligent, a testament to their mother’s care. Stefan is said to be a delight to talk to. The plot thickens somewhat when we learn that Josef Fritzl was abusiness man who dealt in property, and an engineer who built a warren of underground rooms under his house. He put his meticulous planning skills to a repugnant use in the imprisonment of his daughter, carefully crafting her living space prior to her kidnap, and even luring her into the cellar under the pretext of helping him carry a heavy reinforced steel door that was to seal her dungeon.
Indeed, Austrian police suggest that Josef Fritzl was so well organised he was able to take long holidays abroad without fear of his prisoners starving to death, and he even claims that if he was gone for too long, the electronic locking mechanism on the cellar door would automatically unlock. Fritzl’s business associates describe him as a man who was unusually reliable – if he said he would return a tool he would borrowed in two days time, he would return it in two days time. Fritzl’s neighbours describe the family as “keeping themselves to themselves”, growing a huge hedge around their garden, and never visiting local garden parties. And what of Priklopil? He too fits the same personality type. When he died he was working as a communications technician for Siemens.
From the asperger’s syndrome blogs I read there has been silence on this issue, just as there was silence over the Virginia Tech University massacre when the decidedly strange Seung-Hui Cho went on a shooting rampage. Seung-Hui Cho suffered from selective mutism, social anxiety and depression. His family thought he might be mentally ill. According to his grandfather, Cho never made eye contact with him, called him grandfather, or tried to hug him. He was teased for his shyness and strange speech patterns. He appears to have looked down on and hated his peers – as happens commonly when an intelligent individual is bullied and hounded for being different.
I don’t believe that other aspie bloggers haven’t noticed these personality traits. The people whose blogs I read have finely tuned aspie radars and spot patterns quickly. I believe that, like me, they simply don’t know what to say.
You can take your vitamins and throw them down the toilet. Folate makes me manic and gives me eczema. B12 makes me feel a little bit too happy, very intelligent, too awake (great first thing in the morning, terrible problem at night), makes me easily stressed and irritable, and makes me gain weight quickly. After having stable weight for months and months, I suddenly gained several pounds in the space of a two month B12 (adenosylcobalamin) trial earlier this year. On the plus side it actually helped my residual winter eczema somewhat – though not as much as getting some sunshine has.
The weight gain that B12 causes I suspect is connected to B12′s ability to depress a form of glutamate decarboxylase (GAD67) that converts glutamate into GABA. And of course glutamate stimulates weight gain through insulin production. More on the B12 trials in another post.
So the upshot of this is that I’ve been back on a diet for a few weeks now to get rid of the weight. I’m on a ketogenic diet. Properly. Last year I did a moderate version that included a small portion of rice every day. I tried this because without any carbohydrate at all I tended to just flake out and feel starved. I couldn’t really sustain the rice version for long as I tended to feel just a little too hungry all the time. Of course this means I don’t have much variety in my diet right now. Largely I’m living on lamb, chicken, fish, shellfish, eggs, and A2 dairy (butter, cream, cream cheese), and Woodlands organic sheep’s milk yoghurt, which has turned out to be a life-saver (at last! a yoghurt that doesn’t give me headaches and cravings!). I’m not hungry at all. This probably sounds like a scary anorexic diet, but I am getting enough calories and vitamins, I assure you. I’m also feeling better than I have in years. Literally years, because I haven’t really done failsafe gluten-free for very long before, and I haven’t done it ketogenic like this. All my leftover aches and pains have gone – I suspect gluten and A1 milk bother me rather more than I liked to think they do. This time I have no real hunger, so I feel as though the diet is sustainable and I plan to stay on it for at least six months – or until I get back down to my minimum healthy BMI, because I like being slim.
And I’m calm. Totally calm. Ambien calm. It’s like someone found the centre of my emotional balance and nailed me there. No stressing out over minor things. No irritation. I’m also highly motivated. Hence less posts and more stuff getting done around the house. Like painting walls and constructing furniture and spring cleaning and unpacking boxes that are still left form the house move last year – all the stuff that normally tires me out just thinking about it. I’m not manic however – I’m just happy in a good, balanced way.
No vitamin could ever do this or has ever done this for me. The minor improvements I saw in myself on the B12 (which approached megadoses on occasion) are nothing in comparison to the sledgehammer effect of ketosis. And ketosis comes without the unpleasant side effects. My sleep is fine. I’m waking up fine. I feel sharp. And I’m losing weight instead of gaining it.
And why it’s relevant to failsafers!
Our objective was to study brain amino acid metabolism in response to ketosis. The underlying hypothesis is that ketosis is associated with a fundamental change of brain amino acid handling and that this alteration is a factor in the anti-epileptic effect of the ketogenic diet. Specifically, we hypothesize that brain converts ketone bodies to acetyl-CoA and that this results in increased flux through the citrate synthetase reaction. As a result, oxaloacetate is consumed and is less available to the aspartate aminotransferase reaction; therefore, less glutamate is converted to aspartate and relatively more glutamate becomes available to the glutamine synthetase and glutamate decarboxylase reactions. We found in a mouse model of ketosis that the concentration of forebrain aspartate was diminished but the concentration of acetyl-CoA was increased. Studies of the incorporation of 13C into glutamate and glutamine with either [1-(13)C]glucose or [2-(13)C]acetate as precursor showed that ketotic brain metabolized relatively less glucose and relatively more acetate. When the ketotic mice were administered both acetate and a nitrogen donor, such as alanine or leucine, they manifested an increased forebrain concentration of glutamine and GABA. These findings supported the hypothesis that in ketosis there is greater production of acetyl-CoA and a consequent alteration in the equilibrium of the aspartate aminotransferase reaction that results in diminished aspartate production and potentially enhanced synthesis of glutamine and GABA. Response of brain amino acid metabolism to ketosis
There are a number of different studies by Daikhin and Yudkoff that have confirmed the above hypothesis in different ways. They can be found in pubmed. I won’t repeat them all here.
Here is a study that found other differences:
The ketogenic diet (KD) is an established treatment for medically refractory pediatric epilepsy. Its anticonvulsant mechanism is still unclear. We examined the influence of the KD on the CSF levels of excitatory and inhibitory amino acids in 26 children (mean age 6.1 years) with refractory epilepsy. Seventeen amino acids were determined before and at a mean of 4 months after the start of the KD. Seizures were quantified. Highly significant changes were found in eight amino acids: increases in GABA, taurine, serine, and glycine and decreases in asparagine, alanine, tyrosine and phenylalanine. However, aspartate, glutamate, arginine, threonine, citrulline, leucine, isoleucine and valine/methionine remained unchanged. A significant correlation with seizure response was found for threonine (P=0.016). The GABA levels were higher in responders (>50% seizure reduction) than in nonresponders during the diet (P=0.041). In the very good responders (>90% seizure reduction), the GABA levels were significantly higher at baseline as well as during the diet. Age differences were found with significantly larger decreases in glutamate and increases in GABA in connection with the diet in younger children. Our results indicate that the KD significantly alters the levels of several CSF amino acids that may be involved in its mechanism of action and the increase in GABA is of particular interest. The ketogenic diet influences the levels of excitatory and inhibitory amino acids in the CSF in children with refractory epilepsy
Glutamate and aspartate are both ‘bad’ neurotransmitters for people with food chemical intolerance (aspartate is involved in salicylate reactions on NMDA receptors). Ketosis appears to reduce aspartate levels by moving glutamate production away from aspartate and towards GABA and glutamine. Other glutamate-opposing amino acids like taurine, serine and glycine are raised too. GABA and glutamine are both ‘good’, calming neurotransmitters for failsafers.
The ketogenic diet has been studied for many years in relation to intractable epilepsy in children. It has also been hypothesised to help bipolar disorder:
The ketogenic diet, originally introduced in the 1920s, has been undergoing a recent resurgence as an adjunctive treatment for refractory epilepsy, particularly in children. In this difficult-to-treat population, the diet exhibits remarkable efficacy with two-thirds showing significant reduction in seizure frequency and one-third becoming nearly seizure-free. There are several reasons to suspect that the ketogenic diet may also have utility as a mood stabilizer in bipolar illness. These include the observation that several anticonvulsant interventions may improve outcome in mood disorders. Furthermore, beneficial changes in brain-energy profile are noted in subjects on the ketogenic diet. This is important since global cerebral hypometabolism is a characteristic of the brains of depressed or manic individuals. Finally, the extracellular changes that occur in ketosis would be expected to decrease intracellular sodium concentrations, a common property of all effective mood stabilizers. Trials of the ketogenic diet in relapse prevention of bipolar mood episodes are warranted. The ketogenic diet may have mood-stabilizing properties
When the researchers say that anticonvulsant interventions help bipolar disorder, one example is the prescribing of sodium valproate for people who have bipolar disorder. I have a close friend with epilepsy who is familiar with both valproate and ketosis. Valproate is an acetone mimic that produces effects on the brain that are identical to ketosis. The difference is that valproate comes with a range of side effects that a ketogenic diet doesn’t have.
If valproate is used for bipolar disorder it naturally follows that ketosis would help too.
Unfortunately no studies have yet been conducted to back up the use of a ketogenic diet for bipolar disorder. Which is a dreadful shame. It has helped (as in ‘effectively cured whilst diet is maintained’) three members of my family who have bipolar tendencies but are just short of official diagnosis – something that Prozac didn’t do for their depression.
An interesting quote from a blog I came across about natural pesticides compared to artificial ones. I apologise if someone sent me a link to this, I have no idea where it came from!
Dr. Ames began rethinking this war against synthetic chemicals after thousands of chemicals had been subjected to his test. He noticed that plenty of natural chemicals flunked the Ames test. He and Dr. Gold took a systematic look at the chemicals that had been tested on rodents. They found that about half of natural chemicals tested positive for carcinogencity, the same proportion as the synthetic chemicals. Fruits, vegetables, herbs and spices contained their own pesticides that caused cancer in rodents. The toxins were found in apples, bananas, beets, Brussel sprouts, collard greens, grapes, melons, oranges, parsley, peaches — the list went on and on.
Then Dr. Ames and Dr. Gold estimated the prevalence of these natural pesticides in the typical diet. In a paper published in 2000 in Mutation Research, they conclude:
About 99.9 percent of the chemicals humans ingest are natural. The amounts of synthetic pesticide residues in plant food are insignificant compared to the amount of natural pesticides produced by plants themselves. Of all dietary pesticides that humans eat, 99.99 percent are natural: they are chemicals produced by plants to defend themselves against fungi, insects, and other animal predators.
We have estimated that on average Americans ingest roughly 5,000 to 10,000 different natural pesticides and their breakdown products. Americans eat about 1,500 mg of natural pesticides per person per day, which is about 10,000 times more than the 0.09 mg they consume of synthetic pesticide residues. Synthetic v. Natural Pesticides
One of the criticisms often levelled at meat eaters by vegetarians is that meat eating is inefficient and requires more land. Aside from the fact that we are not about to run out of land (famine in Africa and the Far East is almost always induced by wars and politics), it turns out that vegetarianism is not the most efficient use of land space:
A low-fat vegetarian diet is very efficient in terms of how much land is needed to support it. But adding some dairy products and a limited amount of meat may actually increase this efficiency, Cornell researchers suggest.
This deduction stems from the findings of their new study, which concludes that if everyone in New York state followed a low-fat vegetarian diet, the state could directly support almost 50 percent more people, or about 32 percent of its population, agriculturally. With today’s high-meat, high-dairy diet, the state is able to support directly only 22 percent of its population, say the researchers.
The study, published in the journal Renewable Agriculture and Food Systems, is the first to examine the land requirements of complete diets. The researchers compared 42 diets with the same number of calories and a core of grains, fruits, vegetables and dairy products (using only foods that can be produced in New York state), but with varying amounts of meat (from none to 13.4 ounces daily) and fat (from 20 to 45 percent of calories) to determine each diet’s “agricultural land footprint.”
They found a fivefold difference between the two extremes.
“A person following a low-fat vegetarian diet, for example, will need less than half (0.44) an acre per person per year to produce their food,” said Christian Peters, M.S. ’02, Ph.D. ’07, a Cornell postdoctoral associate in crop and soil sciences and lead author of the research. “A high-fat diet with a lot of meat, on the other hand, needs 2.11 acres.”
“Surprisingly, however, a vegetarian diet is not necessarily the most efficient in terms of land use,” said Peters.
The reason is that fruits, vegetables and grains must be grown on high-quality cropland, he explained. Meat and dairy products from ruminant animals are supported by lower quality, but more widely available, land that can support pasture and hay. A large pool of such land is available in New York state because for sustainable use, most farmland requires a crop rotation with such perennial crops as pasture and hay.
Thus, although vegetarian diets in New York state may require less land per person, they use more high-valued land. “It appears that while meat increases land-use requirements, diets including modest amounts of meat can feed more people than some higher fat vegetarian diets,” said Peters.
“The key to conserving land and other resources with our diets is to limit the amount of meat we eat and for farmers to rely more on grazing and forages to feed their livestock,” said Jennifer Wilkins, senior extension associate in nutritional sciences who specializes in the connection between local food systems and health and co-authored the study with Gary Fick, Cornell professor of crop and soil sciences. “Consumers need to be aware that foods differ not only in their nutrient content but in the amount of resources required to produce, process, package and transport them.”
According to the U.S. Department of Agriculture, the average American ate approximately 5.8 ounces of meat and eggs a day in 2005.
“In order to reach the efficiency in land use of moderate-fat, vegetarian diets, our study suggests that New Yorkers would need to limit their annual meat and egg intake to about 2 cooked ounces a day,” Peters said.
The research was supported in part by the National Research Initiative of the USDA Cooperative State Research, Education and Extension Service. Diet with dairy and a little meat may be best for planet
It’s been thought since Victorian times that it takes about two acres of land to feed a man. The Victorians ate a high quality diet of eggs, meat, dairy and bland starches. Unless we are planning to overpopulate the world to hell, we have plenty of space to feed ourselves properly.
Of course New York State is not Derbyshire. Out here in the wilds there is virtually no crop land at all. The locally produced meat is lamb, and the sheep are grazed on rocky moorland you would never be able to grow crops on. I don’t think there is a flat, rock-free piece of field between Sheffield and Leek. The organic farm local to our house in Matlock has a small field where they are actually able to grow potatoes. Probably the most calorifically efficient use of the land. Green vegetables on the other hand aren’t exactly a calorifically efficient use of land, are they?
Using cleaning sprays and air fresheners while doing housework could account for up to one in seven cases of asthma in adults, a study has found.
The modern penchant for using labour-saving cleaning sprays and air fresheners has been found to raise significantly the risk of symptoms.
Just spraying a cleaner once a week can trigger an attack, according to the research. The risk rose the more that the sprays were used.
“Frequent use of household cleaning sprays may be an important risk factor for adult asthma,” said Jan-Paul Zock, of the Municipal Institute of Medical Research, in Barcelona.
“The relative risk rates of developing adult asthma in relation to exposure to cleaning products could account for as much as 15 per cent, or one in seven, of adult asthma cases.”
Furniture sprays, glass-cleaners and air freshener sprays were associated with the highest risk of a person developing asthma after doing the housework. No link was identified between the onset of asthma and the use of cleaning products that were not sprayed.
Cleaning sprays have previously been found to be associated with an increased incidence of asthma among people who clean for a living but it is thought to be the first time the link has been made to everyday use.
Howard Stoate, a GP, MP and chairman of the asthma all-party parliamentary group, said that a link between chemicals and asthma has long been suspected.
He hoped that it might explain why countries such as New Zealand, which have low air pollution levels, have increases in asthma levels.
“There are a lot of gaps in our knowledge about asthma. Anything that fills those has to welcomed. Although asthma is on the increase worldwide no one can say why,” he said.
Asthma UK, a charity dedicated to helping the 5.2 million asthma patients in Britain, said that it was particularly interested in the finding that people without asthma go on to develop it after using the sprays.
“This report … highlights significant findings regarding the link between asthma and the use of spray cleaning products in the home,” Victoria King, of Asthma UK, said. “Although further research is needed, we do already know that air fresheners and bleach trigger symptoms in people who already have asthma.”
The international study involved 3,503 people aged 20 to 44 in ten European countries who used cleaning and air freshener sprays. Their details were first logged, on average, nine years before they were interviewed by the study team.
Two-thirds were women but only 9 per cent were, at the end of the survey period, looking after the home full time.
It was found that 6 per cent of the subjects had developed asthma symptoms and that there was a link between the disease and using sprays in the home at least once a week.
Analysis revealed that using the sprays at least once a week, as 42 per cent of the study group did, increased the risk of asthma symptoms by 30 to 50 per cent.
The study team reported: “Consistently positive associations for most asthma definitions were observed for cleaning sprays in general, and glass-cleaning, furniture and air-refreshing sprays in particular.”
Cleaning sprays and air fresheners contain chemicals such as ammonia, chlorine-releasing agents and sodium hydroxide. Researchers suggested that the chemicals being released into the air in spray form significantly increased their exposure to people.
The results of the study were published in the American Journal of Respiratory and Critical Care Medicine, by the American Thoracic Society. The researchers used data from the European Community Respiratory Health Survey, one of the largest epidemiologic studies of airway disease in the world.
A spokesman for the UK Cleaning Products Industry Association said: “The safety of consumers is the highest priority of our industries and the safety of our products is regularly checked and subject to rigorous controls, as well as stringent European legislation.” Household sprays linked to one in seven cases of asthma
Much as I respect the Truth in Labeling Campaign and similar consumer-led campaigns to remove various additives from food, they are consumer-led rather than science-led, and they do not have a full, scientific understanding of adverse reactions to foods. As a result they can talk absolute nonsense sometimes.
In the 18 years during which the Truth in Labeling Campaign has extensively studied the subject of monosodium glutamate and the many hidden forms of the reactive component of monosodium glutamate, we have concluded that there is likely more than one biochemical mechanism that causes adverse reactions in MSG-sensitive people. However, we believe that the most common reason for adverse reactions may be an intolerance for one or more of the contaminants that invariably are produced when glutamic acid is freed from protein through adulteration, processing and/or fermentation.
If a food ingredient is untreated, unprocessed and unfermented, even if it contains free glutamic acid, it will only contain L-glutamic acid because higher organisms contain only L-glutamic acid. There will be no contaminants. Consequently, MSG-sensitive people can typically eat tomatoes off of the vine even though they contain free glutamic acid (umami), providing that they are not overripe, and cheeses such as Reggiano Parmesan that are made from raw milk rather than pasteurized milk or milk that has been cultured, and that are made from rennet rather than enzymes. Give the same person a domestic cheese made from pasteurized milk, cultured milk, and/or enzymes and an adverse reaction will often follow. (possibly, any processed free glutamic acid (MSG) from fermentation of Reggiano Parmesan cheese is below the tolerance level of most MSG-sensitive people.) MSG Update – “Natural versus manufactured umami” in Wise Traditions Spring 2008
Sometimes I wonder whether the frequent apologist inserts like this that I find in Wise Traditions articles are planted there because someone has specifically asked for a “Weston A. Price Foundation friendly” answer that justifies the organisation’s many mistakes on what constitutes a healthful food that does not harm sick people.
It is certainly true that there is more than one biochemical mechanism for MSG sensitivity. Glutamate intolerance like other food chemical intolerances are multifactoral and very complex, occuring on a continuum from high tolerance to low tolerance, with different individuals affected with different symptoms.
However the idea that there is a difference between ‘natural’ and ‘unnatural’ MSG is of course, utter rubbish. In the stomach monosodium glutamate rapidly dissolves into sodium cations and glutamate anions. Glutamate is the anion of L-glutamic acid. The form glutamate occurs in – whether glutamate or glutamic acid – is not in the slightest bit important as the difference is purely a matter of electrical charge and can change at will. For all intents and purposes the form of glutamate found in artificial additives and in natural wholefoods is absolutely identical to the body.
The idea that people can react to a naturally-occurring compound is obviously a matter of confusion for the author of this article, hence in comes the theory that instead of reacting to MSG, people must be reacting to a mysterious ‘contaminant’. The idea that MSG-sensitive people can eat these naturally-occurring glutamates safely is downright wrong and very bad advice to give to glutamate sensitive individuals. I assure you that people are not reacting to mysterious artificial contaminants, they are reacting to MSG. Comprehensive elimination diets and blind capsule challenges performed by the Royal Prince Alfred Hospital have long confirmed MSG reactions. The same reactions are seen in individuals who eat foods that contain natural glutamates in isolation from other food chemicals – like peas for example, which do not contain amines or significant amounts of salicylates. Mysterious-contaminant-paranoia is a phenomenon I encounter often in individuals who are not educated on food chemical intolerance and have not sorted out what they are reacting to and what they are not reacting to.
People create all sorts of funny rules in their heads for why they might be reacting to one food and not reacting to another. Perhaps this author has discovered that he can tolerate a certain brand of cheese. Cheeses from small producers are often not aged for the same length of time or as flavour-refined as mass-produced cheeses, purely due to time and space constraints. It’s quite possible the author got lucky and found a relativley low glutamate Parmesan cheese. It’s also quite possible that people who have these strong beliefs about ‘natural’ foods being pure still have an unusual reaction but blame it on something else they have eaten. People tend to try to prove their beliefs rather than challenge them. This is called confirmation bias, and the Truth in Labeling website is full of these kinds of mistakes. Unfortunately this does nothing for their cause, as any misleading statements or distortion of the facts makes one look less trustworthy to those in the know including those on the opposing team.
Further, people who obsess over a problem with one particular food chemical rarely see the bigger picture. They may observe that they have reactions to foods when they go out to eat, and always blame this on the presence of MSG in those foods (just as people on the GFCF diet blame all of their eating out reactions on ‘hidden gluten’), when it is likely the foods contain a number of other reactive additives, and be relatively higher in other natural food flavour chemicals like amines, salicylates and SLAs. People rarely just have reactions to MSG and natural glutamates alone, usually they are also somewhat sensitive to other food chemicals due to cross-reactivity as different chemicals can trigger the same biochemical pathways in the body.
The article also contains the following contention:
In this writer’s interaction with countless MSG-sensitive people over more than 18 years, I have only communicated with three people who contended that they could tell when MSG was in a food preparation. However, their method of identification was a feeling of an electrical charge, a tingling on their tongue, rather than an actual taste.
I can taste MSG. Why can’t these people? MSG has a very strong, monotonous flavour a bit like salt. It is a strong meaty taste, but without any nuance or subtlety. I find it unpleasant as it tends to drown out all other flavours. This is probably why it is used by manufacturers, because it disguises off-flavours as a result. I can taste glutamate in processed foods, and I can taste it in old meat, cured meat, and in stocks and broths.
If it is true that these people cannot taste MSG, then the reason these people can’t taste MSG is because they don’t know what to look for. They are so used to eating foods that contain natural glutamates and other strong flavours that MSG containing foods do not taste strong or unusual to them. Fresh meat is relatively tasteless compared to the vacuum packed or hung meat most people eat these days. They are probably also used to reacting to foods that do not contain MSG but contain other reactive chemicals which do not have an MSG taste – for example, one cannot taste food colourings or histamine, and reactive SLAs have many different flavours. Only on a comprehensive food chemical elimination diet do people start to be able to taste the difference between foods that will cause adverse reactions and those that will not.
A 51-year-old postmenopausal non-Hispanic white woman was treated for a hypertensive crisis at a regional medical center in eastern Arizona. She had complained of symptoms for one week prior to admission, including light-headedness, headaches, and high blood pressure by self-measurement. Ten days prior to admission, the patient had been enrolled in a university-sponsored research trial designed to investigate the extent to which vitamin C and soy isoflavones, as supplements to a habitual diet, could provide antioxidant effects by reducing in vivo oxidative damage to cells, either alone or synergistically. During trial screening the patient reported typically consuming soy or soy products twice a week; no regular alcohol consumption; no history of hypertension or cardiovascular disease (although there was a family history of mild hypertension); no current medical supervision or care for any chronic health problems; no current use of over-the-counter or prescription medications and a routine exercise pattern of three times a week for 30-60 minutes. The participant weighed 175 pounds (79.5 kg), stood 5’8″ (1.73 m), with a body mass index of 26.7 kg/m2.Early in the research trial, the patient was randomized to receive 500 mg vitamin C plus 5 mg/kg body weight soy isoflavones. On trial day 3, the patient reported to the investigators that she felt “odd” and “light-headed.” At the time, this was not attributed to the study-related supplements because the participant reported experiencing infrequent headaches for the past 20 years. On trial days 6 and 7 of the treatment period, the participant had her blood pressure checked by an automated machine; the readings were in the range of 140-150/92-98 mmHg vs. her usual BP of 120/82 mmHg. Due to this unexpected occurrence, the investigators requested that she stop consuming the supplements and drop out of the study. The incident was reported the university’s Institutional Review Board Research Compliance Office, and the research trial was allowed to continue. Unbeknownst to the investigators, the participant chose to ignore the request to discontinue the supplements and continued to take the supplements on trial days 8 and 9. On trial day 9 she found her BP to be 159/110 mmHg. That night, she experienced an intense headache, a feeling of anxiety, and difficulty sleeping. Around midday on trial day 10, she stopped by a regional medical center to have her BP checked by a medical professional before going hiking. At that time, her BP was 226/117 mmHg; she reported that “my head feels like it is going to explode” and she was admitted to the emergency room.
One plausible explanation for the hypertensive crisis experienced by this participant is the inhibition of monoamine oxidase by the isoflavones (e.g., daidzin, daidzein) or their metabolites (e.g., equol). Rooke et al. and Gao et al. both reported that daidzin, the plant precursor of the mammalian metabolite daidzein, and some of its structural analogs can inhibit mitochondrial monoamine oxidase in vitro. Additionally, Dewar et al. reported that equol, a mammalian metabolite of daidzein, was an effective inhibitor of rat liver monoamine oxidase in vitro. Since the soy isoflavone supplements used in the research trial consisted of 63% (178 mg aglycone units/g) genistein, 28% (79.1 mg aglycone units/g) daidzein and 9% (24.6 aglycone units/g) glycitein (percentages based on aglycone units), the daidzein in the supplement may have interacted with monoamine oxidase.
Monoamine oxidase is responsible for the deamination of monoamines, including serotonin, epinephrine, norepinephrine, dopamine and tyramine. Its inhibition will cause an increase in the blood levels of these compounds. Since tyramine acts as a vasoconstrictor, an increased tyramine level will cause an increase in blood pressure [5,6]. Review of the two-day food records recorded prior to the participant’s entering the study in addition to dietary information obtained after the hypertensive event indicated the participant’s normal diet typically contained multiple tyramine-containing foods. The participant confirmed that she had consumed several tyramine-containing foods during the study, including the day before and the day of her emergency room admission (Table 2). Thus, the high dose of supplemental isoflavones [397.5 mg isoflavones (aglycone units) containing approximately 111 mg daidzein (aglycone units)], in conjunction with her typical moderate to high tyramine diet, may have contributed to a monoamine oxidase inhibitor-type reaction. Although the studies by Rooke et al., Gao et al.  and Dewar et al. suggest such a reaction might be possible, we believe this is the first report published of a possible monoamine oxidase inhibitor reaction and subsequent blood pressure spike occurring in vivo due to intake of a soy isoflavone supplement. Hypertensive crisis associated with high dose soy isoflavone supplementation in a post-menopausal woman: a case report
Excessive intake of aspartame may inhibit the ability of enzymes in the brain to function normally, suggests a new review that could fan the flames of controversy over the sweetener.
The review, by scientists from the University of Pretoria and the University of Limpopo and published recently in the European Journal of Clinical Nutrition, indicated that high consumption of the sweetener may lead to neurodegeneration. Aspartame is made up of phenylalanine (50 per cent), aspartic acid (40 per cent) and methanol (10 per cent). It is commonly used in food products for the diet or low calorie market, including soft drinks and chewing gums. It was approved for use in foods in the US and EU member states in the early 1980s.The sweetener has caused much controversy amid suspicions on whether it is entirely safe, with studies linking the ingredient and cancer in rats.
It has also previously been found that aspartame consumption can cause neurological and behavioural disturbances in sensitive individuals. Symptoms that have been reported include headaches, insomnia and seizures.
Despite strong concerns being raised from some quarters over the sweetener, both the European Food Safety Authority (EFSA) and the US Food and Drug Administration (FDA) have not changed their guidelines regarding the safety of the ingredient or intake advice.
The new review also challenges finding published last year in the journal Critical Reviews in Toxicology (Informa Healthcase) that considered over 500 studies, articles and reports conducted over the last 25 years – including work that was not published, but that was submitted to government bodies as part of the regulatory approvals process.
The earlier review concluded: “The weight of existing evidence s that aspartame is safe at current levels of consumption… No credible evidence was found that aspartame is carcinogenic, neurotoxic, or has any other adverse effect on health when consumed even at quantities many times the established ADI [acceptable daily intake] levels.”
Writing in the European Journal of Clinical Nutrition, a Nature journal, the scientists behind the new review state: “The aim of this study was to discuss the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders, and also in compromised learning and emotional functioning.”
The researchers found a number of direct and indirect changes that occur in the brain as a result of high consumption levels of aspartame, leading to neurodegeneration.
They found aspartame can disturb the metabolism of amino acids, protein structure and metabolism, the integrity of nucleic acids, neuronal function and endocrine balances. It also may change the brain concentrations of catecholamines, which include norepinephrine, epinephrine and domapine.
Additionally, they said the breakdown of aspartame causes nerves to fire excessively, which can indirectly lead to a high rate of neuron depolarisation.
The researchers added: “The energy systems for certain required enzyme reactions become compromised, thus indirectly leading to the inability of enzymes to function optimally.
“The ATP stores [adenosine triphosphate] in the cells are depleted, indicating that low concentrations of glucose are present in the cells, and this in turn will indirectly decrease the synthesis of acetylcholine, glutamate and GABA (gamma-aminobutyric acid).”
Furthermore, the functioning of glutamate as an excitatory neurotransmitter is inhibited as a result of the intracellular calcium uptake being altered, and mitochondria are damaged, which the researchers said could lead to apoptosis (cell death) of cells and also a decreased rate of oxidative metabolism.
As a result of their study, the researchers said more testing is required to further determine the health effects on aspartame and bring an end to the controversy.
Source: European Journal of Clinical Nutrition
2008, doi: 10.1038/sj.ejcn.1602866
“Direct and indirect cellular effects of aspartame on the brain”
Authors: P. Humphries, E. Pretorius, H. Naude
Thanks to a yahoo group called TaubesTalk for the following news article and abstract:
SYDNEY (AFP) – Australian scientists may have discovered how to help people lose weight without cutting back on food, a breakthrough that could pave the way for fat-burning drugs.
Researchers in Melbourne found that by manipulating fat cells in mice they were able to speed up the animals’ metabolisms.
They found that when a particular enzyme, known as angiotensin converting enzyme (ACE), was removed, mice were able to eat the same amount as other mice but burn more calories and therefore gain less weight.
Animals without the enzyme were on average 20 percent lighter than normal mice and had 50 to 60 percent less body fat, senior researcher at the Howard Florey Institute Michael Mathai said.
“It is very clear that they do have less body fat,” he told AFP.
Mathai, who is also a lecturer in nutrition at Victoria University, said the slimmer mice also appeared to have less chance of developing diabetes because they processed sugar faster than normal mice.
He said the research, to be published Tuesday in the US-based Proceedings of the National Academy of Sciences, could be used to develop drugs to assist weight loss.
Drugs which impair the action of ACE already exist and are mostly used to combat high blood pressure.
“The drugs are out there because they are used for hypertension,” he said.
“So we know their safety and their tolerability. What we don’t know is whether or not they will work in humans. And we don’t know whether it will work in all obese humans.”
Mathai said it could be a question of finding the right dosage of hypertension medication, or developing a new type of drug of the same class, to be used as weight-loss pills.
“This might be one way in which you can increase metabolic rate in combination with managing nutrition to limit the intake of calories,” he said.
Mathai said the research, conducted at the Howard Florey Institute, Victoria University, La Trobe University, Deakin University, the Baker Institute and the University of Melbourne, was yet to pinpoint why the genetic manipulation led to weight loss.
“Because we deleted the gene, the gene is gone from the whole body, that means that it is gone from all tissues including the brain,” he said.
“And so we don’t know whether it’s a direct effect of the deficiency in the tissue or whether it’s something coming from the brain.” Australian scientists report weight loss breakthrough
And the abstract:
Angiotensin II (AII), acting via its G-protein linked receptor, is an important regulator of cardiac, vascular, and renal function. Following injection of AII into rats, we find that there is also a rapid tyrosine phosphorylation of the major insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) in the heart. This phenomenon appears to involve JAK2 tyrosine kinase, which associates with the AT1 receptor and IRS-1/IRS-2 after AII stimulation. AII-induced phosphorylation leads to binding of phosphatidylinositol 3-kinase (PI 3-kinase) to IRS-1 and IRS-2; however, in contrast to other ligands, AII injection results in an acute inhibition of both basal and insulin-stimulated PI 3-kinase activity. The latter occurs without any reduction in insulin receptor or IRS phosphorylation or in the interaction of the p85 and p110 subunits of PI 3-kinase with each other or with IRS-1/IRS-2. These effects of AII are inhibited by AT1 receptor antagonists. Thus, there is direct cross-talk between insulin and AII signaling pathways at the level of both tyrosine phosphorylation and PI 3-kinase activation. These interactions may play an important role in the association of insulin resistance, hypertension, and cardiovascular disease. Cross-talk between the insulin and angiotensin signaling systems
I think this may be why low carbohydrate diets help so many people with food chemical intolerance. Lower your insulin levels, and I bet you lower your ACE output.