Monday, April 30, 2007

Brain scans pinpoint cannabis mental health risk | Top News�|�

Brain scans pinpoint cannabis mental health risk|Top News|

By Ben Hirschler

LONDON (Reuters) - Brain scans showing how cannabis affects brain function may help explain why heavy consumption of the drug triggers psychosis and schizophrenia in a small number of people, scientists said on Monday.

Psychiatrists are increasingly concerned about the mental health impact of smoking large amounts of modern super-strength marijuana, or skunk, particularly among young people.

Until now, the mechanism by which cannabis works on the brain has been a mystery but modern scanning techniques mean experts can now detect its impact on brain activity.
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Professor Philip McGuire and Zerrin Atakan of London's Institute of Psychiatry said their work using magnetic resonance imaging, or MRI, showed patients given the active cannabis compound tetrahydrocannabinol (THC) had reduced function in the inferior frontal cortex brain region.

This area is associated with controlling inappropriate emotional and behavioral responses to situations.

"What THC seems to be doing is switching off that part of the brain, and that was associated with how paranoid people became," McGuire told reporters.

Their research will be presented at a two-day International Cannabis and Mental Health Conference at the Institute of Psychiatry this week.


Similar findings from other teams also highlight the link between THC dose and the risk of schizophrenia-like symptoms, conference organizer Professor Robin Murray said.

"It's no longer a contentious issue. The expert community, by and large, accepts that cannabis contributes to the onset of psychotic symptoms in general and the severe form of psychosis, schizophrenia," he said.

Brain health dramatically improved by intake of omega-3 fatty acids and fish oils

Brain health dramatically improved by intake of omega-3 fatty acids and fish oils

It's no secret that long-term diet and nutrition choices have an effect on the way we look and feel; but new studies show that nutrition can also affect the way we think. As it turns out, there really is such a thing as “food for thought.”

It may seem strange that what we put in our stomachs can have such a powerful effect on what goes on in our minds, but research is increasingly showing that emotional, mental and psychiatric disorders like depression, bipolar disorder and schizophrenia may more likely be the result of dietary deficiencies than genetic predispositions. The same is true of people who struggle with memory loss, have trouble learning new tasks, have Alzheimer’s disease or simply suffer from a lot of blue moods. The dietary deficiency that tends to frequently show up in these patients is a lack of omega-3 oils -- abundant fatty acids found in cold-water fish like salmon, herring and cod.

Omega-3s and brain health
The omega-3 fatty acid known as docosahexaenoic acid (DHA) is an important ingredient for optimal brain function. Earl Mindell, RPh PhD, writes in Earl Mindell's Supplement Bible, “There's a reason why fish is known as brain food. It is a rich source of docosahexaenoic acid (DHA), a fatty acid that is found in high concentration in the gray matter of the brain. DHA is instrumental in the function of brain cell membranes, which are important for the transmission of brain signals.” By making cell membranes more fluid, omega-3 fatty acids, especially DHA, improve communication between the brain cells, according to Mind Boosters author Dr. Ray Sahelia. As a result, lack of omega-3 in the body can cause a communication breakdown in the brain, which is probably the last place you'd want such a breakdown to happen.

Omega-3 fatty acids are so important to the development and proper maintenance of the brain that “some scientists even postulate that it was the ingestion of omega-3 EFAs that allowed the brain to evolve to the next stage in human development,” according to Superfoods Rx authors Steven G. Pratt and Kathy Matthews. While omega-3s were abundant in our diets before the 20th century, they are now seriously lacking. The Editors of FC&A Medical Publishing write in The Folk Remedy Encyclopedia, “Just like a machine, your brain needs oil -- in the form of omega-3 and omega-6 fatty acids -- to run smoothly. Unfortunately, the average diet doesn't usually contain the right balance of these fatty acids. If you eat a typical modern diet, you probably get plenty of omega-6 through corn, soybean, and other oils in processed food. But omega-3 oils, which are just as important, are often missing.”

Schizophrenia, Syndrome X, and Omega-3 Fatty Acids :: psychiatry online

1926-a.pdf (application/pdf Object)

Schizophrenia, Syndrome X,
and Omega-3 Fatty Acids
TO THE EDITOR: In an interesting study, Martina C.M. Ryan,
M.B., M.R.C.Psych., et al. (1) found an increased prevalence of
impaired glucose tolerance and insulin resistance in patients
with drug-naive, first-episode schizophrenia in relation to
healthy comparison subjects. This finding is in line with the
results of a recent review showing that features of the metabolic
syndrome X are more common in subjects with schizophrenia
than in the general population (2). Dr. Ryan and colleagues
discussed the influence of diet (1), but we believe that
they omitted the possible role of polyunsaturated fatty acids
of the omega-3 and omega-6 series, in particular, eicosapentaenoic
acid and arachidonic acid. Substantial evidence suggests
that impaired polyunsaturated fatty acid metabolism is
related to both schizophrenia and the metabolic syndrome X.
In recent reviews, low consumption of omega-3 polyunsaturated
fatty acid was concluded to be associated with hypertriglyceridemia,
cardiovascular disease, and probably also to
insulin resistance and type 2 diabetes (3–5). Of interest, lowered
omega-3 polyunsaturated fatty acid levels have also
been reported in the erythrocytes of drug-naive psychotic patients
(6) and in medicated young schizophrenic patients in
comparison with normal comparison subjects (7). Furthermore,
placebo-controlled trials have found eicosapentaenoic
acid to be effective in schizophrenia, depression, and borderline
personality disorder (8–10).

Fatty Acid Deficiencies and ADD

Fatty Acid Deficiencies and ADD

A Purdue University study showed that kids low in Omega-3 essential fatty acids are significantly more likely to be hyperactive, have learning disorders, and to display behavioral problems. Omega-3 deficiencies have also been tied to dyslexia, violence, depression, memory problems, weight gain, cancer, heart disease, eczema, allergies, inflammatory diseases, arthritis, diabetes, and many other conditions. Over 2,000 scientific studies have demonstrated the wide range of problems associated with Omega-3 deficiencies. The American diet is almost devoid of Omega 3's except for certain types of fish. In fact, researchers believe that about 60% of Americans are deficient in Omega-3 fatty acids, and about 20% have so little that test methods cannot even detect any in their blood.

Your brain is more than 60% structural fat, just as your muscles are made of protein and your bones are made of calcium. But it's not just any fat that our brains are made of. It has to be certain types of fats, and we no longer eat these types of fats like we used to. Worse, we eat man-made trans-fats and excessive amounts of saturated fats and vegetable oils high in Omega-6 fatty acids, all of which interfere which our body's attempt to utilize the tiny amount of Omega-3 fats that it gets.

Other parts of our bodies also need Omega-3 fatty acids. Symptoms of fatty acid deficiency include a variety of skin problems such as eczema, thick patches of skin, and cracked heels.


Hunter/gatherers ate greens with lots of Omega-3's. We know this because scientists have actually tested many of the plants and animals eaten by existing and past hunter/gatherer groups. These have been replaced primarily with grains, which contain the wrong kinds of fats.

More Detail Than You May Want to Know: EPA, DHA, and the Omega-3 family of Eicosanoids are important types of Omega-3 fatty acids. Normally our body can manufacture all of these products if it has plenty of the parent Omega-3 fatty acid called Alpha-Linolenic Acid (ALA) found naturally in green leafy vegetables, flax, flaxseed and canola oil, walnuts and Brazil nuts. (Note: DHA is not to be confused with DHEA, a popular hormonal supplement).

Our bodies convert ALA to EPA; EPA to DHA; and DHA to Omega-3 Eichosanoids. There are many things that can interfere with this process, especially vegetable oils in the diet. Note that it is possible to acquire EPA and DHA directly by eating fish oil, certain eggs, or by taking supplements. Fatty fish contain plenty of both substances. Plenty of studies have shown that fish-eating cultures have much better health, including mental health.

DHA is particularly important for brain functions. Scientists have discovered that severely depressed people are lower in DHA, and the more depressed they are, the less DHA they have. One ancient remedy for depression was to feed the patient animal brains, now known to be extremely high in DHA and Omega-3 fatty acids. Incidentally, alcohol is known to deplete DHA stores extremely rapidly.

While the body can theoretically manufacture its own DHA out of the parent ALA fatty acid, things can interfere with this conversion. The most important problem is an excess of Omega-6 fatty acids in the bloodstream, which use the same enzymes for a similar type of conversion. This is why it is extremely important not to have too many Omega-6 fats in your diet (the vegetable oils like sunflower and soybean oil). Other problems might inhibit the conversion process, such as a deficiency in certain vitamins and minerals.

Infants who are fed formula in the United States receive almost no Omega-3's, while infants who are breast fed thrive on milk rich in DHA (the amount depends on the mother's diet). Researchers have found that infants who are fed formulas enriched with Omega-3's or who are breast fed do better visually and intellectually.

Incidentally, pregnant women experience a major loss in DHA as their DHA is rerouted to the fetus. This may be one reason depression is so common after child birth.

Why I think of trans fats as "plastic": Trans-fats are manufactured by bubbling hydrogen gas through super-heated vegetable oil in the presence of nickel. The fat molecules are changed chemically so they are not very reactive, making them good for frying and for sitting on the grocery store shelf a very long time. The electrical properties of these fats are changed as well as their shape.

It's been said that margarine, a trans-fat, is one electron away from plastic. I don't know if that's true or not, but the image has stuck with me. These man-made trans-fats are being used by our bodies as building material, but they're all wrong. Imagine your brain being replaced molecule by molecule with plastic instead of fat. And you wonder why you can't remember where you left your keys.

Don't eat these fats! Put them in the same category as arsenic or PCBs. Plastics that will invade your brain. I may be exaggerating just a bit, but I'm serious about the dangers of trans-fats.

Read your labels. Avoid any product that has oils which have been "hydrogenated" or "partly hydrogenated." You'll be amazed when you see how much of this garbage you've been eating. It's in the majority of prepared foods including breads, crackers potato chips, and cookies. Mayonnaise is a glob of trans-fat. When eating out, your worst foods are deep fried foods (including french fries), donuts, and muffins.

Why it's Bad to Eat Too Many Vegetable Oils: That's right, one more things is bad for you! Vegetable oils contains Omega-6 fatty acids, and we eat lots of these. Sunflower oil, soybean oil, safflower oil and most other vegetable oils contain lots of Omega-6 fatty acids. This is bad for a couple of reasons:

1. Omega-6 fatty acids feed tumors. Cancer growth rates nearly explode in the presence of a high level of Omega-6 fatty acids (which many of us have). On the other hand, Omega-3 fatty acids slow the growth rate of tumors significantly, or even decrease their size.

2. The enzymes used to break parent Omega-6 fatty acids down into various compounds are shared by Omega-3 fatty acids. If you have a lot of Omega-6 fatty acids in your blood stream and only a small amount of Omega-3 fatty acids, the enzymes will probably be used up by the Omega-6 fatty acids, and you will be unable to manufacture DHA out of ALA.

3. Omega-6 fatty acids are broken down into substances which promote inflammation and other problems while Omega-3 fatty acids are broken down into substances that reduce inflammation. Therefore, there should be a balance between the two oil. The typical ratio in the U.S. is currently 22:1 in favor of the Omega-6 fatty acids. The ideal ratio is between 1:1 and 4:1.

Neurobehavioral aspects of omega-3 fatty acids: possible mechanisms and therapeutic value in major depression Alternative Medicine Review - Find Artic

Neurobehavioral aspects of omega-3 fatty acids: possible mechanisms and therapeutic value in major depression Alternative Medicine Review - Find Articles

Omega-3 fatty acids are an essential component of CNS membrane phospholipid-acyl chains and, as such, are critical to the dynamic structure of neuronal membranes. (3) DHA is continuously secreted by astrocytes, bathing the neuron in omega-3 fatty acid. (58) The binding of serotonin to the astroglial 5HT2A receptor can mobilize DHA to supply the neuron. (59) Alterations in membrane lipids can alter function by changing fluidity. Proteins are embedded in the lipid bi-layer and the conformation or quaternary structure of these proteins appears to be sensitive to the lipid microenvironment. The proteins in the bi-layer have critical cellular functions, acting as receptors, enzymes, and transporters. (60-64) In addition, EFAs can act as sources for second messengers within and between neurons. (65) An optimal fluidity is required for neurotransmitter binding and the signaling within the cell. (66) Omega-3 fatty acids can alter neuronal fluidity by displacing cholesterol from the membrane. (67)

It is not surprising there are functional consequences when animals are fed a diet deficient in omega-3 fatty acids (Table 3). Reduction in omega-3 intake (in the form of ALA) results in a reduction of omega-3 content throughout the brain cells and organelles along with a compensatory rise in omega-6 fatty acid content. This alteration is accompanied by a 40-percent reduction in the [Na.sup.+][K.sup.+] ATPase of nerve terminals, an enzyme that controls ion transport produced by nerve transmission and that consumes half the energy used by the brain. (63) There is also a 20-percent reduction in 5'-nucleotidase activity, a decrease in fluidity in the surface polar part of the membrane, (63) and a significant reduction in the cell body size of the hippocampal CA1 pyramidal neuron. (68) A 30-percent reduction in the average densities of synaptic vesicles in the terminals of the hippocampal CA1 region has also been observed as a result of an omega-3 deficiency combined with a learning task. (69) Deficiency of omega-3s also results in a 30-35 percent reduction in phosphatidylserine (PS) in the rat brain cortex, brain mitochondria, and olfactory bulb. (70) On the other hand, fish oil supplemented to rats can increase PS composition of the cerebral membrane. (71) This is an interesting finding, given research showing that PS has antidepressant activity in adults. (72,73) PS can activate various enzymes, including protein kinase C, [Na.sup.+][K.sup.+] ATPase, and tyrosine hydroxylase, as well as regulating calcium uptake. It is therefore suggested that altering PS in cerebral membranes can alter neurotransmission. (71)

A number of studies have specifically examined the effect of an omega-3 deficient diet on dopamine and serotonin levels in animals. Animals on such a diet have a reduction in the dopaminergic vesicle pool (74) along with a 40-60 percent decrease in the amount of dopamine in the frontal cortex and an increase in the NA, (75,76) alterations strikingly similar to the animal models of depression described above. Although overall dopamine levels in the NA are higher in an omega-3 deficiency and the animal model of depression, function of the NA-dopaminergic system appears to be abnormal in both. In an omega-3 deficiency, the release of dopamine from the vesicular storage pool under tyramine stimulation is 90-percent lower than in rats receiving an adequate omega-3 intake. (74) In the animal model of depression, although overall NA-dopamine levels are higher, the extracellular levels of dopamine in the NA are lower than normal controls and do not respond to normal serotonin stimulation. (77)

Omega-3 is Essential to the Human Body

Omega-3 is Essential to the Human Body

A Purdue University study has showed that kids low in Omega-3 essential fatty acids are significantly more likely to be hyperactive, have learning disorders, and to display behavioral problems. Omega-3 deficiencies have also been tied to many conditions, including the following:
dyslexia violence
depression memory problems
weight gain cancer
heart disease eczema
allergies inflammatory diseases
arthritis diabetes

Over 2,000 scientific studies have demonstrated the wide range of problems associated with Omega-3 deficiencies. The American diet is almost devoid of Omega 3's, except for certain types of fish.

In fact, researchers believe that about 60% of Americans are deficient in Omega-3 fatty acids, and about 20% have so little that test methods cannot even detect any in their blood.

The human brain is more than 60% structural fat, just as your muscles are made of protein and your bones are made of calcium. But it's not just any fat that our brains are made of. It has to be certain types of fats, and we no longer eat these types of fats like we used to.

Worse, we eat man-made trans-fats and excessive amounts of saturated fats and vegetable oils high in Omega-6 fatty acids, all of which interfere which our body's attempt to utilize the tiny amount of Omega-3 fats that it gets.

Other parts of our bodies also need Omega-3 fatty acids. Symptoms of fatty acid deficiency include a variety of skin problems such as eczema, thick patches of skin, and cracked heels.

To get the necessary Omega-3 fatty acids, you must eat meat that is allowed to "free-range", or in the case of cattle, to be grass-fed. You cannot buy this grass-fed beef at your local grocery store.

But you can buy grass-fed beef online, shipped overnight to your door, at Grassfed Organics.

Signs of Fatty Acid Imbalance (from the book "Smart Fats")
Dry skin Alligator skin "Chicken skin" on back of arms
Dandruff Lowered immunity Dry eyes
Frequent urination Fatigue Poor wound healing
Irritability Dry, unmanageable hair Frequent infections
Attention deficit Hyperactivity Learning problems
Soft nails Brittle, easily frayed nails Patches of pale skin on cheeks
Allergies Excessive thirst Cracked skin on heels or fingertips

Imagine your brain conducting some routine maintenance on your dopamine and serotonin receptors (implicated in both ADD and mood disorders). These receptors are composed of an Omega-3 fatty acid called DHA.

If you don't have much DHA in your blood, man-made trans-fat molecules may be used as a construction material instead. But trans-fats (hydrogenated oils) are shaped differently than DHA: they are straight while DHA is curved.

The dopamine receptor becomes deformed and doesn't work very well. Repeat this scenario day after day, year after year, and you could wind up with problems like depression and problems concentrating. This problem is most severe for a child whose brain is still developing.

A lack of highly unsaturated fats is particularly noticeable in connection with brain and nerve functioning. An adjustment in diet to one with oil and protein contents high in unsaturated fats brings the best results in children.

Omega 3 Resource Center

Omega 3 Resource Center

Benefits of Omega-3's

-Brain development and growth
-Behavior regulation
-Delays age-associated deterioration in serotonin and dopamine systems (memory, attention, cognition, behavior)
-Increased density of serotonin and dopamine receptors in the brain and nervous system.
-May increase endogenous dopamine levels by 40-75%

-Reduces anxiety
-Delays the progression of degenerative eye conditions such as retinal detachment and macular degeneration.

May have therapeutic benefit for:

--Alzheimer's disease


--attention deficit-hyperactivity disorder

--bipolar disorder

--chronic fatigue syndrome

--chronic pain


--diabetic neuropathy


--insulin resistance

--irritable bowel syndrome

--memory problems

--migraine headaches

--reproductive problems


--thyroid hormone function

omega-3 omega-6 | essential fats

omega-3 omega-6 | essential fats

Nature or nurture? There is an age-old debate about whether performance is primarily ‘in your genes’ or develops in response to training. The common consensus is somewhere in between: that we inherit a set of genes which determine our potential, but it’s our training and nutrition that allow us to reach that potential. However, new evidence suggests this fatalistic approach to our genetic make-up is misplaced; fascinating research is emerging from the world of nutrition to suggest that essential fats in our diet can exert significant control over key metabolic genes in our cells, particularly those involved with fat storage, fat burning and glycogen synthesis. In plain English this means that, while you might not be born with the ideal genetic make-up for your chosen sport or event, correct fatty acid nutrition could help to ‘reprogramme’ your genetic code!

There are two principal essential fats: alpha-linolenic acid (sometimes called omega-3) and linoleic acid (omega-6). These two fats are essential because their chemical structure means that they can be used to make hormone-like substances called prostaglandins, which go on to regulate a host of other functions in the body. However, these fats cannot be synthesised by the body, which is why we rely on getting them ‘ready-made’ from the diet.

The complex structure of the fats also makes them very chemically reactive; put simply, they readily undergo chemical change and ‘fall apart’ when exposed to heat, light or air. This means that storing, cooking or processing foods rich in essential fatty acids (EFAs) inevitably leads to a loss in nutritional value. The problem is that we need more of these EFAs per day than any other single nutrient – measured in tablespoons, not milligrams! And the task of obtaining enough of them in unadulterated form in today’s world of tinned, dried, frozen, fast and processed food is a major challenge.


The role of EFAs in human nutrition has long been recognised; dietary omega-3 and omega-6 fats are needed for the synthesis of prostaglandins, which help regulate certain aspects of metabolism, such as blood viscosity, inflammatory processes, blood cholesterol and fat levels, and water balance. Additionally, it is now widely accepted that a low ratio of EFAs to saturated fatty acids is associated with an increased risk of coronary heart disease (CHD).
New findings on EFAs and obesity

However, more recent research on EFA nutrition has yielded some intriguing new findings. One of these is that increased intakes of these essential fats appear to reduce tissue levels of triglycerides (stored fats), which improves the sensitivity of insulin (the hormone that drives amino acids and glucose into muscle cells), so reducing the risk of obesity and CHD(1). Initially, these beneficial effects of EFAs were thought to be due to changes in the fatty acid composition of the cell membranes, leading to subsequent alterations in hormonal signalling. However, when researchers dug a little deeper it became apparent that something else was going on.

They discovered that these fats, particularly those of the omega-3 family, play essential roles in the maintenance of energy balance and glucose metabolism. In particular, they observed a phenomenon known as ‘fuel partitioning’, whereby dietary EFAs were able to direct glucose (from digested carbohydrates) towards glycogen storage while at the same time directing other fatty acids in the body away from triglyceride synthesis (ie fat storage) and towards fatty acid oxidation! In addition, these studies suggested that omega-3 fatty acids have the unique ability to enhance thermogenesis (the burning of excess fat to produce heat), thereby reducing the efficiency of body fat deposition(2-7). In simple terms, this fuel partitioning phenomenon appears to conserve carbohydrate while simultaneously shedding fat – exactly what most athletes would give their right arm for!

Further study of this fuel partitioning effect led to the discovery that the EFAs were somehow boosting the production of enzymes involved with fatty acid oxidation (such as carnitine palmitoyltransferase, which helps transport fatty acids into the mitochondria of the cells for burning) while at the same time down-regulating the production of enzymes involved in fat synthesis, such as fatty acid synthase (8-12).

At first it was assumed that this ‘up-regulation’ of fat burning/glycogen synthesising enzymes and ‘down-regulation’ of fat storage enzymes occurred through hormonal signalling; in other words that the EFAs were somehow altering the cell membranes, causing a change in chemistry and leading to altered enzyme production by the genes responsible. However, these changes in gene transcription occur too quickly to be explained in this way; there seemed to be a much more direct effect. And eventually researchers discovered, to their amazement, that these EFAs were able to control gene expression directly via a steroid-like substance called PPARĪ±.

PPARĪ± is known as a ‘lipid-activated transcription factor’. This means it switches on key genes by binding to DNA, but only when it has been activated itself by binding to lipids such as EFAs. And it turns out that the genes it switches on are precisely those which code for enzymes involved in fat burning! Not only was this a remarkable discovery in itself, it was also the first time science had clearly demonstrated that nutritional components of the diet can exert direct control over the function of genes.

Johann Hari: How multiculturalism is betraying women - Independent Online Edition > Johann Hari

Johann Hari: How multiculturalism is betraying women - Independent Online Edition > Johann Hari

Johann Hari: How multiculturalism is betraying women
It would be easy to congratulate ourselves on our tolerance of the fanatically intolerant
Published: 30 April 2007

Do you believe in the rights of women, or do you believe in multiculturalism? A series of verdicts in the German courts in the past month, have shown with hot, hard logic that you can't back both. You have to choose.

The crux case centres on a woman called Nishal, a 26-year-old Moroccan immigrant to Germany with two kids and a psychotic husband. Since their wedding night, this husband beat the hell out of her. She crawled to the police covered in wounds, and they ordered the husband to stay away from her. He refused. He terrorised her with death threats.

So Nishal went to the courts to request an early divorce, hoping that once they were no longer married he would leave her alone. A judge who believed in the rights of women would find it very easy to make a judgement: you're free from this man, case dismissed.

But Judge Christa Datz-Winter followed the logic of multiculturalism instead. She said she would not grant an early divorce because - despite the police documentation of extreme violence and continued threats - there was no "unreasonable hardship" here.

Why? Because the woman, as a Muslim, should have "expected" it, the judge explained. She read out passages from the Koran to show that Muslim husbands have the "right to use corporal punishment". Look at Sura 4, verse 34, she said to Nishal, where the Koran says he can hammer you. That's your culture. Goodbye, and enjoy your beatings.

This is not a freakish exception. Germany's only state-level Minister for Integration, Armin Laschet, says this is only "the last link, for the time being, in a chain of horrific rulings handed down by the German courts".

The German magazine Der Spiegel has documented a long list of these multicultural verdicts. Here are just a few:

A Lebanese-German who strangled his daughter Ibthahale and then beat her unconscious with a bludgeon because she didn't want to marry the man he had picked out for her was sentenced to mere probation. His "cultural background" was cited by the judge as a mitigating factor.

A Turkish-German who stabbed his wife Zeynep to death in Frankfurt was given the lowest possible sentence, because, the judge said, the murdered woman had violated his "male honour, derived from his Anatolian moral concepts". The bitch. A Lebanese-German who raped his wife Fatima while whipping her with a belt was sentenced to probation, with the judge citing his ... you get the idea.

Their victims are forced to ask - like Soujourner Truth, the female slave who famously challenged early women's rights activists to consider black women as their sisters - "Ain't I a woman?"

In Germany today, Muslim women have been reduced to third-class citizens stripped of core legal protections - because of the doctrine of multiculturalism, which says a society should be divided into separate cultures with different norms according to ethnic origin.

In our genes -- Harpending and Cochran 99 (1): 10 -- Proceedings of the National Academy of Sciences

In our genes -- Harpending and Cochran 99 (1): 10 -- Proceedings of the National Academy of Sciences

The D4 dopamine receptor (DRD4) locus may be a model system for understanding the relationship between genetic variation and human cultural diversity. It has been the subject of intense interest in psychiatry, because bearers of one variant are at increased risk for attention deficit hyperactivity disorder (ADHD) (1). A survey of world frequencies of DRD4 alleles has shown striking differences among populations (2), with population differences greater than those of most neutral markers. In this issue of PNAS Ding et al. (3) provide a detailed molecular portrait of world diversity at the DRD4 locus. They show that the allele associated with ADHD has increased a lot in frequency within the last few thousands to tens of thousands of years, although it has probably been present in our ancestors for hundreds of thousands or even millions of years.


There are at least two hypotheses to explain the world distribution of 7R. The first, due to Chen et al. (2), is that it is a dispersal morph. They argue that the allele increases the likelihood that its bearers migrate. As modern humans colonized the earth, bearers of 7R were more likely to be movers so that populations far away from their ancient places of origin have, in effect, concentrated 7R. The world high frequencies in South America reflect the great distance of South America from the original human homeland: similarly migrations from China led to the presence of the allele in southeast Asian and Pacific populations, whereas none remained in China. This hypothesis does not account for the apparent long persistence at low frequency of 7R in human ancestors before the population movements occurred that were responsible for population frequency differences.

The second hypothesis is that 7R bearers enjoy a reproductive advantage in male-competitive societies, either in competition for food as children or in face-to-face and local group male competition. Societies in which this advantage would be present were rare before the spread of agriculture, but common after it. This hypothesis requires a brief review of human ecological history. We acknowledge our abuse of detail and of ethnographic diversity in the summary that follows.

Modern humans were successful colonizers of much of the Old World by 40,000 years ago. They lived by hunting and gathering and, later, by agriculture. The archaeological evidence suggests that agriculture appears soon after the end of the Pleistocene, but the antiquity of occasional tropical gardening is not known. Where human densities were low, agriculture was most often extensive, involving shifting cultivation of gardens that were then left fallow for years. Increasing human densities led to agricultural intensification with ever higher inputs of labor to ever scarcer land, resulting in plow agriculture and organized irrigation.

Among most hunting and gathering people both sexes work to provision offspring; in particular males allocate much of their reproductive effort to parental effort. These "dad" societies contrast with "cad" societies in which males allocate reproductive effort to mating effort, that is to competition with other males for access to females.

The general theory of the "war between the sexes" is described by Dawkins (11), whereas the human version of it is described in a landmark paper by Whiting and Whiting (12) and elaborated by others (13, 14). In general, in societies where males are dads, men and women live together with their offspring; they eat and sleep together; the males are not particularly gaudy; and they do not make fancy weapons and art. Pair bonds are durable, divorce rates are low; and nuclear families are the primary context for care of children.

In cad societies, the public relations between men and women are aloof; men and women often do not eat and sleep together; and males are involved in personal adornment, fancy and decorative weapons and art, and local raiding and warfare. In many such groups, for example, men eat and sleep in a men's house rather than with families. Marriages are not durable, and children from an early age are likely to be left to the care of siblings and other children. The latter societies are called "peer-rearing" societies in the literature, whereas dad societies are more often "parent-rearing" societies.

Most foraging people are dad societies, the exceptions being cases where there are periodic rich resource streams like salmon runs on the North American northwest coast. There is some controversy in the literature about whether apparently parental males in dad societies are really parental or whether they are instead engaged in many subtle forms of male competition and mate guarding (15). At any rate the end result is that men work and provide food to children.

Friday, April 27, 2007

Hacking Your Body's Bacteria for Better Health -

Hacking Your Body's Bacteria for Better Health -

Modern humans are bacteria-killing machines. We assassinate microbes with hand soap, mouthwash and bathroom cleaners. It feels clean and right.

But some scientists say we're overdoing it. All this killing may actually cause diseases like eczema, irritable bowel syndrome and even diabetes. The answer, they say, is counterintuitive: Feed patients bacteria.

"Probiotics (pills containing bacteria) have resulted in complete elimination of eczema in 80 percent of the people we've treated," says Dr. Joseph E. Pizzorno Jr., a practicing physician and former member of the White House Commission on Complementary and Alternative Medicine Policy. Pizzorno says he's used probiotics to treat irritable bowel disease, acne and even premenstrual syndrome. "It's unusual for me to see a patient with a chronic disease that doesn't respond to probiotics."

Clinical trial data on probiotics is incomplete, but there are many indications that hacking the body's bacteria is beneficial.

In sheer numbers, bacterial cells in the body outnumber our own by a factor of 10, with 50 trillion bacteria living in the digestive system alone, where they've remained largely unstudied until the last decade. As scientists learn more about them, they're beginning to chart the complex symbiosis between the tiny bugs and our health.

"The microbes that live in the human body are quite ancient," says NYU Medical Center microbiologist Dr. Martin Blaser, a pioneer in gut microbe research. "They've been selected (through evolution) because they help us."

And it now appears that our daily antibacterial regimens are disrupting a balance that once protected humans from health problems, especially allergies and malfunctioning immune responses.


, people can end up with unbalanced immune systems.

"Many of the most difficult problems in medicine today are chronic inflammatory diseases," says Blaser. "These include rheumatoid arthritis, lupus, atherosclerosis, eczema and multiple sclerosis. One possibility is that they're autoimmune or genetic diseases. The other possibility is that they are physiological responses to changes in microbiota."

Blaser's specialty is Helicobacter pylori, a strain once common in every human stomach but now rare in the West. Its disappearance may have benefits: H. pylori-related inflammation is associated with peptic ulcers and some stomach cancers. However, H. pylori also reduces acid reflux, which in turn is associated with asthma and esophageal cancers.

H. pylori's decline, says Blaser, correlates with a rapid rise in those afflictions. H. pylori deficiency may also contribute to obesity, he says, because the bacteria help regulate production of two hormones, ghrelin and leptin, that affect metabolism and appetite.

Low levels of Bacteroidetes have also been linked to obesity. Studies indicate that bacterial imbalances are associated with irritable bowel syndrome, post-surgical infections and type 1 diabetes.

The health-food movement has moved ahead with probiotics without regard for clinical trial results. Women commonly use supplements like acidophilus to treat yeast infections. Other probiotics are making their way into products such as Kashi Vive cereal "to help you care for your digestive system" and Dannon's Activia yogurt, which in its first year boasted more than $100 million in sales. But scientists say over-the-counter probiotics are of inconsistent quality.

Pizzorno, for example, buys his probiotics from companies that sell directly to doctors. Consumer probiotics don't always contain medically recognized bacterial strains, he said, and often the bacteria they contain are dead.

"Most of the companies don't have any research ongoing at all," says Stig Bengmark, a University of London hepatologist. "They buy cheap bacteria from yogurt companies and say it's good, but it's never proven."

To more precisely hack the gut bacteria, Blaser calls for a Gut Genome Project, modeled after the Human Genome Project. It's a daunting task: The human genome, mapped to great fanfare but still dimly understood, contains a tenth of the genes believed to be in our gut bacteria. But though difficult, such research could prove vital.

Gut bacteria affect obesity :: Entrez PubMed

Entrez PubMed

An obesity-associated gut microbiome with increased capacity for energy harvest.

Center for Genome Sciences, Washington University, St. Louis, Missouri 63108, USA.

The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance. Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity.

Remember this the next time someone tells you weight loss is just a matter of burning more calories than you consume. There's a ton more to the story than that- including, why are some people more hungry than others. I think carbs are a big part of that equation.

Sci-Tech Today | Genetic Risk Factors for Diabetes Found

Sci-Tech Today | Genetic Risk Factors for Diabetes Found

Scientists have found clusters of new gene variants that raise the risk of Type 2 diabetes -- and how the researchers did it is as important as what they found.

In one of the largest studies yet of human genetic variability, the scientists tested the DNA of more than 32,000 people in five countries to pin down spots that harbor genetic risk factors for this complicated killer.

This type of research -- called a "genome-wide association" study -- promises to usher in a new era of genetics. Most breakthroughs so far have come from finding a mutation in a single gene that causes illness. But some of the world's most common killers, such as heart disease and diabetes, are caused by complex interactions among numerous genes and modern lifestyles -- and teasing out the genetic culprits until now has been almost impossible.

"We have been for all of the last decade or more looking under the lamppost to try to find those genes ... and lots of times the lamplight was not actually where we wanted it," said Dr. Francis Collins, genetics chief at the National Institutes of Health, a co-author of the research unveiled Thursday.

This new approach "allows us to light up the whole street, and look what we find."

What? Four previously unknown gene variants that can increase people's risk of Type 2 diabetes, and confirmation that six other genes play a role, too.

Gene explains why people are night owls

Gene explains why people are night owls :: Telegraph UK

A genetic mutation called the "after-hours gene" may explain why some people are night owls, it is revealed in Science journal today.

It could also hold clues for pharmacologists working to develop drugs to help people adjust to shift work or jet lag. There are further implications for the study of causes of some psychiatric disorders.

The altered gene, named "after hours" or Afh, is a variant of a gene called Fbxl3, which had not been linked to the body clock that keeps our metabolism, digestion and sleep patterns in tune with the rising and setting of the sun.


Pharmaceutical companies are already beginning to study this class of proteins as potential drug targets.

By monitoring when and how often the mice chose to run on an exercise wheel the team spotted a change in some of the animals’ normal rhythms.

Instead of following the typical 24 hour pattern, some of the mice had body clocks that stretched to up to a 27 hour day.

Closer study of the DNA from the mice then revealed that those on a 27-hour-cycle had the after hours version of the Fbxl3 gene, one of a large family that controls the breakdown of specific proteins within body cells.

Dr Patrick Nolan, of the MRC Mammalian Genetics Unit, who led the study said: ‘‘The internal body clocks of mice with the after hours gene run on a longer cycle than mice that have a normal copy of the gene, who like most of us live on a 24 hour schedule.’’

The “cogs” of the body clock consist of interlocked cycles of proteins that wax and wane in cells. One of the key components of this loop is a protein called Cry.

“We found that mice that carried the after hours gene also had a delayed Cry protein breakdown rate, leading to a slowdown in the molecular feedback loops and a lengthening of the body clock cycle.’’

In other research, scientists have identified a part of the brain that affects how we deal with seasonal change.

The research will help our understanding of the causes and consequences of seasonal affective disorder and could also shed light on why we crave more food in winter.

Dr Gerald Lincoln, of Edinburgh University's Centre for Reproductive Biology, said: "Surprisingly, the circannual body clock works on a 10-month cycle.

"We reset our body calendar every summer, when increased light inhibits the production of melatonin. This could explain why sunshine makes us feel happier."

Thursday, April 26, 2007

Intelligence not linked to wealth, according to US study - Yahoo! News

Intelligence not linked to wealth, according to US study - Yahoo! News

"Your IQ has really no relationship to your wealth. And being very smart does not protect you from getting into financial difficulty," Zagorsky said.

The study confirmed previous research which has shown that smarter people tend to earn more money, but pointed out there is a difference between high pay and overall wealth.

"The average income difference between a person with an IQ score in the normal range (100) and someone in the top two percent of society (130) is currently between 6,000 and 18,500 dollars per year," it said.

"But when it came to total wealth and the likelihood of financial difficulties, people of below average and average intelligence did just fine when compared to the super-intelligent."

An irregular pattern of total wealth as well as financial distress levels -- such as maxed out credit cards, bankruptcy and missing bill payments -- emerged among the various degrees of intelligence, the study said.

Wednesday, April 25, 2007

Unhappy Meals - Michael Pollan - New York Times

Unhappy Meals - Michael Pollan - New York Times

From Leaves to Seeds. It’s no coincidence that most of the plants we have come to rely on are grains; these crops are exceptionally efficient at transforming sunlight into macronutrients — carbs, fats and proteins. These macronutrients in turn can be profitably transformed into animal protein (by feeding them to animals) and processed foods of every description. Also, the fact that grains are durable seeds that can be stored for long periods means they can function as commodities as well as food, making these plants particularly well suited to the needs of industrial capitalism.

Put in the simplest terms, we’re eating a lot more seeds and a lot fewer leaves, a tectonic dietary shift the full implications of which we are just beginning to glimpse. If I may borrow the nutritionist’s reductionist vocabulary for a moment, there are a host of critical micronutrients that are harder to get from a diet of refined seeds than from a diet of leaves. There are the antioxidants and all the other newly discovered phytochemicals (remember that sprig of thyme?); there is the fiber, and then there are the healthy omega-3 fats found in leafy green plants, which may turn out to be most important benefit of all.

Most people associate omega-3 fatty acids with fish, but fish get them from green plants (specifically algae), which is where they all originate. Plant leaves produce these essential fatty acids (“essential” because our bodies can’t produce them on their own) as part of photosynthesis. Seeds contain more of another essential fatty acid: omega-6. Without delving too deeply into the biochemistry, the two fats perform very different functions, in the plant as well as the plant eater. Omega-3s appear to play an important role in neurological development and processing, the permeability of cell walls, the metabolism of glucose and the calming of inflammation. Omega-6s are involved in fat storage (which is what they do for the plant), the rigidity of cell walls, clotting and the inflammation response. (Think of omega-3s as fleet and flexible, omega-6s as sturdy and slow.) Since the two lipids compete with each other for the attention of important enzymes, the ratio between omega-3s and omega-6s may matter more than the absolute quantity of either fat. Thus too much omega-6 may be just as much a problem as too little omega-3.

And that might well be a problem for people eating a Western diet. As we’ve shifted from leaves to seeds, the ratio of omega-6s to omega-3s in our bodies has shifted, too. At the same time, modern food-production practices have further diminished the omega-3s in our diet. Omega-3s, being less stable than omega-6s, spoil more readily, so we have selected for plants that produce fewer of them; further, when we partly hydrogenate oils to render them more stable, omega-3s are eliminated. Industrial meat, raised on seeds rather than leaves, has fewer omega-3s and more omega-6s than preindustrial meat used to have. And official dietary advice since the 1970s has promoted the consumption of polyunsaturated vegetable oils, most of which are high in omega-6s (corn and soy, especially). Thus, without realizing what we were doing, we significantly altered the ratio of these two essential fats in our diets and bodies, with the result that the ratio of omega-6 to omega-3 in the typical American today stands at more than 10 to 1; before the widespread introduction of seed oils at the turn of the last century, it was closer to 1 to 1.

The role of these lipids is not completely understood, but many researchers say that these historically low levels of omega-3 (or, conversely, high levels of omega-6) bear responsibility for many of the chronic diseases associated with the Western diet, especially heart disease and diabetes. (Some researchers implicate omega-3 deficiency in rising rates of depression and learning disabilities as well.) To remedy this deficiency, nutritionism classically argues for taking omega-3 supplements or fortifying food products, but because of the complex, competitive relationship between omega-3 and omega-6, adding more omega-3s to the diet may not do much good unless you also reduce your intake of omega-6.

A High-Fat, Low-Carbohydrate Diet Improves Alzheimer's Disease in Mice.

A High-Fat, Low-Carbohydrate Diet Improves Alzheimer's Disease in Mice.

The authors believe that insulin and the related hormone, insulin-related growth factor-1 (IGF-1), are the key players. "Insulin is often considered a storage hormone, since it promotes deposition of fat but insulin may also work to encourage amyloid-beta production."

Richard Feinman, editor of the journal, explains the relation between nutrients: "You might say that fat is the bomb, and insulin (from carbohydrate) is the fuse. Most studies of the deleterious effects of fat have been done in the presence of high carbohydrate. If carbs are high, dietary fat is not oxidized and is instead stored as body fat." When carbohydrates are very low and fat is high, compounds called ketone bodies are generated (ketosis) and these compounds may play a role in the observed reduction in amyloid-beta. In association with a group from University of Washington led by Dr. Suzanne Craft, Henderson has previously shown cognitive improvement in patients with mild AD who were given a diet that raises ketone bodies.

In an accompanying editorial, Feinman says, "Although it is too early to tell how the results will fit into the treatment of AD, the implication for diet in general is also important." The primacy of insulin as a control element is the basis of popular weight-loss diets based on carbohydrate restriction. Such regimens allow dieters to regulate fat and calorie intake by appetite alone as long as carbohydrate intake remains minimal. Feinman points out, "Henderson's effort is one of several recent studies that point the way to understanding metabolism beyond the issues surrounding simple fat reduction."

Weight training makes the ailing heart grow stronger - National -

Weight training makes the ailing heart grow stronger - National -

"As the muscles become stronger and as the blood flow to them becomes better, the heart actually has to do less work for every degree of exercise," said Associate Professor David Hare, a senior cardiologist at the Austin.

Over two to three months, patients start to feel stronger.

Rather than helping a damaged heart recover its normal beating function, Professor Hare said, weight training could teach the muscles how to use the heart's output more efficiently.

Of the 39 participants in the study, those who underwent weight training showed a significant increase in the number of blood vessels that connected to their muscle cells.

Those cells also showed greater efficiency in producing energy from food and oxygen.

"If you've got better extraction of oxygen by the muscle, then the muscle is going to carry out a lot more exercise without putting as much stress on the heart," Professor Hare said.

Before 1990, the accepted wisdom among cardiologists was that total rest was the only way to treat a damaged heart.

Professor Simon Stewart from the Baker Heart Research Institute in Melbourne said the concept had been "turned upside down" by evidence that the heart function was closely connected to the performance of peripheral body systems.

"The research is consistent with the idea that heart failure, though traditionally thought to be just about the heart, also affects the muscles," he said.

"We should be looking at the body as a whole system, rather than just the heart."

Weight of the Evidence: Weight Loss, Cholesterol and Blood Sugar Improvements - What's the Wonder Drug Now?

Weight of the Evidence: Weight Loss, Cholesterol and Blood Sugar Improvements - What's the Wonder Drug Now?

Weight Loss, Cholesterol and Blood Sugar Improvements - What's the Wonder Drug Now?
While the media is hot and heavy to lead their headlines with junk science complete with amateurish conclusions, a study was quietly published Friday in the journal, Molecular and Cellular Biochemistry - Beneficial effects of ketogenic diet in obese diabetic subjects (abstract) - that's remains ignored.

No fanfare, no ballyhoo, in fact, not one headline to call attention to the significant findings, over the course of a year, of a dietary trial in obese subjects with and without type II diabetes.

Findings that included:

For both groups, diabetic and normal glucose:

* Weight loss of 24.55kg in 56-weeks (that's 54-pounds)
* Total Cholesterol down 19.3%
* LDL down 28.2%
* HDL up 52.3%
* Triglycerides down 59%
* Fasting Blood Glucose down 31%

For those with type II diabetes:

* Weigth loss of 24.4kg in 56-weeks (that's 53.7-pounds)
* Total Cholesterol down 28.5%
* LDL down 33%
* HDL up 63.4%
* Triglycerides down 40.8%
* Fasting Blood Glucose down 50.9% (yes, glucose fell more than 50%)

So, what exactly did the researchers have these subjects do that led to such impressive improvements over the course of 56-weeks?

Sixty-four subjects were divided into two groups - thirty one had abnormal glucose levels (type II diabetes) and the remaining thirty-three had normal glucose levels. Both groups were instructed to modify their diet to include only 20g of carbohydrate a day from a list of foods allowed along with 5-tablespoons of olive oil on salads, and allowed 80g-100g of meats, eggs, fish, poultry and full-fat cheese each day. No alcohol was consumed by participants. At week 12, participants were allowed to increase carbohydrate to 40g per day. Throughout the 56-weeks some foods were forbidden - flour, bread, rice, macaroni, noodles, honey, sugar, sweets, cakes, potatoes, all fruit juices and all soft drinks.

Yes, shocker - the study was designed to measure the effects of a ketogenic diet in subjects with and without type II diabetes.

So, with the above findings, it's no wonder this one is being quietly ignored.

How to Give Yourself Diabetes Healthbolt

How to Give Yourself Diabetes Healthbolt:

"Here’s few things that can put you on the fast track to diabetes.

* Watch two or more hours of TV daily. Increased risk: 14%
* Have one bout of major depression. Increased risk: 23%
* Eat lots of processed meat. Increased risk: 43%
* Skip breakfast every morning. Increased risk: up to 50%
* Drinking one soda every day. Increased risk: 83%
* Wake up at night and don’t return to sleep. Increased risk: 98%
* Eat fast food more than twice a week. Increased risk: 100%
* Have the majority of your extra body mass (fat) around your waist instead of evenly distributed. Increased risk: a whopping 330%

We say it a lot around here, but it bears repeating: Eat healthy and exercise to help avoid all of the above."

Low Carb, High Protein Diet Has a Great Defensive Team - Diabetes Health

Low Carb, High Protein Diet Has a Great Defensive Team - Diabetes Health

Low Carb, High Protein Diet Has a Great Defensive Team

Part 4 of a 5 part feature
Richard Bernstein, MD, FACE, FACN, FCCWS
24 April 2007
Recommend this Article:
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Dr. Bernstein's latest book, Diabetes Solution, 3rd Edition, was published in March 2007 by Hachette Book Group, USA. His prior book, Diabetes Diet, was published in 2005 by Little Brown and Co.

When I developed diabetes in 1946, physicians thought that the high illness and death rate of diabetics was due to dietary fat and the supposedly resultant elevation of serum cholesterol. Since the DCCT trial, the scientific literature overwhelmingly supports the role of elevated blood sugar in all long-term diabetic complications.

Yet even today, many physicians ignore the need for normal blood sugars and focus on dietary fat. The 2006 Clinical Practice Recommendations (1) of the ADA advocate large amounts of dietary carbohydrate (45 - 65% of total calories) and small amounts of protein and fat. This recommendation is preceded by the statement that "dietary carbohydrate is the major contributor to postprandial (after meal) glucose concentration."

The high carbohydrate load is justified by the claim that "the brain and central nervous system have an absolute requirement for glucose as an energy source." This statement, while only partially correct (ketones from stored fat keep the brain alive during starvation), ignores the fact that in the absence of dietary carbohydrate, the liver, intestines, and kidneys convert dietary protein into as much glucose as the brain requires.

Low Carb Team Fights Like Cavemen

Virtually the entire evolution of mankind occurred when our ancestors were hunter-gatherers, well before the inventions of agriculture and animal husbandry. (2) These people had scarcely any access to dietary carbohydrate and certainly no access to animal milk, cereal grains, whole-grain and refined breads, refined sugars, and sweet fruits. They ate almost exclusively lean meat and fish, plus small amounts of leafy and other low carbohydrate vegetables. Some humans, such as Eskimos, consumed only fat and protein. Our pre-agriculture ancestors frequently had violent deaths, but no coronary, kidney, or arterial disease, no tooth decay, and no diabetes.

By 1969, when I first began to measure my own blood sugars, I was already suffering from about 15 major and minor long-term complications of diabetes, thanks to the low fat, high carbohydrate diet I had been following for 23 years. By about this time, scientific studies of animals had demonstrated the prevention and even reversal of many diabetic complications by blood sugar normalization.

A1c’s Huddle Around 4.5%

I soon discovered that even multiple daily insulin injections (basal/bolus dosing) would not achieve anything close to steady normal blood sugars. It was not until I lowered my carbohydrate consumption to a daily total of 30 grams (mostly from leafy and cruciferous vegetables) that things fell into place. Today my A1c is 4.5% (normal is 4.2-4.6%), and my target blood sugar is 83 mg/dl (about mid-normal for young non-diabetic adults).

Most of my long-term complications, including advanced kidney disease and severe gastroparesis, have normalized. Those that involved irreversible muscle loss (droopy eyelids, intrinsic minus feet (diabetic foot)) have not gotten worse. My lipid profile, which had been grossly abnormal, now shows: Triglycerides–50; LDL–53; HDL–118; and LDL subparticles - Type A. I see similar results in others who follow a prehistoric diet like my own (except for some type 1's with severe gastroparesis).

Until very recently, researchers were not comparing the effects of low carbohydrate diets to the ADA low fat/low protein diet. Recent results consistently support low carbohydrate, high protein¬ diets–not only for blood sugar control, but also with regard to weight loss and cardiac risk. Many of these studies are posted on the Web site of the Nutrition and Metabolism Society, at

Plenty of Rookies

I am not alone. Thousands of type 1 and type 2 diabetics are following very low carbohydrate diets. Many observe that both fat and protein bring about satiety, while carbohydrate leaves them hungry and craving more carbohydrate. Other studies have focused on the importance of dietary protein for prevention of bone loss (4) and for preventing blood pressure elevation (5).

Richard K. Bernstein, M.D.,

The Ball In Play: Carbs Make Fat, Fat Makes Thin? - Diabetes Health

The Ball In Play: Carbs Make Fat, Fat Makes Thin? - Diabetes Health

Carbs and carbs alone, not fat, increase body weight. It doesn't matter whether the carbs are from sugar, bread, fruit, or vegetables: They’re all rapidly digested and quickly converted to blood glucose. A short time after a carb-rich meal, the glucose in your bloodstream rises rapidly, and your pancreas produces a large amount of insulin to take the excess glucose out.

Just as eating fat doesn’t raise blood glucose, it doesn't raise insulin levels either. This is important because insulin is the hormone responsible for body fat storage. Because fats do not elicit an insulin response, they cannot be stored as body fat.
Insulin takes glucose out of the bloodstream. It is converted first into a starch called glycogen, which is stored in the liver and in muscles. But the body can store only a limited amount of glycogen, so the excess glucose is stored as body fat. This is the process of putting on weight.

When your blood glucose level returns to normal, after about 90 minutes, the insulin level in your bloodstream is still near maximum. As a result, the insulin continues to stack glucose away in the form of fat. Ultimately, the level of glucose in your blood falls below normal, and you feel hungry again. So you have a snack of more carbohydrates, and the whole process starts over again. You're getting fatter, but feeling hungry at the same time. Ultimately, insulin resistance caused by continually high insulin levels in your bloodstream impairs your ability to switch on a satiety center in the brain. You enter a vicious cycle of continuous weight gain combined with hunger. Under such circumstances, it is almost impossible not to overeat.

Taking Off Weight: Only Cutting Carbs Can Do It

So you've put the weight on–now you need to take it off again. Here again, “healthy eating” hampers your attempts because a carbohydrate-based diet prevents you from losing excess fat.

To lose fat, your body must use that fat as fuel. It will only use its stored fat as fuel if you deprive it of its present supply of fuel: blood glucose.

There are two ways to cut your body's glucose supply. You can starve, which is what low-calorie, low-fat dieting is. Alternatively, you can reduce the starches and sugars from which glucose is made, and make up the difference with another fuel: fat.

The latter approach has two advantages over the traditional calorie-controlled diet. First, you don’t have to go hungry. Second, by feeding your body on fats, your body will stop trying to find glucose and will naturally begin using its own stored fat.

When you eat carbs, your capacity to use fat is limited. Increasing blood glucose during dieting stimulates insulin release. Even at very low concentrations of insulin, fat synthesis is activated and break-up of fat is inhibited. This means that if you eat a carbohydrate-based low-fat diet, you force your body into a fat-making mode, not a fat-using mode.

Insulin inhibits the production of fat-burning enzymes, thereby preventing your body's fat cells from releasing their fat. This stops your body from burning your stored fat and makes it impossible for you to lose the weight you have put on.

Baby Foods That Prevent Obesity and Diabetes in Adulthood to Hit the Market Soon

Baby Foods That Prevent Obesity and Diabetes in Adulthood to Hit the Market Soon

Infant formula and other baby foods that provides permanent protection from obesity and diabetes into adulthood could be on shop shelves soon, reports Lisa Melton in Chemistry & Industry.

The foods, under development at the Clore Laboratory at the University of Buckingham, will be supplemented with leptin, the hunger hormone. Those who take the foods early in life should remain permanently slim. 'Like those people who are lean by nature even though they overeat? like we all do – they will tend to be inefficient in terms of using energy,' says Mike Cawthorne, who heads the Metabolic Research group at Clore.

Cawthorne's group has already demonstrated that supplementing infant rats' diets with leptin means that they never get fat or develop diabetes. Even animals fed a high-fat diet remained slim.

Leptin, the fat hormone that turns off hunger in the brain, is produced in the body throughout life. Its discovery was heralded as a major breakthrough, but research in adults proved disappointing because individuals soon seemed to resist its hunger-quenching effect.

But Cawthorne says this time things are different. Providing leptin earlier enough effectively hard-wires the body's energy balance. In fact, whether one is fat or thin may be determined before birth. Feeding the hormone to pregnant rats has been found to have a lifelong impact on their offspring's predisposition to obesity. Animals born of leptin-treated mothers remain lean even when fed a fat-laden diet, while those from untreated dams gained weight and developed diabetes.

Lifestyle changes can help tame the diabetes epidemic

Lifestyle changes can help tame the diabetes epidemic

The following are the “fairly simple” lifestyle changes you can make to prevent/reverse T2D, pre-diabetes or insulin resistance:

1. Nurture a consciousness of health (physical, psychological, emotional and spiritual) in your family.

2. Strive for a balanced lifestyle that includes: enough sleep, building solid relationships, eating meals in peace.

3. If your heart is healthy, get a pedometer and walk everywhere you can, working up to 10,000 steps per day (about 5 miles) or do other aerobic activity, such as swimming or bicycling 45-60 minutes per day.

4. For optimal hormone balance, build muscle mass to slow the aging process.

5. Especially if you are overweight at the waist, get your fasting insulin taken; if it is higher than 10, cut out obvious carbohydrates (potatoes, bread, pasta, breakfast cereals, etc) from your diet.

6. Ideal meals consist of: healthy protein (i.e. wild salmon, beans, lentils, organic meat, poultry and eggs), healthy fats (i.e. oils: extra virgin olive, macadamia nut, cold-pressed canola, coconut, fish, flax; nuts and seeds, avocadoes), low glycemic load, high soluble fiber carbohydrates (i.e. oat bran, quinoa, other whole grains, beans, lentils, vegetables, berries, cherries, etc.). The combination of fats, proteins, and soluble fiber slows the absorption of carbohydrates.

7. Meals made from scratch will almost always be healthier than restaurant/fast food/packaged, processed foods - often loaded with hydrogenated oils and sodium, and without potassium.

8. If diabetic/pre-diabetic, monitor your blood sugar 2 hours after at least one meal per day, in a notebook, listing all foods/drinks for that meal. Analyze which meals are glucose healthy and which need to be changed.

9. If stress is a problem in your life, do saliva testing (more reliable than blood) for cortisol/DHEA hormones, to check status of your adrenal glands. Let go of controlling others, anger and resentment. Forgive yourself and others. If you don’t forgive, your health will be jeopardized.

If you implement these lifestyle changes and attitudes, your blood sugar balance will improve.

Chronic depression or depression that worsens over time may cause diabetes in older adults

Chronic depression or depression that worsens over time may cause diabetes in older adults

The study differed from prior research in several ways. It is the first to examine the connection between increasing symptoms of depression over time and the incidence of diabetes.

Previous studies linking diabetes to depression have been based on a one-time measure of depressive symptoms. A single measure could be based on an episode or event that has caused a person to feel blue for a limited amount of time.

Carnethon's study measured depressive symptoms at a single point in time as well as depressive symptoms over time. This approach paints a more accurate depiction of depressive symptoms. By measuring depressive symptoms before diabetes developed, she and colleagues were better able to investigate the causal effect between mood and diabetes.

The Northwestern study also factored out other known lifestyle causes of diabetes such as being overweight or getting little physical exercise.

"We know that overweight and obesity are the primary risk factors for diabetes and most people with Type 2 diabetes are overweight or obese," Carnethon said. "But even after we adjusted for [statistically accounted for] body mass index (measure of height versus weight), we still saw a residual association between depression and diabetes."

In addition, the study considered a key biological factor , a high level of inflammation common in depressed people -- that might have explained the link between depression and diabetes. Inflammation is estimated by the levels of an inflammatory protein in the blood called C-reactive protein. But even after accounting for levels of the protein, depressive symptoms were still associated with the development of diabetes.

Carnethon theorizes that the culprit responsible for diabetes in persons who are depressed is a high level of a stress hormone, cortisol. High levels of cortisol may decrease insulin sensitivity and increase fat deposits around the waist (a risk factor for diabetes). While her study was limited to older adults, she believes high cortisol levels in depressed younger adults may also put them at risk for diabetes.

Insulin enables glucose (sugar) to enter the body's cells to be used as fuel. When people are under acute stress or are depressed, the cells in the pancreas are suppressed and secrete less insulin to enable the body to sweep glucose out of the bloodstream. Compounding the problem, high cortisol levels decrease the muscles' sensitivity to insulin, which also could result in elevated glucose levels, Carnethon said.

"When you're depressed or under stress your body is trying to keep glucose in the bloodstream because it needs it for immediate energy," Carnethon noted. "So, it's blocking insulin action. And you may even be producing more glucose because your body thinks it needs the sugar."

Carnethon said the study shows the importance of screening older adults for depressive symptoms. "It's not a normal condition for older adults to be depressed," she said. "I think a lot of people say, "Oh, they're old, they should be depressed. What does it matter if they're a little bit down, Well, it does matter and you should treat it aggressively because it has effects on health beyond that of mood." -- Major Discovery: New Planet Could Harbor Water and Life -- Major Discovery: New Planet Could Harbor Water and Life

An Earth-like planet spotted outside our solar system is the first found that could support liquid water and harbor life, scientists announced today.

Liquid water is a key ingredient for life as we know it. The newfound planet is located at the "Goldilocks" distance—not too close and not too far from its star to keep water on its surface from freezing or vaporizing away.

And while astronomers are not yet able to look for signs of biology on the planet, the discovery is a milestone in planet detection and the search for extraterrestrial life, one with the potential to profoundly change our outlook on the universe.

”The goal is to find life on a planet like the Earth around a star like the Sun. This is a step in that direction,” said study leader Stephane Udry of the Geneva Observatory in Switzerland. “Each time you go one step forward you are very happy.”

Tuesday, April 24, 2007

Fatty Acid Trip: Adventures in High-EPA Fish Oil - Blog Archive - Clinical trial boosts omega-3’s ADHD benefit claims

Fatty Acid Trip: Adventures in High-EPA Fish Oil Blog Archive Clinical trial boosts omega-3’s ADHD benefit claims

The new study from the University of South Australia recruited 132 kids with ADHD aged 7 to 12 for the randomised, placebo-controlled, double-blind intervention study. One hundred and four children completed the trial.

For the first 15 weeks of study, the kids were given daily supplements of either polyunsaturated fatty acids (omega-3 and omega-6, 3000 milligrams per day), PUFAs plus multivitamins and minerals, or placebo capsules (palm oil).

After 15 weeks all the groups crossed-over to the PUFA plus multivitamins and minerals supplement.

The supplement was derived from high-EPA marine fish oil and virgin evening primrose oil (GLA). The formulation contained Eicosapentaenoic acid (EPA), Docosahexaenioc acid (DHA), GLA, and vitamin E.

Parents were asked to rate their child’s condition after 15 and 30 weeks with the 14 ADHD scales of the Conner’s Parent Rating Scales. After 15 weeks of eyeq supplements, improvements were recorded in half of these scales.
After 30 weeks (placebo group switching to eyeq supplements) the parental ratings of behaviour improved significantly in nine out of 14 scales.

No significant improvements were recorded in the Conners Teacher Ratings Scale, but the researchers state that parental ratings are considered more accurate for identifying ADHD in children than teachers.

“The present study is the largest PUFA trial to date with children falling in the clinical ADHD range on Conners Index. The result support those of other studies that have found improvements in developmental problems symptomatic of ADHD with PUFA supplementation,” wrote Sinn.

“These results have significant implications for children with ADHD-related symptoms, parents, and clinicians.”

Dr. Sinn said that many questions remain unanswered. “This work needs to be replicated in other scientifically controlled trials in populations of children with different constellations of symptoms and other developmental disorders that overlap with ADHD,” she told this website.

“We need more understanding about biological mechanisms, degree of relative PUFA deficiency and which children are most likely to respond, and also the relative importance of the omega-3 fatty acids EPA and DHA, and the inclusion of omega-6 fatty acid GLA, in the supplement that has received successful outcomes in the UK and Adelaide trials.”

She added that a new trial would be starting this year to continue this work, with the taking of blood and urine samples to gain more understanding of fatty acid and biological metabolic profiles of responders versus non-responders, extending neuropsychological assessments to gain more understanding of cognitive and learning benefits, and comparing EPA with DHA.

Who's Spinning Intel?

Who's Spinning Intel?

Although there were certainly disagreements between the CIA and Feith's shop, both argued in 2002 that there was a relationship between Saddam's Iraq and al Qaeda. George Tenet, then the director of central intelligence, stated the CIA's position quite clearly in an October 7, 2002 letter to then head of the Senate Intelligence Committee, Senator Bob Graham (D-FL). Tenet explained, "We have solid reporting of senior level contacts between Iraq and al-Qaeda going back a decade." Iraq and al Qaeda "have discussed safe haven and reciprocal non-aggression." Tenet warned, "We have credible reporting that al-Qaeda leaders sought contacts in Iraq who could help them acquire WMD capabilities. The reporting also stated that Iraq has provided training to al-Qaeda members in the areas of poisons and gases and making conventional bombs." And, "Iraq's increasing support to extremist Palestinians, coupled with growing indications of a relationship with al-Qaeda, suggest that Baghdad's links to terrorists will increase, even absent US military action."

Tenet was far from alone in these assessments. Michael Scheuer, the one-time head of the CIA's bin Laden unit, also used to be certain that Iraq and al Qaeda were working together. Scheuer's first book on al Qaeda, Through Our Enemies' Eyes, which was published in 2002, went into elaborate detail about the support the Iraqi regime was providing to al Qaeda. Among the areas of concern was Iraq's ongoing support for al Qaeda's chemical weapons development projects in the Sudan.


The idea that Feith's analysts cooked up the connection, while the CIA shunned the very notion, is pure fantasy--a fantasy dreamed up by Senator Levin and some former CIA members who have repeatedly made clear their disdain for the Bush administration.

But all of this is almost entirely beside the point. Instead of focusing on Levin's "who said what in Washington" game, we'd be better served by focusing on the best evidence available: Saddam's own intelligence files. Here, the Post's account is
thoroughly lacking.

The story leads off with this startling conclusion, purportedly gleaned from the inspector general's report:

"Captured Iraqi documents and intelligence interrogations of Saddam Hussein and two former aides 'all confirmed' that Hussein's regime was not directly cooperating with al-Qaeda before the U.S. invasion of Iraq "

Taking the denials of Saddam and his goons at face value is, of course, ridiculous. But exactly which "captured Iraqi documents" confirmed that Saddam's regime and al Qaeda were "not directly cooperating?" The Post doesn't say. And the inspector general did not perform a thorough review of the Iraqi intelligence documents captured during the Iraq war.

Here is just a small sample of what some of the Iraqi intelligence documents and other evidence collected in postwar Iraq has revealed:

1. Saddam's Terror Training Camps & Long-Standing Relationship With Ayman al-Zawahiri. As first reported in THE WEEKLY STANDARD, there is extensive evidence that Saddam used Iraqi soil to train terrorists from throughout the Middle East. Among the terrorists who received Saddam's support were members of al Qaeda's Algerian affiliate, formerly known as the GSPC, which is still lethally active, though under a new name: al Qaeda in the Islamic Maghreb.

Joe Klein, a columnist for Time magazine and an outspoken critic of the Bush administration, has confirmed the existence of Saddam's terrorist training camps. He also found that Iraqi intelligence documents demonstrated a long-standing relationship between Saddam and al Qaeda bigwig Ayman al-Zawahiri.

Other evidence of Saddam's terror training camps was reported in a paper published by the Pentagon's Iraqi Perspectives Project. A team of Pentagon analysts discovered that Saddam's paramilitary Fedayeen forces were hosting camps for thousands terror of from throughout the Middle East.

2. A 1992 IIS Document lists Osama bin Laden as an "asset." An Iraqi Intelligence memorandum dated March 28, 1992 and stamped "Top Secret" lists a number of assets. Osama bin Laden is listed on page 14 as having a "good relationship" with the Iraqi Intelligence Service's section in Syria.

3. A 1997 IIS document lists a number of meetings between Iraq, bin Laden and other al Qaeda associates. The memo recounts discussions of cooperating in attacks against American stationed in Saudi Arabia. The document summarizes a number of contacts between Iraqi Intelligence and Saudi oppositionist groups, including al Qaeda, during the mid 1990's. The document says that in early 1995 bin Laden requested Iraqi assistance in two ways. First, bin Laden wanted Iraqi television to carry al Qaeda's anti-Saudi propaganda. Saddam agreed. Second, bin Laden requested Iraqi assistance in performing "joint operations against the foreign forces in the land of Hijaz." That is, bin Laden wanted Iraq's assistance in attacking U.S. forces in Saudi Arabia.

We do not know what, exactly, came of bin Laden's second request. But the document indicates that Saddam's operatives "were left to develop the relationship and the cooperation between the two sides to see what other doors of cooperation and agreement open up." Thus, it appears that both sides saw value in working with each other. It is also worth noting that in the months following bin Laden's request, al Qaeda was tied to a series of bombings in Saudi Arabia.

The document also recounts contacts with Mohammed al-Massari, a known al Qaeda mouthpiece living in London.

4. A 1998 IIS document reveals that a representative of bin Laden visited Baghdad in March 1998 to meet with Saddam's regime. According to the memo, the IIS arranged a visit for bin Laden's "trusted confidant," who stayed in a regime-controlled hotel for more than two weeks. Interestingly, according to other evidence discovered by the U.S. intelligence community, Ayman al-Zawahiri was also in Baghdad the month before. He collected a check for $300,000 from the Iraqi regime. The 9-11 Commission confirmed that there were a series of meetings (perhaps set up by Zawahiri, who had "ties of his own" to the Iraq regime) in the following months as well.

5. Numerous IIS documents demonstrate that Saddam had made plans for a terrorist-style insurgency and coordinated the influx of foreign terrorists into Iraq. In My Year in Iraq, Ambassador Paul Bremer says a secret IIS document he had seen "showed that Saddam had made plans for an insurgency." Moreover, "the insurgency had forces to draw on from among several thousand hardened Baathists in two northern Republican Guard divisions that had joined forces with foreign jihadis."

Cobra II, a scathing indictment of the Bush administration's prosecution of the Iraq war by New York Times authors Michael Gordon and General Bernard Trainor, offers additional detail about the terrorists who made their way to Iraq in advance of the war. "Documents retrieved by American intelligence after the war show that the Iraqi Ministry of Defense coordinated border crossings with Syria and provided billeting, pay, and allowances and armaments for the influx of Syrians, Palestinians, and other fighters."

Still another IIS document contains Saddam's orders to "utilize Arab suicide bombers" against the Americans. Saddam's agents were also ordered to provide these terrorists with munitions, cash, shelter, and training.

These are just five examples of the types of documents that have been discovered in postwar Iraq. There are many more examples not listed here. They all undermine the conventional wisdom that there was never any relationship between Saddam's Iraq and al Qaeda.

But you won't see Senator Carl Levin calling attention to any of these documents. And the Washington Post has shown no interest in bringing them to his attention either. Instead, Levin and the Post like to pretend that the relationship between Saddam and al Qaeda was cooked up by neoconservatives bent on war. The Post even initially--and incorrectly--reported that a copy of a memo from Feith's shop was leaked to THE WEEKLY STANDARD prior to war. (In reality, Stephen Hayes reported on the memo months after the war began. The implication of the Post's misreporting was clear: this was all about justifying war.

But instead of worrying about a memo written by Feith's analysts, perhaps the Post should take more interest in what Saddam's files have to say. They're a lot more interesting.

Thomas Joscelyn is a terrorism researcher and economist living in New York.

John Kerry: Building 7 Was Deliberately Demolished | Alternative News Sources

John Kerry: Building 7 Was Deliberately Demolished | Alternative News Sources

At a recent speaking engagement in Austin Texas, Senator John
Kerry responded to a question about WTC Building 7 by concluding that according
to his information, the building was brought down as a result of a controlled
demolition, directly contradicting the official line that the structure fell as
a result of fire and debris damage.

WTC Building 7 was a 47-story building in the WTC complex that
collapsed at 5:20pm on September 11. The building had been
reinforced and was not hit by a plane yet collapsed in a uniform implosion
within its own footprint in a matter of seconds after sustaining relatively
light debris and fire damage following the collapse of the twin towers.

News networks like BBC and CNN were

reporting that the building had collapsed before it fell , indicating that
the media were being handed a script of events that had yet to even unfold.

Ground zero EMT’s, firefighters and police were all told hours in advance to
clear a collapse zone for Building 7 as it was going to be “brought down.”

Questioned on WTC 7 by members of Austin 9/11 Truth Now at a
Book People event in Austin Texas, Kerry responded, “I do know that that wall, I
remember, was in danger and I think they made the decision based on the danger
that it had in destroying other things, that they did it in a controlled

Monday, April 23, 2007

People with two copies of a particular gene have a 70% higher risk of being obese

People with two copies of a particular gene have a 70% higher risk of being obese

Scientists have identified the most clear genetic link yet to obesity in the general population as part of a major study of diseases funded by the Wellcome Trust, the UK's largest medical research charity.

People with two copies of a particular gene variant have a 70% higher risk of being obese than those with no copies.

Obesity is a major cause of disease, associated with an increased risk of type 2 diabetes, heart disease and cancer. It is typically measured using body mass index (BMI). As a result of reduced physical activity and increased food consumption, the prevalence of obesity is increasing worldwide. According to the 2001 Health Survey for England, over a fifth of males and a similar proportion of females aged 16 and over in England were classified as obese. Half of men and a third of women were classified as overweight.

Scientists from the Peninsula Medical School, Exeter, and the University of Oxford first identified a genetic link to obesity through a genome-wide study of 2,000 people with type 2 diabetes and 3,000 controls. This study was part of the Wellcome Trust Case Control Consortium, one of the biggest projects ever undertaken to identify the genetic variations that may predispose people to or protect them from major diseases. Through this genome-wide study, the researchers identified a strong association between an increase in BMI and a variation, or "allele", of the gene FTO. Their findings are published online today in the journal Science.

The researchers then tested a further 37,000 samples for this gene from Bristol, Dundee and Exeter as well as a number of other regions in the UK and Finland.

The study found that people carrying one copy of the FTO allele have a 30% increased risk of being obese compared to a person with no copies. However, a person carrying two copies of the allele has a 70% increased risk of being obese, being on average 3kg heavier than a similar person with no copies. Amongst white Europeans, approximately one in six people carry both copies of the allele.

Can Oily Fish Really Cause Diabetes? - UK News Headlines

Can Oily Fish Really Cause Diabetes? - UK News Headlines

ating oily fish that has been exposed to high levels of environmental pollutants can cause diabetes - particularly if you are overweight, a study shows.

Scientists say chemicals known as POPS (persistent organic pollutants) stored in body fat - not obesity itself - could be contributing to the rising number of cases of Type 2 diabetes which affects more than 1.9 million Brits.

If true it could turn the conventional wisdom of how obesity causes diabetes on its head, reports New Scientist.

POPs are toxic and include polychlorinated biphenyls (PCBs) and the pesticide DDT. They have been banned in developed countries but can accumulate in the fatty tissue of animals.

They are most likely to end up in people by the consumption of fatty fish such as salmon.

Last year Dr Duk-Hee Lee at Kyungpook National University in Daegu, South Korea, and her colleagues reported people
with higher levels of six different POPs were more likely to have diabetes than people with low levels.

Now a follow-up study published in Diabetes Care suggests an association in non-diabetic people between certain pesticides, PCBs and insulin resistance – a precursor to diabetes.

Fat people with POPs in their blood were more likely to develop insulin resistance than thin people with POPs - but the expected association between obesity and insulin resistance disappeared in people with no POPs.

"This suggests the possibility POPs stored in fat tissue, not obesity itself, may be a key factor for the development of type 2 diabetes," said Dr Lee.

Sunday, April 22, 2007

ScienceDaily: Recurrent Middle Ear Infections Can Have A Major Impact On Children's Development

ScienceDaily: Recurrent Middle Ear Infections Can Have A Major Impact On Children's Development

Science Daily — A study by the University of Western Sydney has revealed that recurring middle ear infections in early childhood can have a detrimental impact on language and literacy skill development in later life.

Study author, Dr Heather Winskel, from the University's School of Psychology, says middle ear infection or otitis media (OM) is the most common childhood illness.

"At least 70% of children are likely to experience at least one episode of otitis media before they are three-years-old and for many children it is a recurrent problem," says Dr Winskel.

"The peak incidence of OM occurs when children are between 6 and 18 months, which is the most critical period of language development, when the infant is tuning in to the speech sounds that characterise their native language. This process allows young children to break into the stream of speech and eventually map sound onto meaning.

"Fluctuating hearing loss due to OM during the early years of life presents the child with an intermittent speech signal that is difficult to process."

According to Dr Winskel, while earlier studies have indicated that ongoing middle ear infections in young children appear to be linked with poor language and literacy skills these studies have also produced conflicting results.

Saturday, April 21, 2007

E-motional Design Blog Archive ::COOL VIDEO!:: Nazi Robot Attack

E-motional Design - Art is the WebLimit Nazi Robot Attack

Cool video.
What if the Nazi's had mech robots?

Friday, April 20, 2007

Pot's Active Ingredient Halts Lung Cancer Growth, Study Says - NORML

Pot's Active Ingredient Halts Lung Cancer Growth, Study Says - NORML

Pot's Active Ingredient Halts Lung Cancer Growth, Study Says

April 19, 2007 - Los Angeles, CA, USA

Los Angeles, CA: The administration of THC significantly reduces lung tumor size and lesions, according to preclinical data presented this week at the annual meeting of the American Association for Cancer Research (AACR) in Los Angeles.

Investigators at Harvard University's Division of Experimental Medicine reported that THC inhibited the growth and spread of cells in vitro from two different lung cancer cell lines and from patient lung tumors. They also reported that THC administration reduced the growth of lung tumors in mice by more than 50 percent compared to untreated controls over a three-week period.

Researchers noted that THC appeared to block a specific cancer-causing protein in a manner similar to the pharmaceutical anti-cancer drugs Erbitux (Cetuximab) and Vectibix (Panitumumab).

Results of a large-scale, case-controlled population study published last year found that smoking cannabis, even long-term, is not positively associated with increased incidence of lung-cancer. Investigators in that study noted that one subset of moderate lifetime users had an inverse association between cannabis use and lung cancer, leading them to speculate that cannabinoids may possess certain protective properties against the development of lung cancer in humans.

Separate preclinical studies indicate that compounds in marijuana inhibit cancer cell growth in animals and in culture on a wide range of tumoral cell lines ­-- including human breast carcinoma cells, human prostate carcimona cells, and human colectoral carcinoma cells, among others. Most recently, investigators at Madrid's Complutense University, School of Biology, reported in the British Journal of Cancer that THC administration decreases recurrent glioblastoma multiforme (brain) tumor growth in patients diagnosed with the disease.

AJScreensaver - Free Software Downloads and Software Reviews -

AJScreensaver - Free Software Downloads and Software Reviews -

Cool clock download for your computer. Check out the one that shows year/month/date/day/hour/minute/second on one continous moving screen. Cool!

Thursday, April 19, 2007 / In depth - Iraq may hold twice as much oil / In depth - Iraq may hold twice as much oil

Iraq could hold almost twice as much oil in its reserves as had been thought, according to the most comprehensive independent study of its resources since the US-led invasion in 2003.

The potential presence of a further 100bn barrels in the western desert highlights the opportunity for Iraq to be one of the world’s biggest oil suppliers, and its attractions for international oil companies – if the conflict in the country can be resolved.

If confirmed, it would raise Iraq from the world’s third largest source of oil reserves with 116bn barrels to second place, behind Saudi Arabia and overtaking Iran.

The study from IHS, a consultancy, also estimates that Iraq’s production could be increased from its current rate of less than 2m barrels a day to 4m b/d within five years, if international investment begins to flow.


Production costs in Iraq are low, particularly compared to the more complex offshore developments.

IHS estimates that they are less than $2 a barrel.


Ron Mobed of IHS said: “Obviously the security situation is very bad, but when you look at the sub-surface opportunity, there isn’t anywhere else like this. Geologically, it’s right up there, a gold star opportunity.”

Of Iraq’s 78 oilfields identified as commercial by the government, only 27 are currently producing. A further 25 are not yet developed but close to production, and 26 are not yet developed and far from production.

Iraq’s government has estimated that it would need $20bn-$25bn of investment from foreign companies to get production up to its full potential.

Production methods have advanced greatly in the past two decades, and methods such as horizontal drilling have yet to be deployed in Iraq. The introduction of modern technology by foreign companies has the potential to deliver steep increases in oil recovery.


Oil production in parts of the western desert region that are attached to Sunni Arab-majority provinces could help resolve some of the differences between Iraq’s sectarian political blocs.

The Sunni have until now been strongly hostile to the federalism espoused by most Kurds and some Shia, arguing that it would deprive their less well-resourced heartland in the centre of the country of resources.