Friday, August 31, 2007

Reward deficiency syndrome: a biogenetic model for...[J Psychoactive Drugs. 2000] - PubMed Result

Reward deficiency syndrome: a biogenetic model for...[J Psychoactive Drugs. 2000] - PubMed Result

The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms. The net effect of neurotransmitter interaction at the mesolimbic brain region induces "reward" when dopamine (DA) is released from the neuron at the nucleus accumbens and interacts with a dopamine D2 receptor. "The reward cascade" involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits GABA at the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or "reward site." It is well known that under normal conditions in the reward site DA works to maintain our normal drives. In fact, DA has become to be known as the "pleasure molecule" and/or the "antistress molecule." When DA is released into the synapse, it stimulates a number a DA receptors (D1-D5) which results in increased feelings of well-being and stress reduction. A consensus of the literature suggests that when there is a dysfunction in the brain reward cascade, which could be caused by certain genetic variants (polygenic), especially in the DA system causing a hypodopaminergic trait, the brain of that person requires a DA fix to feel good. This trait leads to multiple drug-seeking behavior. This is so because alcohol, cocaine, heroin, marijuana, nicotine, and glucose all cause activation and neuronal release of brain DA, which could heal the abnormal cravings. Certainly after ten years of study we could say with confidence that carriers of the DAD2 receptor A1 allele have compromised D2 receptors. Therefore lack of D2 receptors causes individuals to have a high risk for multiple addictive, impulsive and compulsive behavioral propensities, such as severe alcoholism, cocaine, heroin, marijuana and nicotine use, glucose bingeing, pathological gambling, sex addiction, ADHD, Tourette's Syndrome, autism, chronic violence, posttraumatic stress disorder, schizoid/avoidant cluster, conduct disorder and antisocial behavior. In order to explain the breakdown of the reward cascade due to both multiple genes and environmental stimuli (pleiotropism) and resultant aberrant behaviors, Blum united this hypodopaminergic trait under the rubric of a reward deficiency syndrome.

Association of polymorphisms of dopamine D2 receptor (DRD2), and dopamine transporter (DAT1) genes with schizoid/avoidant behaviors (SAB)

Association of polymorphisms of dopamine D2 receptor (DRD2), and dopamine transporter (DAT1) genes with schizoid/avoidant behaviors (SAB)

The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms in the brain. Dysfunction of the D2 dopamine receptors leads to aberrant substance-seeking behaviors (ethanol, drugs, tobacco, and food) and other related behaviors (pathological gambling, Tourette's disorder, attention-deficit/hyperactivity disorder). This is the first study supporting a strong association between the dopamine D2 receptor Taq A1 allele with schizoid/avoidant behavior (SAB). Additionally, an albeit weaker association between the 480-bp VNTR 10/10 allele of the dopamine transporter (DAT1) gene with SAB was similarly found.



Found this on Dr-Bob message board. rating scale is from Dr. Thomas E. Brown, who has a site at


(Note: in this report the term ADD-H is used to signify "Attention Deficit Disorder WITHOUT Hyperactivity")

The AAD (Attention Activation Disorder) construct includes problems in the following areas:

Activating and organizing to work
Sustaining attention and concentration
Sustaining energy and effort
Irritability, depressed mood, rejection sensitivity Activating recall of aims and learned information

"Bright children and adolescents who suffer from attention deficit disorder are at a special risk of having their ADD problems go unrecognized and untreated. Within a pattern of under-achievement, their natural intellectual abilities produce intermittent successes which can mask ADD problems, especially if the person is not hyperactive. This study involved a population of high-IQ children, adolescents, and adults who were underachieving and had symptoms of ADD-H.

Research by Lahey et al. (1988) has shown that Attention Deficit Disorder is not unidimensional and that a subgroup of ADD patients exhibits a pattern of inattention and sluggish tempo WITHOUT hyperactivity. Barkley (1990) has demonstrated that this subgroup also shows less aggression, impulsivity, and overactivity at home and at school, and more of a problem with memory, perceptual-motor speed, and central processing speed. Barkley has suggested that the symptoms of ADD-H are sufficiently different from those of ADHD to warrant considering these as two separate and unique disorders, rather than as subtypes of a single attention disturbance."


- Has difficulty getting started on tasks; e.g., homework,
- Feels overwhelmed; e.g., "No way I can do this now" by tasks
which should be managable.
- When first presented with many things to do, has difficulty
deciding which to do first and then getting started.
- Procrastinates excessively; keeps putting things off.
- Slow to react or get started; sluggish, slow moving, doesn't
just jump into things.
- Excessively perfectionist; has to get things "just so." - Sleeps very soundly; hard to wake up in the morning.
- Appears apathetic or unmotivated.
- Misunderstands directions for assignments or tasks.


- When trying to pay attention to someone, e.g., class or
conversation, mind drifts off and briefly loses focus.
- Involuntary "spacing out" occurs intermittently when reading
or listening.
- Easily sidetracked; disrupts a task in progress and switches
to doing something else without any reason.
- When reading, loses track of what has just been read, so needs
to read it again.
- Easily loses track of the main point in reading books,
magazines, and newspapers.
- Gets lost in daydreaming, preoccupied with own thoughts.
- Easily distracted from a task by background noise or activities;
needs to check out whatever else is going on.
- Stares into space; seems "out of it." - Does not appear to be listening even when it is important
to do so.


- Feels sleepy or fatigued, even after having had adequate sleep.
- Unable to complete assignments or tests in allotted time; needs
extra time to finish adequately.
- Criticized by others as being "lazy." - Inconsistent quality of work; performance quite variable; e.g.,
high grades mixed with low grades for no apparent reason.
- Criticized by others for "not working up to potential." - Energy tends to fade quickly; "runs out of steam." - Needs to be reminded by others; e.g, teachers, to get started or
to keep working on assigned tasks.
- Starts tasks; e.g., homework assignments, chores, etc., but
doesn't finish them completely.


- Easily irritated
- Sensitive to criticism from others. Feels it deeply or for a
long time, or gets overly defensive.
- Usually "laid back" in dealing with others but has outbursts
of intense anger.
- Has difficulty expressing anger appropriately to others.
- Mood is discouraged, depressed, "down." - Tends to be a loner among peers; keeps to self socially.
- Appears apathetic or unmotivated.


- Information learned well on one day cannot be recalled easily
when it is wanted; e.g., knows material well on night before
test, but cannot recall it adequately for the next day.
- "Freezes" when taking tests or exams; for a while is unable to
get organized and begin.
- Forgets things which were intended to be done; e.g., turn off
appliances, return phone calls, keep appointments, do
assignments, etc.
- Has difficulty memorizing; e.g., vocabulary, math facts,
names, dates, etc.

-------------------------------------------------------- Dr. Thomas E. Brown, Ph.D.
Department of Psychology
Yale University
P.O. Box 6694
Hamden, CT 06517

Thursday, August 30, 2007

The effect on health of alternate day calorie restriction : Eating less and more than needed on alternate days prolongs life :: CAT.INIST


The effect on health of alternate day calorie restriction : Eating less and more than needed on alternate days prolongs life
Auteur(s) / Author(s)
JOHNSON James B. ; LAUB Donald R. ; JOHN Sujit ;
Résumé / Abstract
Restricting caloric intake to 60-70% of normal adult weight maintenance requirement prolongs lifespan 30-50% and confers near perfect health across a broad range of species. Every other day feeding produces similar effects in rodents, and profound beneficial physiologic changes have been demonstrated in the absence of weight loss in ob/ob mice. Since May 2003 we have experimented with alternate day calorie restriction, one day consuming 20-50% of estimated daily caloric requirement and the next day ad lib eating, and have observed health benefits starting in as little as two weeks, in insulin resistance, asthma, seasonal allergies, infectious diseases of viral, bacterial and fungal origin (viral URI, recurrent bacterial tonsillitis, chronic sinusitis, periodontal disease), autoimmune disorder (rheumatoid arthritis), osteoarthritis, symptoms due to CNS inflammatory lesions (Tourette's, Meniere's) cardiac arrhythmias (PVCs, atrial fibrillation), menopause related hot flashes. We hypothesize that other many conditions would be delayed, prevented or improved, including Alzheimer's, Parkinson's, multiple sclerosis, brain injury due to thrombotic stroke atherosclerosis, NIDDM, congestive heart failure. Our hypothesis is supported by an article from 1957 in the Spanish medical literature which due to a translation error has been construed by several authors to be the only existing example of calorie restriction with good nutrition. We contend for reasons cited that there was no reduction in calories overall, but that the subjects were eating, on alternate days, either 900 calories or 2300 calories, averaging 1600, and that body weight was maintained. Thus they consumed either 56% or 144% of daily caloric requirement. The subjects were in a residence for old people, and all were in perfect health and over 65. Over three years, there were 6 deaths among 60 study subjects and 13 deaths among 60 ad lib-fed controls, non-significant difference. Study subjects were in hospital 123 days, controls 219, highly significant difference. We believe widespread use of this pattern of eating could impact influenza epidemics and other communicable diseases by improving resistance to infection. In addition to the health effects, this pattern of eating has proven to be a good method of weight control, and we are continuing to study the process in conjunction with the NIH.
Revue / Journal Title
Medical hypotheses (Med. hypotheses) ISSN 0306-9877

Wednesday, August 29, 2007

Amantadine for Executive Dysfunction Syndrome in Patients With Dementia -- Drayton et al. 45 (3): 205 -- Psychosomatics

Amantadine for Executive Dysfunction Syndrome in Patients With Dementia -- Drayton et al. 45 (3): 205 -- Psychosomatics



Executive dysfunction syndrome, also known as "frontal lobe syndrome," is commonly seen in patients with brain diseases from many causes.1 Executive dysfunction syndrome has been associated with damage to "frontal-subcortical" brain circuits believed to be the anatomical basis of executive control function.2 A variety of neuropsychiatric symptoms indicative of executive dysfunction have been associated with damage to these circuits, including cognitive disturbance, personality change, mood symptoms, and a series of challenging behaviors. Among patients with degenerative dementia, especially advanced dementia, symptoms of executive dysfunction syndrome are common and present a challenging clinical dilemma. While executive dysfunction syndrome occurs with some frequency in patients with Alzheimer's disease,3,4 it is one of the cardinal clinical manifestations of frontotemporal degeneration. Frontotemporal degeneration is a group of disorders with a common histopathology5,6 that involves the degeneration of the frontal and anterior temporal lobes.5,6 This disease has been referred to in the literature by various names, including non-Alzheimer's dementia, semantic dementia, or Pick's disease.5,6 The prevalence of frontotemporal degeneration among all cases of dementia has been estimated to range between 3% and 22%. Frontotemporal degeneration usually presents during the fifth to seventh decades of life and has a strong familial link.5,6 The symptoms of executive dysfunction syndrome usually precede cognitive decline in patients with frontotemporal degeneration.6 Behavioral disinhibition, decreased judgment, and poor insight are common. Executive functioning is usually selectively impaired during the early stages of frontotemporal degeneration. However, in an older person with dementia, it is very difficult to distinguish executive dysfunction syndrome due to Alzheimer's disease from that due to frontotemporal degeneration on clinical grounds, other than by careful history taking.7

The treatment of executive dysfunction syndrome, especially in the context of frontotemporal degeneration, has been very challenging and mostly unsuccessful.1 Reports have suggested that selective serotonin reuptake inhibitors, bromocriptine, carbamazepine, lithium, and other agents may have efficacy in treating executive dysfunction syndrome. However, there is a dearth of controlled trials in this area, and there have been only a few case series reported. In general, treatments have focused on manipulation of the dopamine, serotonin, or cholinergic neurotransmitter systems that are thought to be modulators of the frontal-subcortical loops involved in the pathogenesis of executive dysfunction syndrome.1

We report here the results from an open, uncontrolled chart review study of our experience using the antiviral drug amantadine to treat executive dysfunction syndrome in patients with dementia. Several years ago, clinicians on our team began to use amantadine empirically, outside its labeled use, for the treatment of these symptoms without a formal protocol. This was based on a report that amantadine helped executive dysfunction syndrome in patients with traumatic brain injury8 and by a case series suggesting that dopamine "augmentation" with bromocriptine reduces problem behaviors related to executive dysfunction syndrome.9 The precise mechanism of amantadine's brain action is unknown. It appears to have dopamine-modulating activity in the peripheral and CNS by augmenting the release and inhibiting the cellular reuptake of dopamine.10 Amantadine is also a N-methyl-D-aspartic acid receptor antagonist, which may indirectly enhance dopaminergic transmission and confer neuroprotective effects, similar to its analogue, memantine.11 Moreover, amantadine is known to alter the function of nicotinic acetylcholine receptors in muscle and has a weak antagonist effect on mammalian hippocampal nicotinic acetylcholine receptors. This may signify protective effects in neurodegenerative disorders or in cholinergic toxicity.12

Interesting. Bromocriptine also heals insulin resistance, in addition to apparently helping executive dysfunction

ScienceDaily: Why Red Beans And Rice Can Be Nauseating

ScienceDaily: Why Red Beans And Rice Can Be Nauseating

Scientists have discovered how lectins, a family of proteins believed to be a natural insecticide that is abundant in undercooked legumes and grains, can make you feel temporarily miserable.

"It's known that it can be a toxin," Dr. Paul L. McNeil, cell biologist at the Medical College of Georgia, says of the lectin protein that's commonly found in vegetables. Lectins, which bind strongly to carbohydrates that decorate cell surfaces, have a particular affinity for the heavy-carbohydrate coats of epithelial cells that line the gastrointestinal tract.

Researchers have long known that ingesting too much undercooked lectin can cause nausea, diarrhea and vomiting. What they didn't know was how lectin caused food poisoning.

Work published Aug. 1 in PloS One shows lectins disable GI tract cells, which are constantly bombarded while digesting food, from repairing tears in cells walls from all the activity. Repair normally occurs in seconds: internal membranes move up to patch the tear, the cell recovers and the one-cell layer lining of the GI tract remains intact.

"If those individual cells cannot repair tears, they die," says Dr. McNeil. "That means you have gaps in the integrity of the surface area of the epithelium and you are exposing the nasty internal world of your GI tract to your blood supply."

The epithelial lining is a continuous, natural barrier between digesting food in the GI tract and the blood supply. When intact, it allows only good stuff like nutrients to pass through.

"Your body senses that lack of barrier function and tells you to eliminate the entire contents of the GI tract," says Dr. McNeil, noting that lectin's apparent role as a natural insecticide and as a source of food poisoning are related. "If you get vomiting and diarrhea you are going to eliminate the entire contents of your gastrointestinal tract, right" And, you are not going to eat red beans again the next day, right" That is probably the point if they are natural insecticides. Alcohol will do the same thing. When you drink too much alcohol, you can destroy the lining of your stomach."

Tuesday, August 28, 2007

Depression and Diabetes :: Clinical Geriatrics

Clinical Geriatrics

Recent studies have suggested that certain psychiatric disorders occur with increased frequency among older adults with type 2 diabetes mellitus for several reasons.1,2 First, diabetes is considered to be one of the most psychologically and behaviorally demanding of the chronic medical illnesses. Multiple coping strategies are necessary to deal with the losses that can occur with aging. Because 95% of the management of diabetes is conducted by the patient, a diagnosis of diabetes can lead to increased levels of anxiety, depressive symptoms, and lowered self-esteem. This is often true in individuals who are predisposed to psychiatric disorders or those with limited social supports.


The association between diabetes and depression dates back to 1674, when Dr. Thomas Willis believed that depression caused diabetes. Persons with depression are twice as likely as the general population to develop diabetes.3 The lifetime prevalence of depression among adults with diabetes is estimated to be 28.5%,1 which is almost three times the prevalence rate for the general adult population in the United States1,7 and 14 times the rate for older adults.

Depressive symptoms include sad mood, anhedonia, insomnia with early morning awakening, anorexia, helplessness, hopelessness, excessive guilt, and/or death wishes or suicidal ideas. Depressive symptoms have been significantly and consistently associated with hyperglycemia.5,8 Hypercortisolemia, often associated with depression, is known to increase blood sugar levels, and this may in part explain this finding. Alternatively, due to the degree of self-management needed, comorbid depression in diabetes may lead to poorer outcomes and increased risk of complications because of lower adherence to glucose monitoring, exercise, diet, and medication regimens.9 Depressive symptoms have been associated with decreased quality of life, and higher serum cholesterol and triglycerides10 in elderly persons with diabetes, as well as an increased risk of stroke, particularly in black men with diabetes. In fact, the lowest adherence to dietary and exercise recommendations is among older adults with the highest levels of depressive symptom severity.11,12

Diabetes is also a risk factor for cerebrovascular disease. The associated vascular cerebrocortical abnormalities preferentially occur in the frontal lobes and have been linked with a subtype of depression seen in older adults that presents with psychomotor retardation, loss of interest, paranoia at times, and executive dysfunction.13 This executive dysfunction can further interfere with adherence to diabetes self-management, because planning, sequencing, and organizing are all adversely affected.14


Several prospective studies have found that obesity in middle age, as well as diabetes in later life, can increase the risk for developing dementia in at least two different ways.21-23 First, animal studies have suggested that depletion of the neuronal insulin receptor mimics some aspects of the neurodegeneration seen in Alzheimer’s disease.24 This provides support for the idea that Alzheimer’s disease may be caused in part by neuronal insulin resistance. Type 2 diabetes is a risk factor for Alzheimer’s disease, particularly among carriers of the ApoE-4 gene.25 Second, the presence of multiple cardiovascular risk factors at midlife substantially increases the risk of late-life dementia in a dose-dependent manner,26 and type 2 diabetes is associated with a twofold increased risk of vascular dementia.27


Any identified reversible causes of cognitive impairment, such as medications, nutritional deficiencies, and metabolic disturbances, should be addressed. Neuropsychological testing should be considered if the etiology of cognitive impairment is unclear.

Although Alzheimer’s disease is the most common cause of dementia, in the older person with diabetes the prevalence of vascular dementia or a mixed dementia is high. Additionally, cholinergic deficits do occur in vascular dementia due to ischemia of basal forebrain nuclei and of cholinergic pathways, and do respond modestly to the cholinesterase inhibitors used to treat Alzheimer’s disease.


Risk reduction for dementia in diabetes, especially control of glucose hypertension and dyslipidemias, are likely to be a more effective way to prevent cognitive deterioration in vascular dementia. Additional education should be provided regarding the importance of weight control, exercise, and nutrition in disease self-management.


Studies have consistently found that rates of diagnosed diabetes in patients with schizophrenia exceed general population figures,33,34 even before the widespread use of the newer second-generation (or atypical) antipsychotics. Among older psychiatrically hospitalized patients, increased prevalence rates of diabetes were also found in patients with schizoaffective and bipolar disorder.35 Although most risk factors for diabetes are similar to those seen in the general population, the prevalence of those risk factors is much higher among patients with serious mental illness. For example, patients with schizophrenia are more likely than age-matched controls to be overweight, consume fewer fruits and vegetables, be sedentary,36,37 and have other cardiovascular risk factors, especially tobacco use.38 As a result, patients with schizophrenia have higher mortality rates, at younger ages, than the general population.38

More recently, the use of the newer atypical antipsychotic medications appears to increase the risk of acquiring or exacerbating type 2 diabetes,39 rarely causing diabetic ketoacidosis.


For a variety of reasons, several psychiatric disorders frequently co-occur with diabetes mellitus. Diabetes risk reduction, including nutritional/physical activity counseling, control of blood pressure, lowering cholesterol and triglyceride levels, weight loss, and increased physical activity can have a positive impact on both the diabetes and the psychiatric illness. Screening for cardiovascular and metabolic risk factors is particularly important when atypical antipsychotics are to be prescribed. Desired benefits of these medications must be weighed against the potential adverse effects, especially the possibility of cerebrovascular events, in older adults with dementia and behavioral disturbances. The identification and treatment of the psychiatric illness can often improve diabetes outcomes.

Monday, August 27, 2007

Drop Foreseen in Median Price of U.S. Homes - New York Times

Drop Foreseen in Median Price of U.S. Homes - New York Times

The median price of American homes is expected to fall this year for the first time since federal housing agencies began keeping statistics in 1950.

Economists say the decline, which could be foreshadowed in a widely followed government price index to be released this week, will probably be modest — from 1 percent to 2 percent — but could continue in 2008 and 2009. Rather than being limited to the once-booming Northeast and California, price declines are also occurring in cities like Chicago, Minneapolis and Houston, where the increases of the last decade were modest by comparison.

The reversal is particularly striking because many government officials and housing-industry executives had said that a nationwide decline would never happen, even though prices had fallen in some coastal areas as recently as the early 1990s.

While the housing slump has already rattled financial markets, it has so far had only a modest effect on consumer spending and economic growth. But forecasters now believe that its impact will lead to a slowdown over the next year or two.

“For most people, this is not a disaster,” said Nigel Gault, an economist with Global Insight, a research firm in Waltham, Mass. “But it’s enough to cause them to pull back.”

In recent years, many families used their homes as a kind of piggy bank, borrowing against their equity and increasing their spending more rapidly than their income was rising. A recent research paper co-written by the vice chairman of the Federal Reserve said that the rise in home prices was the primary reason that consumer borrowing has soared since 2001.

Now, however, that financial cushion is disappearing for many families. “We are having to start from scratch and rebuild for a down payment,” said Kenneth Schauf, who expects to lose money on a condominium in Chicago he and his wife bought in 2004 and have been trying to sell since last summer. “We figured that a home is the place to build your wealth, and now it’s going on three years and we are back to square one.”

On an inflation-adjusted basis, the national median price — the level at which half of all homes are more expensive and half are less — is not likely to return to its 2007 peak for more than a decade, according to Moody’s, a research firm.

Unless the real estate downturn is much worse than economists are expecting, the declines will not come close to erasing the increases of the last decade. And for many families who do not plan to move, the year-to-year value of their house matters little. The drop is, of course, good news for home buyers.

It does, however, contradict the widely held notion that there is no such thing as a nationwide housing slump.


Housing prices have previously declined for long stretches in various regions. Most recently, prices fell in California and in the Northeast during the recession of the early 1990s.

The current slump is different from that one, though, in both depth and breadth. In fact, the national median price rose only slightly faster than inflation from 1950 to the mid-1990s.

But as interest rates fell and lending standards became looser, prices started rising rapidly in the late 1990s, even in places like Chicago, which had rarely seen a real estate boom. The result was a “euphoric popular delusion” that real estate was a can’t-miss investment, said Edward W. Gjertsen II, president of the Financial Planners Association of Illinois. “That’s just human nature.”


For all the attention that the uninterrupted growth in national house prices received, some economists argue that it was misplaced. The Case-Shiller index, which many experts consider more accurate than the government measure, did show a drop in prices in the early 1990s. (Unlike the government’s measure, it includes mortgages of more than $417,000, which are not held by Fannie Mae or Freddie Mac.)

After adjusting for inflation — the most meaningful way to look at any price, economists say — even the government’s index fell in the early 1990s.

Dean Baker, an economist in Washington who has been arguing for the last five years that houses were overvalued, said the idea that house prices could go only up had fed the bubble.

“It was very misleading,” said Mr. Baker, co-director of the Center for Economic and Policy Research, a liberal research group. There are a lot of people, he said, who bought “homes at hugely inflated prices who are going to take a hit. You also have a lot of people who borrowed against those inflated prices.”

Overeating, dopamine and exercise

Stamp Out Overeating

It might sound unlikely but while exercise can help work up an appetite, it could also be a key to preventing over-eating and obesity.

A doctor and colleagues from the Department of Medicine at the Brookhaven National Laboratory in New York have found that one of the reasons some people overeat is because of a deficiency of a natural chemical in the brain, known as dopamine.

Dopamine is a chemical that helps regulate the feelings of fullness when we eat, so that we eat until we're reasonably comfortable and don't overindulge. (Science is yet to discover why this doesn't work at Christmas.)

The group found that severely obese people had a reduced number of dopamine receptors in their brains compared with non-obese people. This meant the obese people had to eat more food in order to experience the same feelings of fullness as their non-obese counterparts.

The researchers could not conclude whether the brain changes they detected were a consequence or cause of obesity, but suggested that strategies aimed at improving or controlling dopamine function might prove beneficial for treating obese people. Unfortunately, many of the drugs shown to alter dopamine levels are highly addictive. This is where exercise enters the equation.

Studies on animals have shown exercise can increase dopamine release and the number of dopamine receptors, factors which can stop the desire to over-eat. This led the authors to suggest obese people may be able to boost their dopamine response through exercise instead of eating.

routines and ADD

Here's a great post from Sarah Wright's blog about routines and ADD!

Four Tricks to Get Back On Track
August 26th, 2007

Well, here it is. Almost Labor Day. Many families, including my own, are now looking at starting up their “regular” routines again. And many are looking forward to it. I know I am. I had a great summer that included traveling, camping, visiting with people I am fond of whom I don’t get to see very often, chauffeuring my son all over the place, and getting to some projects I really wanted to get done.

What I didn’t do though, is work on this blog. And it isn’t because I didn’t think about it or didn’t want to. What I did was a very ADHD thing. I took time off from a routine, thinking it would only be for a couple of weeks, and then the routine totally fell apart. It’s now been a couple of months since I wrote regularly.

Has this ever happened to you? You’ve got a good thing going. You can trust yourself to do what ever it is on a regular basis. And then in a matter of days it’s like you never had that habit or routine at all? This happens to everyone some of the time, but people with ADHD are particularly prone to this kind of lapse.

We all know that the level of payoff or consequence of letting a routine go doesn’t affect a darn thing. What does matter is the more immediate the payoff or consequence, the easier it is to do something. It doesn’t matter if the payoff or consequence is big, if it’s not immediate, it’s hard to take it seriously. Unfortunately, even with immediate payoff or consequence, there’s no guarantee of follow through.

So now that I’m working to get back on track myself, I thought I’d share four of my strategies for developing routines:

1. Make it easy, make it quick.
2. Find ways to make it interesting.
3. Up the ante of doing or not doing it.
4. Get a buddy to do it with you.

Here are some applications to help you get the idea.

1. Assuming you brush your teeth regularly already(!), put your pills out next to the tooth brush so it makes it easy to both remember them and take them (the “easy and quick” trick).
2. If you need to exercise and like numbers, keep statistics on your progress (the “make it interesting” trick).
3. If housekeeping is your bugaboo, invite people over on a regular basis so you’ll have to clean up or be embarrassed (the “up the ante” trick).
4. If doing the dishes is something you usually put off, get someone to do them with you (the “buddy” trick).

Sunday, August 26, 2007

Obesity Doesnt Always Equal Diabetes -

Obesity Doesnt Always Equal Diabetes -

Obesity Doesnt Always Equal Diabetes
08.24.07, 12:00 AM ET

FRIDAY, Aug. 24 (HealthDay News) -- Obesity doesn't mean a person is destined to develop diabetes, experiments in mice suggest. Instead, it may all depend on where the fat is stored.

Mice that overate and were very obese still didn't become diabetic, because the activity of two hormones let them store extra calories in fat tissue rather than in their livers or heart muscle.

"What this mouse model shows is what we have appreciated clinically for a while," said lead researcher Philipp Scherer, a professor of internal medicine and director of the Touchstone Center for Diabetes Research at the University of Texas Southwestern Medical Center at Dallas.

"Basically, it shows that for individuals who have the ability to expand their adipose [fat] tissue mass appropriately for the number of calories they take up, those individuals fare much better than someone who has a more reduced capacity to expand their adipose tissue," Scherer said.

If fat isn't stored in the adipose tissue, it ends up in the liver and muscles. That, in turn, causes significant insulin resistance that can lead to diabetes, Scherer explained.


Scherer noted that in people as in mice, where fat is stored is largely determined by genetics. "You have a lot of obese individuals who are not type 2 diabetics, and you have lean individuals that can be type 2 diabetics," he said. Type 2 diabetes is the most common form of the disease, and it is most often tied to overweight or obesity.

All of this means that measuring fat as an indicator of general health might not hold up anymore, Scherer said. "It's really a matter of where we deposit these excess calories," he said. "Fat is a little like real estate, it's all about location, location, location."

Saturday, August 25, 2007

high fructose corn syrup = diabetes! maybe... Sugary Sodas High in Diabetes-Linked Compound

Sugary Sodas High in Diabetes-Linked Compound
08.24.07, 12:00 AM ET

FRIDAY, Aug. 24 (HealthDay News) -- Sodas sweetened with high fructose corn syrup contain high levels of a potentially dangerous compound often found in the blood of diabetics, a new study concludes.

It could be cause for concern, experts say, because the "reactive carbonyls" in these sugary drinks could bump up diabetes risk, particularly in children.

High fructose corn syrup (HFCS) "is the most popular sweetener used in foods and beverages today, it has been used in the United States for many years," said Chi-Tang Ho, a professor of food science at Rutgers University in New Brunswick, N.J.

Virtually all carbonated soft drinks in the United States are sweetened with HFCS, mostly because it dissolves easily, is sweeter than other types of sugar, and is more economical. Although the study did not specifically investigate the risk of diabetes with HFCS drinks, Ho suggested that steering clear of them might be a healthy move.

His team tested 11 carbonated soft drinks that contained HFCS and found they contained high levels of reactive carbonyls -- compounds that are normally elevated in the blood of people with diabetes.

The study was expected to be presented Thursday at the American Chemical Society annual meeting in Boston.

The reactive carbonyls in the blood of diabetics have been linked to complications of diabetes, such as tissue damage, Ho said.

In his study, Ho found that just one can of HCFS-sweetened carbonated beverage contained about five times the amount of reactive carbonyls found in the blood of a person with diabetes. In comparison, sucrose -- ordinary table sugar -- contains no reactive carbonyls, he said.

Ho suggests that parents check the labels of all the beverages their children consume and discourage them from drinking those containing HCFS. Instead, substitute diet carbonated beverages, water or fruit juices.

Ho also noted that other types of beverages may contain high levels of HFCS, as well. So-called "hydrating" sports drinks often contain HFCS. Ho is particularly concerned about high-caffeine energy drinks.

"I worry about kids in high school," he said. "They rely on energy drinks to do their homework and stay awake. The level of [HFCS] is so high."

Adding a beneficial antioxidant compound found in tea called "epigallocatechin gallate," or EGCG, to drinks that contain HFCS appears to lower reactive carbonyl levels, Ho said. That could mean that drinking beverages that contain both tea extracts and HFCS may not be as harmful as drinking HCFS-sweetened sodas, he said. However, further research is needed to prove that.

Beverages that contain both fruit juice and HFCS also appear to have fewer reactive carbonyl levels, possibly because of beneficial compounds called phytochemicals found naturally in fruit juice, Ho said.

Lona Sandon is assistant professor of clinical nutrition at the University of Texas Southwestern Medical Center at Dallas, and a spokeswoman for the American Dietetic Association. She said the Rutgers study is still inconclusive.

"It doesn't address the risk [of diabetes], it simply shows a possible mechanism for why there might be more risk in children who drink more HFCS-sweetened sodas," she said.

"Although there are other epidemiologic studies showing a correlation between sweetened soda and diabetes, it is not a proven cause-and-effect," Sandon said.

Friday, August 24, 2007

Scientists Find Link Between Dopamine and Obesity

Scientists Find Link Between Dopamine and Obesity

Scientists Find Link Between Dopamine and Obesity

UPTON, NY -- Dopamine, a brain chemical associated with addiction to cocaine, alcohol, and other drugs, may also play an important role in obesity. According to a study by scientists at the U.S. Department of Energy's Brookhaven National Laboratory, obese people have fewer receptors for dopamine, a neurotransmitter that helps produce feelings of satisfaction and pleasure. The findings, which will appear in the February 3, 2001 issue of The Lancet, imply that obese people may eat more to try to stimulate the dopamine "pleasure" circuits in their brains, just as addicts do by taking drugs.

"The results from this study suggest that strategies aimed at improving dopamine function might be beneficial in the treatment of obese individuals," says physician Gene-Jack Wang, the lead scientist on the study.

Brookhaven scientists have done extensive research showing that dopamine plays an important role in drug addiction. Among other things, they¹ve found that addictive drugs increase the level of dopamine in the brain, and that addicts have fewer dopamine receptors than normal subjects.

"Since eating, like the use of addictive drugs, is a highly reinforcing behavior, inducing feelings of gratification and pleasure, we suspected that obese people might have abnormalities in brain dopamine activity as well," says psychiatrist Nora Volkow, who was also involved in the study.
The lower PET scan images, labeled FDG, show glucose metabolism in the brains of obese and control (comparison) subjects. There are no differences. The upper PET scans show where the radiotracer C-11 raclopride binds to dopamine receptors. These images show that obese subjects have fewer dopamine receptors than control subjects.

To test this hypothesis, the scientists measured the number of dopamine receptors in the brains of ten severely obese individuals and ten normal controls. Their method consisted of giving each volunteer subject an injection containing a radiotracer, a radioactive chemical "tag" designed to bind to dopamine receptors in the brain. Then, the researchers scanned the subjects' brains using a positron emission tomography (PET ) camera. The PET camera picks up the radioactive signal of the tracer and shows where it is bound to dopamine receptors in the brain. The strength of the signal indicates the number of receptors.

Obese individuals, the scientists found, had fewer dopamine receptors than normal-weight subjects. And within the obese group, the number of dopamine receptors decreased as the subjects' body mass index, an indicator of obesity, increased. That is, the more obese the individual, the lower the number of receptors.

"It's possible that obese people have fewer dopamine receptors because their brains are trying to compensate for having chronically high dopamine levels, which are triggered by chronic overeating," says Wang. "However, it's also possible that these people have low numbers of dopamine receptors to begin with, making them more vulnerable to addictive behaviors including compulsive food intake."

You know, this makes alot of sense too. I've been theorizing that insulin insensitivity causes dopamine problems. For instance, insulin lowers dopamine levels. But it's also possible that low dopamine, which means less of the reward chemicals in the brain, also called reward deficiency syndrome, causes people with low dopamine to eat more, and/or do drugs and stuff. Could also be both, in a vicious cycle.

Executive dysfunction in hyperhomocystinemia responds to homocysteine-lowering treatment -- Boxer et al. 64 (8): 1431 -- Neurology

Executive dysfunction in hyperhomocystinemia responds to homocysteine-lowering treatment -- Boxer et al. 64 (8): 1431 -- Neurology

Executive dysfunction in hyperhomocystinemia responds to homocysteine-lowering treatment
A. L. Boxer, MD, PhD, J. H. Kramer, PsyD, K. Johnston, MD, J. Goldman, MS, MPhil, R. Finley, BPh and B. L. Miller, MD

From the Memory and Aging Center, Department of Neurology (Drs. Boxer, Kramer, and Miller, J. Goldman and R. Finley), UCSF, and Genetics Department (Dr. Johnston), Permanente Medical Group, San Francisco, CA.

Address correspondence and reprint requests to Dr Boxer, Memory and Aging Center, Department of Neurology, UCSF, Box 1207, San Francisco, CA 94143-1207; e-mail:

An elevated serum homocysteine level is a risk factor for the development of cognitive impairment. Reported is a late-onset case of hyperhomocystinemia due to a vitamin B12 metabolic deficit (cobalamin C) with cognitive impairment, primarily in frontal/executive function. After homocysteine-lowering therapy, the patient’s functional and neuropsychological status improved in conjunction with a decrease in leukoariosis on his MRI scan. These findings suggest that homocysteine-related cognitive impairment may be partially reversible.

Wednesday, August 22, 2007

ScienceDirect - Comprehensive Psychiatry : Seasonality and circadian preference in adult attention-deficit/hyperactivity disorder: clinical and neuropsychological correlates

ScienceDirect - Comprehensive Psychiatry : Seasonality and circadian preference in adult attention-deficit/hyperactivity disorder: clinical and neuropsychological correlates



The objective of the study was to measure both seasonal mood change and circadian preference, and their clinical and neuropsychological correlates, in adults with ADHD during the fall/winter months.


Twenty-nine adults with attention-deficit/hyperactivity disorder (ADHD) were assessed in the fall/winter season using self-report measures of ADHD, mood, seasonality, and circadian preference. Neuropsychological tests were also completed. Correlations between chronobiologic variables and clinical/neuropsychological measures were performed.


Consistent with prior work in adult ADHD, high rates of seasonal depression were reported in this sample. Based on the morningness-eveningness questionnaire, which assesses circadian preference 11 (40.7%, N = 27) subjects were designated as evening types and only 5 (18.5%) as morning types, a distribution highly discrepant with general population studies. Later circadian preference, independent of seasonality, was strongly correlated with both self-reported symptoms of ADHD and neuropsychological deficits, including impulsive responding and poor target discrimination. None of these findings was attributable to state depression.


In the fall/winter period, a mood-independent delay in circadian phase may contribute significantly to core pathology in many adults with ADHD. These findings establish a potential target for chronobiologic treatments such as light therapy in this complex population.

Monday, August 20, 2007

Night owls likely to be problem children

Night owls likely to be problem children

The researchers found several factors were related to anti-social behaviors in the study group, particularly in the boys who tended to exhibit more rule-breaking behaviors than did their peers.

The findings are published in the Developmental Psychology journal. For girls, a preference for evening activities was associated with a higher incidence of relational aggression or aggressive behavior toward their peers.

Boys who experienced prolonged high levels of cortisol - smaller decreases in cortisol levels from the time of awakening until 4 pm - tended to have more behavior problems than did their peers, the report indicates. The association was not true for girls, however.

Normally, levels of cortisol, the stress hormone associated with circadian rhythms, peak in the morning upon awakening and plateau during the afternoon and evening hours.

Abnormalities in cortisol secretion have also been associated with clinical depression and anti-social behavior in earlier studies, the researchers note.

Study: Virus may contribute to obesity -

Study: Virus may contribute to obesity -

WASHINGTON (AP) -- In the buffet of reasons for why Americans are getting fatter, researchers are piling more evidence on the plate for one still-controversial cause: a virus.

For several years, researchers have looked at a possible link between obesity and adenovirus-36.

New research announced Monday found that when human stem cells -- the blank slate of the cell world -- were exposed to a common virus they turned into fat cells. They didn't just change, they stored fat, too.

While this may be a guilt-free explanation for putting on pounds, it doesn't explain all or even most of America's growing obesity problem. But it adds to other recent evidence that blames more than just super-sized appetites and underused muscles for expanding waistlines.

For several years, researchers have looked at a possible link between obesity and this common virus, called adenovirus-36, from a family of viruses that cause colds and pinkeye in people. They had already found that a higher percentage of fat people had been infected with the virus than nonfat people. They had exposed animals to the virus and got them to fatten up and even found a a gene in the virus that causes animals to get obese.


If a viral cause of obesity can be confirmed, a vaccine could be developed, maybe within five to 10 years, to prevent the virus from making some people fat, Dhurandhar said. However, it wouldn't help people already obese, he said.

Outside experts are intrigued but worry about people blaming viruses for all obesity, when this may be just one of many causes. It doesn't mean it's OK to overeat, blame a bug or wait for some kind of antivirus medicine, they said.

"The cause for obesity in everyone is the same," said Dr. Samuel Klein, director of the Center for Human Nutrition at the Washington University School of Medicine in St. Louis. "You eat more calories than you burn up; You can't get away from that basic law of physics."

But there are many causes that trigger overeating and extra storage of fat in the body, including the virus, Klein said. However, he said he considers the virus only a small factor, easily outweighed by genetics and even childhood eating habits.

Dhurandhar said some of his earlier research found that 30 percent of obese Americans had developed antibodies to the virus, showing they had been exposed to it at some point. But for non-obese people, only 11 percent had antibodies, he said.

That means for some people it is not their fault they are fat, Dhurandhar said.

But Klein said that's not completely right.

"We don't want obese people to feel that it's all their fault because it is not all their fault ... but clearly the buck finally lies with the person," Klein said.

Yeah, Dr. Klein, calories in, calories out. Too bad only carb calories raise your triglycerides, lower your HDL, cause your bloodsugar and insulin to skyrocket, cause insulin resistance, cause unbelievable hunger pangs, and only carbs can get turned into body fat. Other than that, yeah just a calorie. Go on a 1,000 calorie a day diet eating cupcakes, see how that works for you.

About the virus, yeah, that's interesting. Could be a factor, but not the whole ball of wax I think. Read a little of a book called the potbelly something or other about this same general idea. Cortisol was implicated in helping the virus spread. Lack of sleep compromises your immune system. I'm sure in the end weight problems are multi-factorial.

Half of dogs and cats in the UK are now overweight | News | This is London

Half of dogs and cats in the UK are now overweight | News | This is London

IngentaConnect Insulin Resistance and Executive Dysfunction in Older Persons

IngentaConnect Insulin Resistance and Executive Dysfunction in Older Persons


To evaluate the association between insulin resistance (IR) and executive dysfunction in a large, population-based study of older persons without diabetes mellitus (DM) or dementia.


IR is independently associated with frontal cortex function evidenced by poor TMT times in older persons without DM or dementia.

Sunday, August 19, 2007

ScienceDaily: Chronic Fatigue Syndrome Linked To Impaired Stress Response

ScienceDaily: Chronic Fatigue Syndrome Linked To Impaired Stress Response

Subtle alterations of a hormonal stress response system called the HPA axis may play a role in chronic fatigue syndrome, according to a study in the November/December issue of Psychosomatic Medicine.

A smoothly functioning hypothalamus-pituitary-adrenal, or HPA, axis helps the body remain stable under physiological and psychological stress through the actions of three hormones. First, the brain portion called the hypothalamus secretes a hormone that stimulates the pituitary gland to secrete a second hormone. This second hormone causes the adrenal glands to create cortisol.

Problems can occur at any point in this process and result in a variety of diseases.

{including possibly chronic fatigue syndrome}


Chronic fatigue syndrome is characterized by debilitating fatigue that can include including muscle aches, low-grade fever and sleep disturbances. Its cause is not understood.


Participants were also given a series of insulin injections known as the insulin tolerance test. "The ITT is considered the gold standard for testing the integrity of the entire HPA axis," Gaab says.

The researchers found significantly lower response levels of one of the HPA hormones, called ACTH, among the chronic fatigue patients compared with the healthy volunteers, during both stress tests as well as the ITT test. In fact, the chronic fatigue patients had significantly lower levels of the hormone before the testing even began.

"These results suggest that on a central level, subtle dysregulations of the HPA axis exist" in chronic fatigue syndrome patients, Gaab says, adding that future studies should include repeated evaluation of the HPA axis over the course of the syndrome.

Gaab and colleagues note that the possible role of cortisol in chronic fatigue syndrome still merits investigation, as low doses of hydrocortisone have shown some positive results in chronic fatigue patients.

Interesting. Sometimes I've seen the HPA axis referred to as the LIMBIC-HPA access. Interesting to me because according to the Dr. Amen test I have limbic system ADD. The limbic system can generate a chronic depressive state. I find it interesting that this is so closely connected to the HPA access, and related to insulin insensitivity. Again, I'm interested to find links between ADD, depression and insulin insensitivity.

Psychiatric Times :: The Role of Cortisol and Depression: Exploring New Opportunities for Treatments

Psychiatric Times

It is now established that in conditions in which there are raised endogenous or exogenous corticosteroids (including Cushing's disease and severe mood disorders), there is also a significant degree of cognitive impairment (Wolkowitz et al., 1990). Studies in experimental animals have shown deficits in learning and memory following chronic administration of glucocorticoids (Lupien and McEwen, 1997), as well as marked atrophy of neurons in the hippocampal formation. It has been postulated that a similar neurodegenerative effect of cortisol may underlie some of the cognitive deficits observed in humans suffering from severe mood disorders (Sapolsky et al., 1986).

While there is substantial evidence to indicate that the hippocampus is particularly sensitive to elevation of glucocorticoids, the effects on other areas of the brain are less clear. Recent clinical data have reported that cortisol treatment induces cognitive deficits in healthy humans, and these deficits appear to be mediated in part via the frontal lobe, suggesting that this brain area may also be sensitive to the neurodegenerative effects of cortisol (Young et al., 1999). The deficits in healthy volunteer study participants are reversible, but this may not be the case with the cognitive deficits induced by hypercortisolemia associated with mood disorders (Ferrier et al., 1999; Young et al., 1999). A more recent study indicated that the frontal lobes are adversely affected by cortisol, which may illustrate a similar pattern of degeneration to that which occurs in the hippocampus (Young et al., in press). Moreover, the traditional assumption that patients with severe mood disorders make a full inter-episode recovery has recently been challenged. Although cognitive deficits do show some improvement on remission of affective symptoms (paralleling the return of normal HPA function), this improvement is not sustained. Studies have identified a specific deficit in executive control in a cohort of patients prospectively verified as euthymic (Thompson et al., 2001), replicating an earlier finding by our group (Ferrier et al., 1999).

This one is a little dense, but basically cortisol creates depression. It also messes with your prefrontal cortex and executive functions of the brain. Like ADD does. Alcohol, caffeine, lack of sleep and external stressors increase cortisol.

Friday, August 17, 2007

Alcohol and Cortisol

June Russell's Health Facts
Alcohol - Cortisol

[Alcohol and Cortisol] [Importance of Cortisol]
Alcohol and Cortisol

Hormones are chemical messengers that control and coordinate the functions of all tissues and organs. Each hormone is secreted from a particular gland and is distributed throughout the body to act on tissues at different sites. Two areas of the brain, the hypothalamus and the pituitary, release hormones as do glands in other parts of the body, for example, the thyroid, thyroid glands, gonads, pancreas, and parathyroid. In order for hormones to function properly, the amount and timing of their release must be finely coordinated, and the target tissues must be able to respond to them accurately. Alcohol can impair the functions of the hormone-releasing glands and of their target tissues, thereby causing serious medical consequences.
{“Alcohol and Hormones,” Alcohol Alert from NIAAA, - Jul. 2000}

Beer and liquor tend to raise levels of cortisol.
{Prevention magazine, Dec. 1999}

Alcohol encourages cortisol surges and hormone imbalances.
{"Keeping your Adrenals Healthy," Healing Foods and Movements, Catherine Fahey,, Apr. 2003}

Cheating on sleep for only a few nights increases brain levels of cortisol, a potentially harmful stress hormone, and high levels of cortisol can damage brain cells in areas of the brain responsible for memory and learning. Adequate exercise and regular sleeping hours facilitate sleep, while caffeine, alcohol and stimulant drugs impair sleep and raise cortisol levels.
{"Wake Up To the Need For Sleep," San Francisco Examiner, June 7, 1998, excerpted from Spectrum magazine, on - Apr. 2003}
The Importance of Cortisol

Chronic stress causes an over-production of a hormone called cortisol, which has a profound negative effect on the brain. It contributes to the death of brain cells, interferes with the functioning of neurotransmitters, and starves the brain of its only source of fuel, glucose.
{“Physical Fitness for Your Brain,” New Age Journal, 1997- 1998 Special Edition}

The adrenals secrete the body’s four main stress hormones: adrenaline, norepinephrine, DHEA and cortisol. These hormones are secreted cyclically, with the highest levels dispatched in the morning and the lowest levels at night. Any disruption in the amount of adrenal output can cause serious health problems. Cortisol, the body’s principal anti-inflammatory hormone, rises during periods of stress, as we grow older, and during periods of chronic pain. Some of the deleterious effects of cortisol imbalance on health are low energy, muscle atrophy, poor bone repair and increased bone loss, thyroid dysfunction, depressed immune system, poor sleep quality, poor skin regeneration and impaired growth hormone release.

Studies show that prolonged depression or stress leads to elevated levels of cortisol, a ‘stress’ hormone produced by the adrenal glands. This in turn appears to shrink or atrophy the hippocampus, the part of the brain associated with many kinds of memory and learning. This process is particularly damaging in the elderly {Reviews in the Neurosciences}, but there is no strong evidence that the hippocampus shrinks as a part of normal aging. Studies show that all people with Alzheimer’s disease have damage to the hippocampus, but their cortisol production varies.
{“Fact or Fiction? All Memory Loss is Age-related,” Vitamin Research Products, June 2000}

Cortisol is a natural steroid that raises blood sugar levels and suppresses inflammation, but it also suppresses the immune system.
{"Treating Adrenal Exhaustion," - May 2003}

Cortisol, the hormone produced by your body in times of high stress, can interfere with your ability to remember words, phone numbers and other details.
{"Mental Fitness," - Jan. 2003}

To reverse the consequences of aging you need to reduce the hormones such as insulin, cortisol and eicosanoids and there is no magic pill to reduce these hormones, only a consistent dietary program on a lifetime basis.
{Dr. Barry Sears, author of the "Zone Diet," Dr. Sears, June E-magazine, June 16, 2003}

Clinical and Ethical Implications of Impaired Executive Control Functions for Patient Autonomy -- Workman et al. 51 (3): 359 -- Psychiatr Serv

Clinical and Ethical Implications of Impaired Executive Control Functions for Patient Autonomy -- Workman et al. 51 (3): 359 -- Psychiatr Serv

Executive control functions have been defined as "those processes which orchestrate relatively simple ideas, movements, or actions into complex goal-directed behavior"(1). Without them, behaviors important to independent living can be expected to break down into their component parts; patients become overdependent on environmental cues and are easily distracted and perseverative (2,3).

Executive functions have been associated with three prefrontal-subcortical subtypes, the dorsolateral prefrontal, the orbitofrontal, and the anterior cingulate (mesiofrontal) (4,5,6). Damage to the dorsolateral subtype impairs abstraction and hypothesis generation. Orbitofrontal lesions lead to impaired emotional control. Irritability and mood swings in the absence of pervasive mood disorder are common sequelae. Mesiofrontal lesions lead to apathy, indifference, and impairment of goal-directed attention. Patients become passive and disorganized (7,8). In 1994 the American Psychiatric Association added executive control functions to the list of cognitive domains that should be considered when making a diagnosis of dementia (9).

Impairments in executive control functions are not limited to dementia, where they contribute greatly to patient morbidity, caregiver burden, and institutionalization (3,10,11). Nor are they limited to traumatic brain injury of the frontal lobes. Specific systemic illnesses that appear to be related to declines in frontal lobe abilities include hypertension, diabetes, and chronic obstructive pulmonary disease (12). Impaired executive control functions can also be recognized in major depression, Parkinson's disease, subcortical strokes, and psychotic disorders (3,13,14).

That's what I'm looking for. A link between diabetes and ADD.

Individuals with impaired executive control functions often do well on many standard cognitive assessments and function adequately in a structured setting.

Yup. Routine and structure help big time. One guy at the ADD support group I've visited said he was happy in the army. They tell you what to do all the time. I find that disturbing because I'm a very contrarian, independent person. But when I have the freedom I want I don't know what to do with it.

Wednesday, August 15, 2007

Study finds link between lack of sleep, weight gain

Study finds link between lack of sleep, weight gain

Study finds link between lack of sleep, weight gain

Sleep quality, quantity affect hormones regulating appetite and metabolism.

By Marjie Gilliam, Cox News Service

Is there a correlation between lack of sleep and weight gain?

Every two years for 16 years, the Nurses Health Study collected data from more than 68,000 women ages 40 to 65, which included information on sleep habits and body weight. The study found that participants who slept five hours a night were 32 percent more likely to experience a weight gain of 33 pounds or greater, and 15 percent more likely to become obese, compared with participants who slept seven hours a night.

The group that slept for six hours were 12 percent more likely to experience major weight gain and 6 percent more likely to become obese when compared with those who slept seven hours a night. One possible explanation for these differences is that lack of sleep causes the body to burn calories less efficiently. Variations in eating habits and exercise among the groups also explained some of the weight gain, but no single factor can be pinpointed.

The amount and quality of sleep affects hormones that regulate appetite and metabolism. A study at the University of Chicago found that participants who slept only four hours a night for two nights had an 18 percent decrease in leptin and a 28 percent increase in ghrelin. Leptin is a hormone that suppresses appetite by affecting how full and satisfied we feel after eating. Ghrelin is a hormone that stimulates appetite.

With sleep deprivation, levels of leptin fall, while ghrelin levels increase. Participants in the study, all healthy young men, showed a 24 percent increase in appetite along with elevated cravings for sweets, salty foods and starchy foods such as bread and pasta. Leptin is only one of a large number of hormones that can influence body weight, while environment and lifestyle behaviors remain the primary causes of weight gain.

Mental health suffers, too

When a person is fatigued from too little sleep, he or she is also less likely to exercise, making it easier to put on extra pounds. Lack of sleep affects other hormones, such as cortisol, insulin and growth hormone, potentially causing a desire for high-calorie foods.

It is believed that decreased amounts of REM sleep can lead to increased food intake. REM stands for "Rapid Eye Movement" and is the "dream" phase of the sleep cycle. During REM, sleep brain activity increases with less muscle activity.

Aside from the potential increase in body weight, sleep deprivation can have serious effects on physical and mental health. When the brain has to work harder in an effort to counteract sleep deficit, its ability to function deteriorates quickly. Memory, concentration and problem-solving capabilities decrease. The ability to handle everyday stress, maintain a healthy immune system and control emotions is also compromised.

Read the book "Lights out!". This article touches directly on that. Lack of sleep indicates "summer" to the body. Summer is when you would find carbs in the wild, and you would crave them due to the short nights. This helps you to pack on weight for the winter lean months, and long nights of sleep and living off your fat pad. But now, with TV and light bulbs, we never go to sleep.

Also, lately I find myself interested in cortisol, as it can produe depression, stress, confusion, weight gain, etc. It can be increased by lack of sleep, AND by coffee. I'm starting to think caffeine is implicated in weight loss and the many maladies of our time.

Monday, August 13, 2007

SPECT Brain SPECT Imaging Information and Resources

SPECT Brain SPECT Imaging Information and Resources

5. Limbic ADD, with symptoms of inattention and/or hyperactivity-impulsivity and negativity, depression, sleep problems, low energy, low self-esteem, social isolation, decreased motivation and irritability. Brain SPECT imaging typically shows increased central limbic system activity and decreased prefrontal cortex activity. This subtype typically responds best to stimulating antidepressants such as buprion or imipramine, or venlafaxine if obsessive symptoms are present.

I took the test in Dr. Amen's book, and I have this suptype of ADD according to my results. Seems to fit.

Saturday, August 11, 2007

Prevalence of attention deficit/hyperactivity disorder among adults in obesity treatment

BioMed Central | Full text | Prevalence of attention deficit/hyperactivity disorder among adults in obesity treatment


Bariatric patients showing poor "focus" during treatment more often failed to lose weight or maintain reduced weight. Evaluation of these patients identified a number having attention deficit/hyperactivity disorder (ADHD), evidently a potent factor limiting successful weight control. After searches found no published reports describing comorbid ADHD and obesity, this report was conceived to begin exploring the prevalence and characteristics of these patients.


Clinical records of 215 patients receiving obesity treatment during 2000 were reviewed. Data collected and analyzed included age, sex, beginning and ending body mass index (BMI), number of clinic visits, months of treatment, and diagnostic category (ADHD, some ADHD symptoms, non-ADHD). DSM-IV criteria were used, except age of onset was modified to <= 12 years.


Whole sample ADHD prevalence was 27.4% (CI:21.1,32.9), but 42.6% (CI: 36.3% to 48.9%) for BMI >= 40. Mean weight loss among obese patients with ADHD (OB+ADHD) was 2.6 BMI (kg/m2) vs. 4.0 for non-ADHD (NAD) (p < 0.002). For BMI >= 40, OB+ADHD had BMI loss 2.9 vs. 7.0 (NAD) (p < 0.004). OB+ADHD had more clinic visits, with a trend toward longer treatment duration.


ADHD was highly prevalent among obese patients and highest in those with extreme obesity. Comorbid obesity and ADHD symptoms rendered treatment less successful compared to NAD counterparts. Reasons for the comorbidity are unknown, but may involve brain dopamine or insulin receptor activity. If replicated in further studies, these findings have important implications for treatment of severe and extreme obesity.

Wow! 42% of morbidly obese have ADD! Does one cause the other? Or are they both caused by another factor, like insulin insensitivity? Lack of sleep? Carbs? Caffeine? Lack of exercise?

Sunday, August 05, 2007

Mind Hacks: Lays me down with my mind she runs

Mind Hacks: Lays me down with my mind she runs

article in last month's American Scientist offered an interesting theory of why some people are driven to find knowledge - because of the kick of natural opioids in the brain.

Sadly, the article is not freely available online, but the theory is outlined by neuroscientist Professor Irving Biederman in a pdf file he's put online, and in a summary from Eureka Alert.

The idea is that the moment of finally understanding something causes a release of natural endorphins in the brain, providing a response to knowledge acquisition that conditions us to want more.

In other words, intellectual curiosity may be driven by an addiction to an opioid high.

Biederman's theory was inspired by the well-known discovery that opioid receptors increase along the ventral visual pathway in the brain - the one that is most strongly associated with recognition and meaning.

At the moment, the theory is still largely speculative, although remains an interesting take on why humans are naturally curious.

Calcium, vitamin D may lower diabetes risk | Health | Reuters

Calcium, vitamin D may lower diabetes risk | Health | Reuters

NEW YORK (Reuters Health) - Calcium and vitamin D, whether from food or supplements, may help lower the risk of developing type 2 diabetes, according to a research review.

A number of studies have found links between type 2 diabetes risk and calcium, vitamin D and dairy food intake. When the results from these studies are combined, the new review found, people with the highest intakes of vitamin D and calcium had an 18 percent lower risk of diabetes than those with the lowest intakes.

Similarly, people who ate the most dairy food had a 14 percent lower diabetes risk than those who ate the least dairy.

Though it's not clear why calcium and vitamin D are linked to diabetes risk, lab research has pointed to some possibilities, according to the review authors, led by Dr. Anastassios G. Pittas of Tufts-New England Medical Center in Boston.

Both nutrients may be important in the functioning of insulin-producing cells in the pancreas, and in the body's proper use of insulin, the researchers explain in their report, published in the Journal of Clinical Endocrinology & Metabolism.

Saturday, August 04, 2007

You Did NOT Eat Your Way to Diabetes!

You Did NOT Eat Your Way to Diabetes!

Don't fall for the toxic myth that you caused your diabetes by reckless overeating

While people with diabetes often are seriously overweight, there is accumulating evidence that their overweight is yet another symptom, not the cause of the process that leads to type 2 diabetes.

But the chances are that you've been told that you caused your diabetes by letting yourself get fat.

This is a truly toxic myth. By blaming you for your condition it causes guilt and hopelessness. Even worse, the belief that people with diabetes have brought their disease on themselves inclines doctors to assume that since you did nothing to prevent your disease, you won't make the effort to control it--a belief that may lead to your getting extremely poor care.

The myth that diabetes is caused by overeating also hurts the one out of five people who are not overweight when they contract type 2 diabetes. Because doctors only think "Diabetes" when they see a patient who fits the stereotype--the grossly obese inactive patient--they often neglect to check people of normal weight for blood sugar disorders even when they show up with classic symptoms of high blood sugar such as recurrent urinary tract infections or neuropathy.

Where Did This Toxic Myth Come From?
The way this myth originated is this. Because people with type 2 diabetes are often overweight, and because many people who are overweight have a syndrome called "insulin resistance" in which their cells do not respond strongly to insulin and require larger amounts of insulin to process blood sugar, the conclusion was drawn years ago that insulin resistance is the cause of type 2 diabetes.


Why Obesity Doesn't Necessarily Cause Diabetes
While people who have diabetes are often heavy, one out of five people diagnosed with diabetes are thin or normal weight. And though heavy people with diabetes are likely to be insulin resistant, the majority of people who are overweight will never develop diabetes, though they are likely to be just as insulin resistant as those who do--or even more so.

In fact, the message that diabetes researchers in academic laboratories are coming up with about what really causes diabetes is quite different from what you read in the media. What they are finding is that there are many different metabolic flaws that appear to develop into the syndrome that we call type 2 diabetes. Most of them appear to be genetic in origin. This means that unless you have damaged or abnormal genes, you can eat until you drop and never develop diabetes.

Twin Studies Back up a Genetic Cause for Diabetes
Studies of identical twins showed that twins have an 80% concordance for Type 2 diabetes. In other words, if one twin has type 2 diabetes, the chance that the other will have it two are 4 out of 5. While you might assume that this might simply point to the fact that twins are raised in the same home by mothers who feed them the same unhealthy diets, studies of non-identical twins found NO such correlation. The chances that one non-identical twin might have type 2 diabetes were much lower, though these twins, born at the same time and raised by the same caregivers were presumably also exposed to the same unhealthy diets.

This kind of finding begins to hint that there is more than just bad habits to blame here.


Insulin Resistance Develops in Thin Children of People with Type 2 Diabetes
Lab research has come up with some other intriguing findings that challenge the idea that obesity causes insulin resistance which causes diabetes.

One of these studies took two groups of thin subjects with normal blood sugar who were evenly matched for height and weight. The two groups differed only in that one group had close relatives who had developed type 2 diabetes, and hence, if there were a genetic component to the disorder, were more likely to have it. The other group had no relatives with type 2 diabetes. The researchers then and examined the subjects' glucose and insulin levels during a glucose tolerance test and calculated their insulin resistance. They found that the thin relatives of the people with Type 2 diabetes already had much more insulin resistance than did the thin people with no relatives with diabetes. (4)

Mitochondrial Dysfunction is Found in Lean Relatives of People with Type 2 Diabetes
Why this might be was made clear by a landmark 2004 study which looked at the cells of the "healthy, young, lean" but insulin-resistant relatives of people with type 2 diabetes and found that their mitochondria, the "power plant of the cells" that is the part of the cell that burns glucose, appeared to have a defect. While the mitochondria of people with no relatives with diabetes burned glucose well, the mitochondria of the people with an inherited genetic predisposition to diabetes were not able to burn off glucose as efficiently, but instead caused the glucose they could not burn and to be stored in the cells as fat.(5)

More Evidence that Abnormal Insulin Resistance Precedes Weight Gain and Probably Causes it
Thanks to Susan of for posting about this study the day it was published. A study done at Yale University School of Medicine by Gerald I. Shulman and Kitt Falk Petersen, published in the prestigeous Proceedings of the National Academy of Science (PNAS) journal on July 16, 2007 reports on a study that compared energy usage by lean people who were insulin resistant and lean people who were insulin sensitive.

Using new imaging technologies, the researchers found that lean but insulin resistant subjects converted glucose from high carbohydrate meals into triglycerides--i.e. fat. Lean insulin-sensitive subjects, in contrast, stored the same gluocse in the form of muscle and liver glycogen.

The researchers conclude that "the insulin resistance, in these young, lean, insulin resistant individuals, was independent of abdominal obesity and circulating plasma adipocytokines, suggesting that these abnormalities develop later in the development of the metabolic syndrome."

In short, obesity looked to be a result, not a cause of the metabolic flaw that led these people to store high carb meals as fat rather than burn the glucose from these meals for energy.

The researchers suggested controlling insulin resistance with exercise. It would also be a good idea for people who are insulin resistant, or have a family history of Type 2 diabetes to cut back on their carb intake, knowing that the glucose from the carbs they eat is more likely to turn into fat.

Beta Cells Fail to Reproduce in People with Diabetes

A study of pancreas autopsies that compared the pancreases of thin and fat people with diabetes with those of thin and fat normal people found that fat, insulin-resistant people who did not develop diabetes apparently were able to grow new beta-cells to produce the extra insulin they needed. In contrast, the beta cells of people who developed diabetes were unable to reproduce. This failure was independent of their weight.(6)


A New Model For How Diabetes Develops

These research findings open up a new way of understanding the relationship between obesity and diabetes.

Perhaps people with the genetic condition underlying type 2 diabetes inherit a defect in the beta cells that make those cells unable to reproduce normally to replace cells damaged by the normal wear and tear of life.

Perhaps, too, a defect in the way that their cells burn glucose inclines them to turn excess blood sugar into fat rather than burning it off as a person with normal mitochondria might do.

Put these two facts together and you suddenly get a fatal combination that is almost guaranteed to make a person fat.

Studies have shown that blood sugars only slightly over 100 mg/dl are high enough to render beta cells dysfunctional.(7) In a normal person who had the ability to grow new beta cells, any damaged beta cells would be replaced by new ones, which would keep the blood sugar at levels low enough to avoid further damage. But the beta cells of a person with a genetic heritage of diabetes are unable to reproduce So once blood sugars started to rise, more beta cells would succumb to the resulting glucose toxicity, and that would, in turn raise blood sugar higher.

As the concentration of glucose in their blood rose, these people would not be able to do what a normal person does with excess blood sugar--which is to burn it for energy. Instead their defective mitochondria will cause the excess glucose to be stored as fat. As this fat gets stored in the muscles it causes the insulin resistance so often observed in people with diabetes--long before the individual begins to gain visible weight. This insulin resistance puts a further strain on the remaining beta cells by making the person's cells less sensitive to insulin. Since the person with an inherited tendency to diabetes' pancreas can't grow the extra beta cells that a normal person could grow when their cells become insulin resistant this leads to ever escalating blood sugars which further damage the insulin-producing cells, and end up in the inevitable decline into diabetes.

Low Fat Diets Promote the Deterioration that Leads to Diabetes in People with the Genetic Predisposition
In the past two decades, when people who were headed towards diabetes begin to gain weight, they were advised to eat a low fat diet. Unfortunately, this low fat diet is also a high carbohydrate diet--one that exacerbates blood sugar problems by raising blood sugars dangerously high, destroying more insulin-producing beta-cells, and catalyzing the storage of more fat in the muscles of people with dysfunctional mitochondria. Though they may have stuck to diets to low fat for weeks or even months these people were tormented by relentless hunger and when they finally went off their ineffective diets, they got fatter. Unfortunately, when they reported these experiences to their doctors, they were almost universally accused of lying about their eating habits.

It has only been documented in medical research during the past two years that that many patients who have found it impossible to lose weight on the low fat high carbohydrate can lose weight--often dramatically--on a low carbohydrate diet while improving rather than harming their blood lipids. (8)

The low carb diet does two things. By limiting carbohydrate, it limits the concentration of blood glucose which often is enough to bring moderately elevated blood sugars down to normal or near normal levels. This means that there will be little excess glucose left to be converted to fat and stored.

It also gets around the mitochondrial defect in processing glucose by keeping blood sugars low so that the body switches into a mode where it burns ketones rather than glucose for muscle fuel.
Relentless Hunger Results from Roller Coaster Blood Sugars

There is one last reason why you may believe that obesity caused your diabetes, when, in fact, it was undiagnosed diabetes that caused your obesity.

Long before a person develops diabetes, they go through a phase where they have what doctors called "impaired glucose tolerance." This means that after they eat a meal containing carbohydrates, their blood sugar rockets up and may stay high for an hour or two before dropping back to a normal level.

What most people don't know is that when blood sugar moves swiftly up or down most people will experience intense hunger. The reasons for this are not completely clear. But what is certain is that this intense hunger caused by blood sugar swings can develop years before a person's blood sugar reaches the level where they'll be diagnosed as diabetic.

This relentless hunger, in fact, is often the very first diabetic symptom a person will experience, though most doctors do not recognize this hunger as a symptom. Instead, if you complain of experiencing intense hunger doctors may suggest you need an antidepressant or blame your weight gain, if you are female, on menopausal changes.

This relentless hunger caused by impaired glucose tolerance almost always leads to significant weight gain and an increase in insulin resistance. However, because it can take ten years between the time your blood sugar begins to rise steeply after meals and the time when your fasting blood sugar is abnormal enough for you to be diagnosed with diabetes, most people are, indeed, very fat at the time of diagnosis.

With better diagnosis of diabetes (discussed here) we would be able to catch early diabetes before people gained the enormous amounts of weight now believed to cause the syndrome. But at least now people with diabetic relatives who are at risk for developing diabetes can go a long way towards preventing the development of obesity by controlling their carbohydrate intake long before they begin to put on weight.

Metabolic And Insulin Resistance Syndrome Linked To Cancer Diabetes Sleep Disorders and Heart Disease

Metabolic And Insulin Resistance Syndrome Linked To Cancer Diabetes Sleep Disorders and Heart Disease

Researchers will present evidence at the 5th Annual World Congress on the Insulin Resistance Syndrome (WCIRS) that a relatively common syndrome can lead to higher risk for cardiovascular disease, breathing and sleep disorders, liver disease, Poly cystic Ovarian Syndrome, type 2 diabetes, certain cancers, Alzheimer's Disease and more.

The confirmation that Insulin Resistance Syndrome increases disease risk will be presented at the conference in Boston from October 11-13, 2007. Dr. Reaven discovered Insulin Resistance Syndrome, often referred to as the Metabolic Syndrome or Syndrome X, back in 1988. Since then researchers have been studying the far-reaching effects of this condition.

Diabetes Update: Did Your Plastic Water Bottle Give You Diabetes?

Diabetes Update: Did Your Plastic Water Bottle Give You Diabetes?

Did Your Plastic Water Bottle Give You Diabetes?
Today's news carried a story about how 12 scientists have published a warning that a compound called bisphenol A, an estrogen mimic which is found in many plastics, has been conclusively linked with reproductive tract damage in many animals.

A chilling line from the report states "The scientists - including four from federal health agencies - reviewed about 700 studies before concluding that people are exposed to levels of the chemical exceeding those that harm lab animals. Infants and fetuses are most vulnerable, they said."

In addition the report explains, "The compound, bisphenol A or BPA, is one of the highest-volume chemicals in the world and has found its way into the bodies of most human beings.

"Used to make hard plastic, BPA can seep from beverage containers and other materials. It is used in all polycarbonate plastic baby bottles, as well as other rigid plastic items, including large water cooler containers, sports bottles and microwave oven dishes, along with canned food liners and some dental sealants for children."

Here is a link to the version of this story that appeared in the San Francisco Chronicle:

Scientists say plastic compound causes reproductive problems

What the article failed to mention is that several studies have also found that bisphenol A increases insulin resistance. For example, a study published in January 2006 in the journal Environmental Health Perspectives has a title that says it all:
"The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance".

Another article published in 2004 in The British Journal of Pharmacology, Bisphenol A affects glucose transport in mouse 3T3-F442A adipocytes concluded "it was demonstrated that BPA, one of the chemicals that we intake incidentally, affects the glucose transport in adipocytes [fat cells], and also that the environmental chemicals may be identified as one of the environmental factors that affect diabetes and obesity."

There are more studies out there along the same lines. What they have in common is that they were published in journals that don't get a lot of attention from the press and that no drug company or agribusiness powerhouse benefits from promoting these results to the media so these findings did not get the PR push that would get them into the news.

But if you have a weight problem linked to insulin resistance, they should get you thinking.

Yeah, I know. Plastic water bottles, no stick pans, where does it end? This is something to watch, but my gut isn't so sure on this one.

Wednesday, August 01, 2007

FuturePundit: Low Latent Inhibition Plus High Intelligence Leads To High Creativity?

FuturePundit: Low Latent Inhibition Plus High Intelligence Leads To High Creativity?

Low Latent Inhibition Plus High Intelligence Leads To High Creativity?

Jordan Peterson of the University of Toronto and colleages at Harvard University have found that decreased latent inhibition of environmental stimuli appears to correlate with greater creativity among people with high IQ. (same press release available here and here)

The study in the September issue of the Journal of Personality and Social Psychology says the brains of creative people appear to be more open to incoming stimuli from the surrounding environment. Other people's brains might shut out this same information through a process called "latent inhibition" - defined as an animal's unconscious capacity to ignore stimuli that experience has shown are irrelevant to its needs. Through psychological testing, the researchers showed that creative individuals are much more likely to have low levels of latent inhibition.

"This means that creative individuals remain in contact with the extra information constantly streaming in from the environment," says co-author and U of T psychology professor Jordan Peterson. "The normal person classifies an object, and then forgets about it, even though that object is much more complex and interesting than he or she thinks. The creative person, by contrast, is always open to new possibilities."

Previously, scientists have associated failure to screen out stimuli with psychosis. However, Peterson and his co-researchers - lead author and psychology lecturer Shelley Carson of Harvard University's Faculty of Arts and Sciences and Harvard PhD candidate Daniel Higgins - hypothesized that it might also contribute to original thinking, especially when combined with high IQ. They administered tests of latent inhibition to Harvard undergraduates. Those classified as eminent creative achievers - participants under age 21 who reported unusually high scores in a single area of creative achievement - were seven times more likely to have low latent inhibition scores.

The authors hypothesize that latent inhibition may be positive when combined with high intelligence and good working memory - the capacity to think about many things at once - but negative otherwise. Peterson states: "If you are open to new information, new ideas, you better be able to intelligently and carefully edit and choose. If you have 50 ideas, only two or three are likely to be good. You have to be able to discriminate or you'll get swamped."