Wednesday, November 26, 2008

Estrogenic Stimulation of Hypothalamic-Limbic System Metabolism in Ageing Diabetic C57BL/KsJ Mice

Estrogenic Stimulation of Hypothalamic-Limbic System Metabolism in Ageing Diabetic C57BL/KsJ Mice:

"The therapeutic influences of estrogen treatment on age- and diabetes-related declines in regional brain glucose utilization (RBGU) rates were evaluated in 8- to 20-week-old female C57BL/KsJ normal ( /?) and diabetic (db/db) mice.

[...]

A gradual decline in the basal rate of brain glucose utilization was observed in all control (oil- and E-treated) groups between 8 and 20 weeks. Expression of the hyperglycemic-obese diabetes syndrome in db/db mice resulted in a significant reduction in regional brain glucose utilization RBGU rates between 8 and 20 weeks relative to control values.

[...]

These data demonstrate that the normal development-related decline in regional brain carbohydrate metabolism is accelerated by the diabetes syndrome, and that Estrogen therapy can modulate the syndrome-associated suppression of glucose utilization in steroid-sensitive CNS loci. These data suggest that the depressive influences of the diabetes syndrome on brain carbohydrate utilization rates may be therapeutically modified in recognized CNS regions possessing steroid-sequestering, metabolically responsive neurons."

I'm not as interested in the estrogen part, but rather this is further proof that the brain's failure to use carbohydrate effectively can be made worse by diabetes(carbohydrate consumption)

Tuesday, November 25, 2008

Behaviour in Fronto-temporal dementia and Semantic dementia

Behaviour in Fronto-temporal dementia and Semantic dementia

FTD - The frontal lobes

The frontal lobes develop later in maturity. They help to control incoming information from the environment, and to guide our actions and behaviour (see diagram). When the frontal lobes don’t work as they should, the system of control begins to break down. This can affect behaviour in a number of ways.

Planning and foresight
People with FTD may lose the ability to plan future actions and anticipate the consequences of their actions. This lack of planning may lead to the following behaviours:

* Inertia, apathy, lack of motivation – people with damage to the frontal lobes can become less proactive
* Purposeless activity, impulsivity – sometimes people act quickly without thinking things through
* Neglect of self care and personal responsibilities – lack of motivation to carry out simple tasks
* Behaviour governed by immediate wants – lack of foresight may result in inappropriate judgements about things such as money or eating

So, inability to anticipate the consequences of actions may lead to poor judgement and decision-making.

Organisation
Frontal lobe dysfunction may also result in disorganised behaviour. FTD sufferers may fail to complete tasks, or may attempt to carry out activities in a rather unusual manner. Even a simple task such as making a cup of tea might present problems, as there are several components involved, and the order in which they are carried out affects the outcome. Difficulties occur because the frontal lobes play an important role in our ability to sequence and organise our thoughts and actions.

Attention
People with FTD may also have impaired attention. It may be difficult to engage them in tasks and they may fail to complete activities because they are easily distracted by something else.

Checking
As mentioned earlier, there can be a loss of motivation and subsequent failure to anticipate the consequences of actions. People with FTD may have little insight into the effects of their behaviour and fail to ‘check’ their conduct. Thus, they may make numerous mistakes, and may be oblivious to their errors.

Abstraction
People with FTD may demonstrate ‘concrete’ or literal thinking. For example, a figure of speech such as ‘too many cooks spoil the broth’ might be interpreted literally as having something to do with cooking. The frontal lobes play an important part in our ability to understand abstract concepts, meaning that people with FTD may interpret things differently, often with reference to their own personal experience. Thus, they may appear self-centred, with little interest in others’ viewpoints.

Flexibility
A common symptom is a loss of flexibility in behaviour. The frontal lobes are very important in allowing us to adapt our behaviour according to the situation. People with FTD often lose this ability, and become quite rigid in their thinking. They may be unable to adjust their actions in unfamiliar situations, and thus behave inappropriately. Also, they may ‘perseverate’ (do/say the same thing over and over again). This is because their brain fails to tell them that the action/information is no longer relevant to the current situation.

Emotions and social behaviour
The frontal lobes are not only important in cognition. They also play a key role in our emotions. Often, one of the most difficult factors that carers encounter is their relatives’ loss of feeling towards them and their family. People who may have once been very affectionate towards their loved ones may become ‘cold’ in manner. There may be a loss of sympathy and empathy, and people may no longer respond appropriately to situations. In contrast to this picture of a ‘loss’ of emotion, it is also common for people with FTD to show inappropriate demonstration of emotion. People may become ‘disinhibited’ and tactless, for example they may laugh loudly or tell jokes at a funeral. They are typically unembarrassed by their behaviour, and lack insight into the effect it has on others.

Sensory information
People with FTD are able to feel normally, but it is our experience that sometimes their responses to stimuli are abnormal. For example, there may be no response to painful stimuli such as scalding hot water. The reason for this behaviour is yet to be clarified, but it is possible that there may be a relationship with impaired attention. There is evidence to suggest that how we behave is governed by attention, for example, a runner focussed on winning a race may complete the circuit without feeling the pain of a sprained ankle, simply because they are not attending to it. Impaired attention may therefore influence FTD sufferers’ reactions to stimuli.

Eating behaviours
It is common for people with FTD to demonstrate odd eating habits. There is often a preference for sweet foods, such as biscuits and chocolate. People may become gluttonous, eating everything that is put in front of them (sometimes including food on others’ plates). This relates to a lack of ability to inhibit behaviour, and also a tendency to respond indiscriminately to environmental stimuli (this is called ‘utilisation behaviour’). In addition, people with FTD may even seek out food, and also may ‘cram’ food into their mouths instead of chewing and swallowing one item at a time. This may relate to problems in sequencing, or may reflect a ‘repetitive’ behaviour as discussed below.

Repetitive behaviours
It is very common for people with FTD to show repetitive behaviours and mannerisms such as humming the same tune, or repeating the same phrases or words. People often develop repetitive routines and rituals, and it is common for carers to report behaviours such as pacing, wandering, and hoarding.

The role of emotion in decision-making: Evidence from neurological patients with orbitofrontal damage

The role of emotion in decision-making: Evidence
from neurological patients with orbitofrontal damage


Most theories of choice assume that decisions derive from an assessment of the future outcomes of various options and alternatives
through some type of cost-benefit analyses. The influence of emotions on decision-making is largely ignored. The studies of
decision-making in neurological patients who can no longer process emotional information normally suggest that people make
judgments not only by evaluating the consequences and their probability of occurring, but also and even sometimes primarily at a
gut or emotional level. Lesions of the ventromedial (which includes the orbitofrontal) sector of the prefrontal cortex interfere with
the normal processing of ‘‘somatic’’ or emotional signals, while sparing most basic cognitive functions. Such damage leads to
impairments in the decision-making process, which seriously compromise the quality of decisions in daily life.

[...]

OK, so here they focused on decision making in frontal lobe impaired subjects. They make the point that in real life, you don't always know what the results of your actions will be, so you have to estimate. They had subjects choose from two decks of cards: cards with a modest, but fairly certain, payoff, and another deck which was a losing deck, but with some big payoffs spread inside. Normal people tended towards the sure thing, while frontal lobe impaired patients chose from the risky deck. They tied this in to emotions, by studying skin response to view emotional responses. They found that both groups of patients felt emotions when they won or lost, but that normal patients felt emotions before picking, especially from the risky deck. Impaired patients seemed blind to this, and just made their choices and THEN felt the emotion. They also show that different halves of the brain focus on negative or positive rewards. So depending on the damaged lobe, right or left, the subject might be totally focused on positive rewards, ignoring negative consequences, or totally focused on negative rewards, ignoring the positive. Either way leads to impaired decision making skills. Authors are also trying to point out the role emotion plays in decision making, especially when results are uncertain, as they are in most scenarios in real life.

Cigarette smoking exacerbates alcohol-induced brain damage

Cigarette smoking exacerbates alcohol-induced brain damage

Heavy alcohol consumption is known to cause brain damage. A new imaging study has compared 24, one-week-abstinent alcoholics (14 smokers, 10 nonsmokers) in treatment with 26 light-drinking "controls" (7 smokers, 19 nonsmokers), and found that cigarette smoking can both exacerbate alcohol-induced damage as well as independently cause brain damage. The damage is most prominent in the frontal lobes (important in planning, decision-making, and multi-tasking among other functions). Independent of alcohol consumption, cigarette smoking also had adverse effects on brain regions involved in fine and gross motor functions and balance and coordination. Roughly 80% of alcohol-dependent individuals report smoking regularly.

Orbitofrontal Cortex and Social Behavior: Integrating Self-monitoring and Emotion-Cognition Interactions -- Beer et al. 18 (6): 871 -- The Journal of Cognitive Neuroscience

Orbitofrontal Cortex and Social Behavior: Integrating Self-monitoring and Emotion-Cognition Interactions -- Beer et al. 18 (6): 871 -- The Journal of Cognitive Neuroscience

The role of the orbitofrontal cortex in social behavior remains a puzzle. Various theories of the social functions of the orbitofrontal cortex focus on the role of this area in either emotional processing or its involvement in online monitoring of behavior (i.e., self-monitoring). The present research attempts to integrate these two theories by examining whether improving the self-monitoring of patients with orbitofrontal damage is associated with the generation of emotions needed to guide interpersonal behavior. Patients with orbitofrontal damage, patients with lateral prefrontal damage, and healthy controls took part in an interpersonal task. After completing the task, participants' self-monitoring was increased by showing them a videotape of their task performance. In comparison to healthy controls and patients with lateral prefrontal damage, orbitofrontal damage was associated with objectively inappropriate social behavior. Although patients with orbitofrontal damage were aware of social norms of intimacy, they were unaware that their task performance violated these norms. The embarrassment typically associated with inappropriate social behavior was elicited in these patients only after their self-monitoring increased from viewing their videotaped performance. These findings suggest that damage to the orbitofrontal cortex impairs self-insight that may preclude the generation of helpful emotional information. The results highlight the role of the orbitofrontal cortex in the interplay of self-monitoring and emotional processing and suggest avenues for neurorehabilitation of patients with social deficits subsequent to orbitofrontal damage.

Again, frontal lobe malfunction is associated with ADD, diabetes, alzheimers, brain damage, etc. Problems with organization and interpersonal relations can be effected. Here, they use videotaping to show the subject how they behaved, and the subject is finally able to identify that their behavior was inappropriate. Self monitoring is impaired in frontal lobe disorders like ADD.

Molecular Switch in Brain May End Smokers’ Cravings - Health News - Health.com

Molecular Switch in Brain May End Smokers’ Cravings - Health News - Health.com

Blocking a neuropeptide receptor in the brain may be one way to quickly lessen the desire for a cigarette, a new study suggests.

Hypocretin-1, or Orexin A, a short chain of amino acids found in nerve tissue, appears to initiate a series of closely linked biochemical reactions that makes lab rats crave nicotine, the addictive chemical in tobacco, according to researchers at the Scripps Florida research institute in Jupiter.

If duplicated in humans, the finding could be lead to new smoking-cessation treatments, the researchers said.

“Blocking hypocretin-1 receptors not only decreased the motivation to continue nicotine use in rats, it also abolished the stimulatory effects of nicotine on their brain reward circuitries,” study leader Paul Kenny, a scientist at Scripps Florida, explained in a news release issued by the institute. “This suggests that hypocretin-1 may play a major role in driving tobacco use in smokers to want more nicotine. If we can find a way to effectively block this receptor, it could mean a novel way to help break people’s addiction to tobacco.”

Very interesting. Hypocretin or Orexin A deficits are the cause of narcolepsy. This compound activates the Hypothalamus, increasing mood, activity, attention, etc. Low Orexin levels make one sleepy, unmotivated, depressed, etc. Glucose lowers Orexin levels, and may even cause the body to destroy Orexin in the brain, causing narcolepsy. Smoking also seems to damage the body through manipulating insulin and glucose levels. People with ADD are more likely to smoke. It could be that they are self medicating due to low orexin levels. This is why my blog is called "it's all connected". I also think it's interesting that they want to create a med to block orexin, to help smokers stop. Woudn't this compound also cause the low arousal and motivation associated with narcolepsy and ADD? You won't want to smoke, or do much of anything else for that matter. Why not enhance orexin a with a low carb, ketogenic diet and exercise instead? Or just get enough sleep? I guess the idea is that no one will do that, and besides, there's no money in it for big pharm.

Sugar feeds cancer

Drug/diet synergy for managing malignant astrocytoma in mice: 2-deoxy-D-glucose and the restricted ketogenic diet. - 7thSpace Interactive

Astrocytomas are largely dependent on glycolysis to satisfy their bioenergetic requirements for growth and survival. Therapies that target glycolysis can potentially manage astrocytoma growth and progression.

Dietary restriction of the high fat/low carbohydrate ketogenic diet (KD-R) reduces glycolysis and is effective in managing experimental mouse and human astrocytomas

[...]

The results suggest that management of malignant astrocytoma with restricted ketogenic diets could be enhanced when combined with drugs that inhibit glycolysis.

Monday, November 24, 2008

Fasting intermittently reduces cell proliferation, a marker for cancer risk, s...( Berkeley -- An apple a day keeps the do...)

Fasting intermittently reduces cell proliferation, a marker for cancer risk, s...( Berkeley -- An apple a day keeps the do...)

A new study by researchers at the University of California, Berkeley, raises such a possibility. It shows that healthy mice given only 5 percent fewer calories than mice allowed to eat freely experienced a significant reduction in cell proliferation in several tissues, considered an indicator for cancer risk. The key was that the mice eating 5 percent fewer calories were fed intermittently, or three days a week.

What is encouraging about the findings is that the reduction in cell proliferation from that intermittent feeding regimen was only slightly less than that of a more severe 33 percent reduction in calories. Until now, scientists have been certain only of a link between a more substantial calorie reduction and a reduction in the rate of cell proliferation.

Saturday, November 22, 2008

Bottoms Up: Individualists More Likely To Be Problem Drinkers

Bottoms Up: Individualists More Likely To Be Problem Drinkers

ScienceDaily (Nov. 21, 2008) — What makes residents of certain states or countries more likely to consume more alcohol? According to a new study in the Journal of Consumer Research, high levels of individualism lead to more problem drinking.

"We looked at the extent to which consumer levels of individualism (vs. collectivism) were related to their beer and problem alcohol consumption," write authors Yinlong Zhang and L.J. Shrum (both University of Texas-San Antonio).

"We found that the higher a region scored on valuing individualism, the greater their beer and alcohol consumption, and this was true even when taking into account the effects of other variables such as income, climate, gender, and religion."

[...]

The researchers found that people with more interdependent mindsets were less likely to over-consume when they were with peers. "The results suggest that people with collectivistic cultural orientations tend to be more motivated to regulate impulsive consumption tendencies than those with individualistic cultural orientations, which in turn makes them less likely to engage in beer or alcohol consumption," the authors conclude.

Calorie Restriction And Exercise Show Breast Cancer Prevention Differences In Postmenopausal Women

Calorie Restriction And Exercise Show Breast Cancer Prevention Differences In Postmenopausal Women

Epidemiological data has suggested that inducing a so-called "negative energy balance" (where less energy is taken in than expended) through eating a low-calorie diet or increasing exercise levels, decreases the postmenopausal breast cancer risk associated with obesity. Although the mechanism responsible for these anti-obesity strategies was unknown, scientists have suspected hormone alteration plays a critical role. Increased fat tissue is known to be associated with alterations in adipokines, proteins secreted by fat tissue that help modify appetite and insulin resistance. For example, increased levels of leptin and decreased levels of adiponectin have been associated with breast cancer risk.

[...]

The calorie-restricted mice and the exercised mice showed no significant difference in percentage of body fat, but both groups had significantly less body fat than the sedentary mice that were fed at will.

In addition, blood levels of leptin, a hormone that plays a role in fat metabolism, were significantly reduced in the calorie-restricted and exercised mice compared to the controls. The calorie-restricted mice also displayed increased blood levels of adiponectin, a hormone produced in fat tissue that regulates some metabolic processes, compared to the exercised mice.

Some of the cell signaling pathways regulated by these hormones converge at mTOR, Nogueira explains. She and her colleagues found that the key proteins found downstream of mTOR activation were less active in both the calorie-restricted and exercised mice compared to the controls.

"These data suggest that although exercise can act on similar pathways as caloric restriction, caloric restriction possesses a more global effect on cell signaling and, therefore, may produce a more potent anti-cancer effect," Nogueira said.

Type 2 diabetes may slow mental processing speed | Health | Reuters

Type 2 diabetes may slow mental processing speed | Health | Reuters

Diabetes may slow brain processing

Some studies have linked diabetes and cognitive dysfunction, but a new study suggests that mental processing speed may be the brain function most severely affected by diabetes. Researchers looked at data from the AGES Reykjavik Study and found that people who had been diagnosed with diabetes were slower to process information than people who didn’t have diabetes. People with undiagnosed diabetes had similar problems, but those with pre-diabetes had mental functioning similar to people without diabetes. Both memory and “executive function or the ability to plan and multitask, were comparable in people with and without diabetes, though people who’d had diabetes more than 15 years also had impaired executive function, according to the report in the American Journal of Epidemiology.

Monday, November 17, 2008

Want To Know What Is In Fast Food, Lots Of Corn! : ChattahBox

Want To Know What Is In Fast Food, Lots Of Corn! : ChattahBox:

"Washington (ChattahBox) - According to a new study, a key ingredient in fast food is apparently corn!

The study focused on three main fast food chains in Boston, Baltimore, Denver, San Francisco, Detroit, as well as Los Angeles.

The study was led by A. Hope Jahren from the University of Hawaii, along with colleague Rebecca Kraft, and found the key ingredient to be corn.

Using a special technique to analyze the food, they found high levels of both carbon and nitrogen, which means corn
.
The corn is able to fatten the cattle in a very short period of time.

This could explain why fast food causes obesity at such a high rate.

Their findings have been published in the Proceedings of the National Academy of Sciences."

Tuesday, November 11, 2008

Metabolic Syndrome and Psychiatric ... - Google Book Search

Metabolic Syndrome and Psychiatric ... - Google Book Search

Major depression

It has long been known that a disproportionately large percentage of patients with diabetes also suffer major depression. The prevalence of major depression in diabetics, regardless of whether their diabetes is type 1 or type 2, is roughly 3 times that seen in the general population. However, the likelihood of depression is often increased in individuals dealing with serious and potentially disabling illnesses. Plus, the significance of the high prevalence of depression in diabetics, and whether it reflects some interaction between the two seemingly disparate conditions has not been entirely clear.

Over recent years it has become apparent that there is a relationship between major depression and metabolic syndrome, which is frequently the precursor of diabetes type 2. Men and women with depression are more likely than those without depression to develop metabolic syndrome. People with depression often have the abdominal obesity, insulin resistance, hypertension, hyperlipidemia, and elevated fasting glucose levels that characterize the syndrome. There is also a strong relationship between depression and insulin resistance. Insulin resistance, a cardinal feature of metabolic syndrome, is four times more likely to occur in depressed individuals. Although Major depression is associated with metabolic syndrome, it is not clear how the two are related. Does depression cause the metabolic syndrome, or do the biochemical changes of metabolic syndrome lead to depression?

Evidence suggests that depression can set the stage for later development of metabolic syndrome. Women who complain of depression, anxiety, and anger are more likely than women without those psychological characteristics to develop metabolic syndrome in subsequent years. Path analyses have shown statistically that the progression from depression to poor health habits to metabolic syndrome is the most likely course of events when depression and metabolic syndrome coexist.

One explanation for how depression might lead to metabolic syndrome is that depression fosters unhealthy lifestyles. Patients with depression often smoke. They are inactive and eat poorly. Although many patients with major depression have poor appetites, some sufferers crave sweets and indulge in "comfort foods" packed with high glycemic index carbohydrates. This is particularly the case in so-called atypical depression. Despite its name, atypical depression may actually be a common form of depression in women. Comorbidity of depression, obesity, and metabolic syndrome occurs more often in women than in men.

Overeating, smoking, drinking, inactivity, and carbohydrate craving are at least partially responsible for the tendency of people with depression to develop metabolic syndrome. However, even when these unhealthy habits are statistically removed from the equation, there is an unexpectedly high incidence of metabolic syndrome among sufferers of major depression. It is possible that some of the same, underlying physiological abnormalities contribute to both major depression and metabolic syndrome.

Insulin resistance and major depression

The insulin resistance of metabolic syndrome may play a role in major depression. Although insulin dramatically affects the way muscle and fat cells take up and metabolize glucose, neuroscientists have come to believe that it had no significant effect on the brains utilization of glucose. However, insulin has subtle, yet potentially important effects on the way the brain uses glucose.

Insulin is actively transported into the brain, and insulin receptors are found in a variety of important areas of the brain. The amount of insulin in the brain is affected by changes in serum insulin levels. Insulin levels in cerebrospinal fluid increase during acute episodes of hyperinsulemia. In chronic hyperinsulinemia, such as occurs in metabolic syndrome, insulin levels in cerebrospinal fluid can decrease. This is likely due to down regulation of the activity of the insulin transport system into the brain. When insulin is reduced to levels below those generally seen during the fasting state in humans, the brain uses less glucose. It is the older areas of the brain, such as the cerebellum and brainstem, that have the highest density of insulin receptors. However, it is the cerebral cortex, where the higher functions of mind reside, that is most strongly affected by the depletion of insulin.

The insulin resistance that defines metabolic syndrome is most clearly seen in muscle, adipose tissue, and liver. Although changes in insulin levels can clearly affect brain activity, there has been a question as to whether the insulin resistance seen in peripheral tissue also occurs in the brain tissue of patients with metabolic syndrome. Recent studies with human subjects have shown that this is the case. When glucose and insulin levels are controlled by clamping techniques, insulin resistant subjects show less cortical excitation than insulin sensitive subject to the same serum levels of insulin. The degree of insulin's affect on cortical activity is in positive correlation with insulin sensitivity as measured by the ability of insulin to stimulate glucose uptake in peripheral tissues. The ability of a specific level of serum insulin to enhance glucose metabolism in the cerebral cortex is also diminished in subjects with peripheral insulin resistance. This resistance to insulin is most apparent in the prefrontal cortex and other areas of the brain involved in motivation and reward.

Perhaps the most compelling evidence of brain tissue becoming resistant to insulin comes from a study in which the response to insulin was evaluated ex viVo using slices of brain removed from hamsters made insulin resistant by feeding them a fructose enriched diet. Direct administration of insulin into brain tissue was less effective in generating insulin induced long-term inhibition in sections from insulin resistant animals than in those for control animals. Existing data do suggest that decreases in insulin activity in the brain, due either to insulin resistance in brain tissue or decreases in the ability of insulin to reach the brain, could play a significant role in the development of major depression.

Consistent with insulin resistance causing depression are findings that chromium, an essential mineral known to enhance the effects of insulin, can help relieve depression. Chromium has been used successfully for treatment of both depression and dysthymia. The latter is a mild but persistent form of depression. Interestingly, the type of depression that may best be helped by chromium is atypical depression. This is the form of depression were commonly seen in women, that is characterized by a depressed mood, lack of motivation, low sex drive, carbohydrate craving, and sleeping too much. The strongest effects of chromium were in countering carbohydrate craving, increased appetite, and decreased sex drive.

Lithium is a medication that has long been used to treat bipolar and affective disorder. It is also used to augment the effects of antidepressants in treatment resistant depression. Lithium mimics several of the effects of insulin in the brain. Both lithium and insulin inhibits the passivity of the increasingly important enzyme, glycogen synthase kinase 3. Moreover, both lithium and insulin stimulates the effects of the enzymes phosphatidylinositol-3-kinase and protein kinase B. it is not known to what degree the benefits of lithium are due to mimicking the effects of insulin. Neither is it known if lithium has any special benefit for patients that suffer both depression and metabolic syndrome or diabetes type 2. Omega-3 deity assets, which have been found to improve some symptoms of both major depression and metabolic syndrome have also been found to enhance the activity of phosphatidylinositol 3 kinase.

HowStuffWorks "How Nicotine Works"

HowStuffWorks "How Nicotine Works"

Effects of Nicotine

Nicotine changes how your brain and your body function. The net results are somewhat of a paradox: Nicotine can both invigorate and relax a smoker, depending on how much and how often they smoke. This biphasic effect is not uncommon. Although the actions of nicotine and ethanol in the body are quite different, you also see dose-dependent effects when you drink alcoholic beverages. Your first drink may loosen your inhibitions and fire you up, but after several drinks, you're usually pretty sedate.

Nicotine and the Body
Nicotine initially causes a rapid release of adrenaline, the "fight-or-flight" hormone. If you've ever jumped in fright at a scary movie or rushed around the office trying to finish a project by your deadline, you may be familiar with adrenaline's effects:

* Rapid heartbeat
* Increased blood pressure
* Rapid, shallow breathing

Adrenaline also tells your body to dump some of its glucose stores into your blood. This makes sense if you remind yourself that the "fight-or-flight" response is meant to help you either defend yourself from a hungry predator or hightail it out of a dangerous situation -- running or brawling both require plenty of energy to fuel your muscles. (For more information, see How Exercise Works.)

Nicotine itself may also block the release of the hormone insulin. Insulin tells your cells to take up excess glucose from your blood. This means that nicotine makes people somewhat hyperglycemic, having more sugar than usual in their blood. Some people think that nicotine also curbs their appetite so that they eat less. This hyperglycemia could be one explanation why: Their bodies and brain may see the excess sugar and down-regulate the hormones and other signals that are perceived as hunger.

Nicotine may also increase your basal metabolic rate slightly. This means that you burn more calories than you usually would when you are just sitting around. (For more information on metabolism, see How Calories Work.) However, losing weight by smoking doesn't give you any of the health benefits that you'd get if you were losing weight by exercising -- it actually does the opposite! Over the long haul, nicotine can increase the level of the "bad" cholesterol, LDL, that damages your arteries. This makes it more likely that you could have a heart attack or a stroke.

Insulin's Brain Impact Links Drugs And Diabetes

Insulin's Brain Impact Links Drugs And Diabetes

Insulin, long known as an important regulator of blood glucose levels, now has a newly appreciated role in the brain.

Vanderbilt University Medical Center researchers, working with colleagues in Texas, have found that insulin levels affect the brain's dopamine systems, which are involved in drug addiction and many neuropsychiatric conditions.

In addition to suggesting potential new targets for treating drug abuse, the findings raise questions as to whether improper control of insulin levels -- as in diabetes -- may impact risk for attention deficit hyperactivity disorder (ADHD) or influence the effectiveness of current ADHD medications.

The antidepressant properties of the ketogenic diet

The antidepressant properties of the ketogenic diet .

Biological Psychiatry , Volume 56 , Issue 12 , Pages 981 - 983

P . Murphy , S . Likhodii , K . Nylen , W . Burnham

Elsevier Article Locator


Background

The ketogenic diet is used to treat epilepsy refractory to anticonvulsant medication. Individuals with epilepsy often have behavioral problems and deficits in attention and cognitive functioning. The ketogenic diet has been found to effect improvements in these domains. It has also been suggested that the ketogenic diet may act as a mood stabilizer.
Methods

The present research used the Porsolt test, an animal model of depression, to determine whether the ketogenic diet has antidepressant properties. Porsolt test scores of rats on the ketogenic diet were compared with those of rats on a control diet.
Results

The rats on the ketogenic diet spent less time immobile, suggesting that rats on the ketogenic diet, like rats treated with antidepressants, are less likely to exhibit “behavioral despair.”
Conclusions

It is concluded that the ketogenic diet may have antidepressant properties.

Monday, November 10, 2008

Insulin Resistance and Executive Dysfunction in Older Persons

Wiley InterScience :: JOURNALS :: Journal of the American Geriatrics Society

ABSTRACT

Objectives: 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.

[...]

Measurements: Anthropometric measurements; plasma fasting levels of glucose, insulin, cholesterol (total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol), and insulin-like growth factor-1 (IGF-1); homeostasis model assessment (HOMA) to estimate degree of IR; Trail Making Test (TMT) A; TMT-B; TMT-B minus TMT-A (DIFF B–A); and Mini-Mental State Examination (MMSE).

Results: IR (HOMA) was associated with longer TMT-B (correlation coefficient (r)=0.11; P=.006) and DIFF B–A times (r=0.10; P=.022). Subjects in the upper tertile of IR were older and had longer TMT-B and DIFF B–A than participants in the lowest tertile. After adjusting for age, sex, and years of formal education, IR was significantly correlated with TMT-A, TMT-B, and DIFF B–A. After adjusting for age, sex, education, body mass index, waist:hip girth ratio, HDL-C, triglycerides, IGF-1, hypertension, drug intake, and physical activity, the results did not significantly change. After introducing MMSE score into the model, IR continued to be an independent determinant of TMT-A (β=11.005; P=.021), TMT-B (β=28.379; P<.001), and DIFF B–A (β=17.374; P=.011).

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

Diabetes and executive dysfunction go hand in hand. Executive dysfunction is a hallmark of ADD.

Erectile Dysfunction Linked To Smoking

Erectile Dysfunction Linked To Smoking

Men who smoke cigarettes run an increased risk of experiencing erectile dysfunction, and the more cigarettes smoked, the greater the risk, according to a study by Tulane University researchers published in the American Journal of Epidemiology.

Frontal Lobe Injury

Frontal Lobe Injury

Consequences of Frontal Lobe Injury

The major role of the frontal lobes is the regulation of behavior. They coordinate attention, memory, language, perception, motor functions, and social behavior as we go about our daily living and vocational activities. In short, they put the human machine to work. When function is impaired, all of the other cognitive systems are affected even though they remain individually intact. The frontal lobes have been likened to the pilot of a Boeing 747, without whom millions of dollars worth of highly complex technology would sit idle at the airport. Recognition and appreciation of these deficits is critical to rehabilitation efforts with the closed head injured population. These deficits can be classed generally and include:

* Problems of Starting--This may manifest as decreased spontaneity and initiation. Such individuals seem to lack motivation and may sit silently without apparent interest in or curiosity about surroundings until they are directed to do something.
* Difficulties in Making Mental or Behavioral Shifts--This includes rigidity or perseveration on a single idea or a single action. Individuals with these problems may be able to successfully verbalize solutions to problems, including plans necessary to meet goals successfully, yet be unable to put any plan into effective action.
* Difficulties with Attention--Individuals with frontal lobe deficits are often captured by extraneous aspects of a task. As a result, they may demonstrate behaviors which seem irrelevant, even bizarre, to the observer. Because they may be highly distractible, they often seem to shift focus continually, never arriving at a point which seems purposeful.
* Problems in Stopping--This may manifest as a more general deficit in self monitoring. It may present as impulsivity or a quickness to anger, speaking too loudly, or carrying a joke or sexual innuendo too far.
* Problems with Social Awareness--This category would include deficits in the ability to appreciate the impact one makes on others, sometimes resulting in rude or insensitive behavior or with a general lack of apparent concern about social conventions.
* Deficient Self-Awareness--Defective self-criticism may be associated with a tendency to be self-satisfied, to experience little or no anxiety, and to fail to appreciate the existence and practical implications of deficits (limited insight).
* A Concrete Attitude--Some patients with frontal lobe lesions retain high-level conceptual abilities but demonstrate a day-to-day literal-mindedness and loss of perspective.

Monday, November 03, 2008

more kids taking medication for ADD and diabetes USATODAY.com

USATODAY.com

The number of children who take medication for chronic diseases has jumped dramatically, another troubling sign that many of the youngest Americans are struggling with obesity, doctors say.

The number of children who take pills for type 2 diabetes — the kind that's closely linked to obesity — more than doubled from 2002 to 2005, to a rate of six out of 10,000 children. That suggests that at least 23,000 privately insured children in the USA are now taking diabetes medications, according to authors of the new study in today's Pediatrics.

Doctors also saw big increases in prescriptions for high cholesterol, asthma and attention deficit and hyperactivity. There was smaller growth for drugs for depression and high blood pressure.

"We've got a lot of sick children," says author Emily Cox, senior director of research with Express Scripts, which administers drug benefit programs for private insurance plans. "What we've been seeing in adults, we're also now seeing in kids."

Type 2 diabetes was once known as adult-onset. But Cox says her records show kids as young as 5 being treated with prescription diabetes drugs.

Cox based her study on prescription records of nearly 4 million children a year, ages 5 to 19, covered by Express Scripts. She says her findings may not apply to the 40% of children who are uninsured or covered by government health plans.

Unless these children make major changes — such as eating healthier and exercising more — they could be facing a lifetime of illness, Cox says.

"These are not antibiotics that they take for seven to 10 days," Cox says. "These are drugs that many are taking for the rest of their lives."

Cox couldn't explain one surprising finding: Most of the increase in drugs for diabetes, attention deficit/hyperactivity and depression was seen in girls. The gender gap was most striking in diabetes: While the number of boys taking medication grew by 39%, the number of girls using them climbed by 147%, Cox found.