World's first medical networking and resource portal

Dr. Pulkit Agarwal's Profile
Special Message:
A complete health care solution with dedicated service to keep you in the best of health. Live healthy... stay healthy
VOTES0000025
PAGE HITS0004400

Smells Like Parkinson’s Disease
Parkinson’s disease has always been primarily seen as a movement disorder resulting in symptoms of shaking, tremors, rigidity, and trouble walking. Interestingly, however, at least 90% of patients with Parkinson’s experience either loss or decreases in the sense of smell. Studies have shown that problems with olfaction actually generally precede the onset of other motor symptoms. Most people are not personally aware of changes in their olfactory acuity, but the increasing range and prevalence of smell tests offer a quick, easy, cheap, and non-invasive diagnostic test, as well as a measure of disease progression. In addition, the shift of focus for researchers from Parkinson’s as a motor disorder to a more global neurodegenerative disorder allows consideration of new paradigms about the causes and disease progression.
The cellular basis of olfactory dysfunction in Parkinson’s remains an enigma. Post-mortem studies have confirmed shrinkage of the olfactory bulb, but this fails to shed light onto the root causes as it only demonstrates the end effect. Experimental models of Parkinson’s have demonstrated various results such as protein aggregation in the olfactory bulb, changes in levels of neurotransmitters, microglial activation, and loss of cells in the olfactory bulb. However, as all of these effects are inter-related, none of these clarify the actual initial cause of damage.
Many of the hypotheses as to why olfactory dysfunction occurs and precedes other symptoms remain grounded in the long-held paradigm of Parkinson’s as a motor disease caused by the loss of dopaminergic neurons in the substantia nigra. For example, in some experimental models an increase in dopamine was found in the olfactory bulb. The researchers suggested this occurs as a compensatory mechanism in response to the loss of dopamine in the substantia nigra. As it has also been shown that sense of smell is particularly vulnerable to changes in dopamine, excess dopamine in the olfactory bulb would, thus, lead to olfactory dysfunction.
However, a number of other theories have been proposed suggesting that perhaps the olfactory bulb is the first brain structure to exhibit signs of damage because Parkinson’s could be caused by respiratory viruses or inhaled toxins that enter the brain through the nose. The cause of Parkinson’s has not been conclusively determined. And while a genetic component has been uncovered, the causes are clearly much more complex with various environmental factors involved. A number of studies have been performed demonstrating Parkinson’s-like symptoms following exposure to viruses, heavy metals, and pesticides in experimental models. Epidemiological studies have also linked pesticides exposure to an increased risk of Parkinson’s. It is certainly an interesting hypothesis that inhaled toxins could cross the blood brain barrier, and that the damage in Parkinson’s could begin first in the olfactory bulb and then spread from there to the substantia nigra. In addition, as the olfactory bulb is heavily involved in adult neurogenesis, any damage to this structure could severely limit the brain’s ability to repair itself by replenishing damaged neurons with new ones. Perhaps, then, Parkinson’s disease does not depend on a single source of damage, but rather multiple insults occurring. For example, genetically induced damage to the dopaminergic neurons in the substantia nigra combined with inhaled toxins damaging the olfactory bulb could, together, cause Parkinson’s, while one or the other would be insufficient.

Category (Brain & Nerves)  |   Views ( 3768 )  |  User Rating
Rate It

Thinking Fast Equals Risky Business
Connections between the speed of thought and feelings of euphoria have been reported in cases of clinical mania. New research now links racing thoughts with risk-taking among the general population.
The speed of modern life has increased dramatically in recent decades, and faster is almost always better. But, is that true when it comes to your own thoughts? In two experiments, reported in Psychological Science, scientists manipulated participants’ thought speeds and assessed their appetites for risk. In the first experiment, three dozen students read aloud at different speeds — twice their normal speed or half their normal speed. Then, each student played a computer-simulated game that required them to blow air into a balloon without popping it. Students were rewarded with five cents each time he or she pumped air into the balloon, but lost money each time the balloon popped. The students who had read quickly were more willing to take risks with the balloon (and the money), attempting and achieving more pumps, but also popping more balloons than the students who had read slowly.
In a second experiment, 52 students watched fast-, medium-, or slow-paced movie clips that contained similar content. The students who watched the fast-paced clips reported a greater intention to engage in real-world risky behaviors, including unprotected sex and illegal drug use. Those students were also more likely to minimize the danger associated with each risky behavior.
Previous studies have shown a link between life in the fast-thinking lane and mood. Experimentally accelerated thought is achieved through instructions to brainstorm freely, exposure to multiple ideas, encouragement to plagiarize others’ ideas, performance of easy cognitive tasks, narration of a silent video in fast-forward, and controlled reading speed. Regardless of the types of thoughts that were induced (money-making schemes, word choice, or feelings of depression or elation), individuals demonstrated an increased positive affect after thinking quickly. Increased speed of thought also amplified feelings of power, creativity, and energy, and inflated self-esteem.
Researchers attribute these findings to the subjective experience of thought speed and the joy-enhancing effects of fast thinking. Likewise, thinking slowly is, apparently, a killjoy.
The need for speed is undeniable today’s fast and furious world. But, at what cost? Are we riskier because we are always thinking faster? Or are we happier? Will letting the brain stop and smell the roses decrease our desire to take risks, or will we just become depressed? Human thought is the product of an integrated, sophisticated network that involves neurons, sensory input, and the brain. Speed is fundamental to the thought process, but it is not the only determinant of effectiveness. Efficiency, timing, and appropriateness must be balanced with speed to keep us safe and running smoothly in whatever lane of life’s highway we choose.

Category (Psychology, Stress & Mental Health)  |   Views ( 1788 )  |  User Rating
Rate It

A Gateway to Weight Loss?
Judging from those hoaky commercials, some products will transform you from a jellyfish into a superhero in a jiffy. But what about the mantra we’re hearing that aggressive weight loss is hopeless, because it results in rebound weight gain? Our brain’s reward centers, our hormones, and our psyches simply can’t resist the evolutionary forces unleashed by artificial famine conditions, they say.
Some research is telling us that people can lose weight fast and that this speedy start bodes well for sustained improvement: More weight loss, and no more rebound than slower dieters that lose less weight. This has been a recurring outcome, even recently. Posts online make the claim more boldly than the researchers. A look past the headlines tells us a more nuanced story.
In a study by Nackers and colleagues, three groups were identified: fast, medium, and slow. The fast group lost more weigh up front, and kept it off just as successfully as the other groups. But this does not mean that an aggressive calory restriction diet is the answer. Here are some points to consider.
The fast group did not consume a drastically lower number of calories than the slow one (1,366.4 vs 1,486.8).
The fast group did not lose a drastic amount of weight, compared to the slow group (13.5 vs. 5.1 kg). Yes, it’s more than double, but it’s over six months.
We should ask what distinguished the slow group from the rest. The slow group attended less meetings, exercised less, and ate more calories. Were they more stressed? Was there a higher rate of depression? Where there other conditions that made them less active? Something was going on. Since the slow group was not as successful at maintaining weight loss, it’s a good guess that the conditions continued throughout the study period. The fast group was 5.1 times more likely to have maintained at least a 10% weight loss at 18 months than the slow group.
There are countless factors that might interfere. One is ADD. There is speculation that people with ADD have higher rates of obesity because their reward system is especially in need of a dopamine fix, and because of less consistent self-discipline. Medication appears to remedy this for many folks.
If there’s a take away, it seems that it would be for us to ask ourselves what might keep us from fully participating in a weight loss program. Those factors are probably the gateway to significant, sustained weight loss.

Category (Diet, Fitness & Nutrition)  |   Views ( 3409 )  |  User Rating
Rate It



None
To
Scrap Flag
Scrap