Prenatal smoking increases the risk of sociopathy

Sorry, but this one doesn’t fly. There is enough evidence to show that the anti-smoking campaign is a manufactured psychopathic ploy to cast doubt on any studies such as those you have cited.

Quite a few years ago when I first began researching pyschopathy, I came across some very interesting findings. As it happens, nicotine is a most interesting substance. Nicotine mimics one of the body’s most significant neurotransmitter, acetylcholine. This is the neurotransmitter most often associated with cognition in the cerebral cortex. LACK of cognition in the cortex is positively correlated to psychopathy. Acetylcholine is the primary carrier of thought and memory in the brain. It is essential to have appropriate levels of acetylcholine to have new memories or recall old memories.

Let’s see if we can connect some dots:

Acetyl-L-Carnitine (ALC) is the acetyl ester of carnitine, the carrier of fatty acids across Mitochondrial membranes. Like carnitine, ALC is naturally produced in the body and found in small amounts in some foods. …Research in recent years has hoisted ALC from its somewhat mundane role in energy production to nutritional cognitive enhancer and neuroprotective agent extraordinaire. Indeed, taken in its entirety, ALC has become one of the premiere “anti-aging” compounds under scientific investigation, especially in relation to brain and nervous system deterioration.

ALC is found in various concentrations in the brain, and its levels are significantly reduced with aging.(1) In numerous studies in animal models, ALC administration has been shown to have the remarkable ability of improving not only cognitive changes, but also morphological (structural) and neurochemical changes. …ALC has varied effects on cholinergic activity, including promoting the release(2) and synthesis(3) of acetylcholine. Additionally, ALC promotes high affinity uptake of choline, which declines significantly with age.(4) While these cholinergic effects were first described almost a quarter of a century ago,(5) it now appears that this is only the tip of the ALC iceberg. [Gissen, VRP’s Nutritional News, March, 1995]

It turns out that Alzheimer’s, a veritable epidemic in our country, is directly related to low levels of acetylcholine. In Alzheimer’s disease, the neurons that make acetylcholine degenerate, resulting in memory deficits. In some Alzheimer’s patients it can be a 90 per cent reduction! But, does anyone suggest smoking and exercising the brain as a possible cure?

Nope.

Another interesting little snippet found in a doctoral dissertation by Galen Knight says:

Thyrotropin is the single most important modulator of thyroid function. However, several of its effects are mimicked by neurotransmitters, acetylcholine and catecholamines…

Which suggests to us that low thyroid function can be partly ameliorated by nicotine.

The next excerpt is the most interesting. It is a from a Bioelectromagnetics Research Laboratory,paper first presented at a workshop to discuss possible biological and health effects of Radio Frequency Electromagnetic waves. The workshop was held by the Department of Bioengineering at the University of Washington, Seattle. The paper was later presented to “Mobile Phones and Health, Symposium,” October 25-28, 1998, University of Vienna, Austria. What they are talking about here is the effects of cell phone towers and the use of cell phones and pagers, etc:

…We carried out a series of experiments to investigate the effect of RFR exposure on neurotransmitters in the brain of the rat. The main neurotransmitter we investigated was acetylcholine, a ubiquitous chemical in the brain involved in numerous physiological and behavioral functions.

We found that exposure to RFR for 45 min decreased the activity of acetylcholine in various regions of the brain of the rat, particularly in the frontal cortex and hippocampus. Further study showed that the response depends on the duration of exposure. Shorter exposure time (20 min) actually increased, rather than decreasing the activity. Different brain areas have different sensitivities to RFR with respect to cholinergic responses [Lai et al., 1987b, 1988b, 1989a,b].

In addition, repeated exposure can lead to some rather long lasting changes in the system: the number of acetylcholine receptors increase or decrease after repeated exposure to RFR to 45 min and 20 min sessions, respectively [Lai et al., 1989a].

Changes in acetylcholine receptors are generally considered to be a compensatory response to repeated disturbance of acetylcholine activity in the brain. Such changes alter the response characteristic of the nervous system. Other studies have shown that endogenous opioids are also involved in the effect of RFR on acetylcholine [Lai et al., 1986b, 1991, 1992b, 1996].

Since acetylcholine in the frontal cortex and hippocampus is involved in learning and memory functions, we carried out experiments to study whether exposure to RFR affects these behavioral functions in the rat. Two types of memory functions: spatial ‘working’ and ‘reference’ memories were investigated.

Acetylcholine in the brain, especially in the hippocampus, is known to play an important role in these behavioral functions. In the first experiment, ‘working’ memory (short-term memory) was studied using the ‘radial arm maze’. This test is very easy to understand. Just imagine you are shopping in a grocery store with a list of items to buy in your mind. After picking up the items, at the check out stand, you find that there is one chicken at the top and another one at the bottom of your shopping cart. You had forgotten that you had already picked up a chicken at the beginning of your shopping spree and picked up another one later. This is a failure in short-term memory and is actually very common in daily life and generally not considered as being pathological. A distraction or a lapse in attention can affect short-term memory.

This analogy is similar to the task in the radial-arm maze experiment. The maze consists of a circular center hub with arms radiating out like the spokes of a wheel. Rats are allowed to pick up food pellets at the end of each arm of the maze. There are 12 arms in our maze, and each rat in each testing session is allowed to make 12 arm entries. Reentering an arm is considered to be a memory deficit. The results of our experiment showed that after exposure to RFR, rats made significantly more arm re-entries than unexposed rats [Lai et al., 1994].

This is like finding two chickens, three boxes of table salt, and two bags of potatoes in your shopping cart.

In another experiment, we studied the effect of RFR exposure on ‘reference’ memory (long-term memory) [Wang and Lai, submitted for publication]. Performance in a water maze was investigated. In this test, a rat is required to locate a submerged platform in a circular water pool. It is released into the pool, and the time taken for it to land on the platform is recorded. Rats were trained in several sessions to learn the location of the platform. The learning rate of RFR-exposed rats was slower, but, after several learning trials, they finally caught up with the control (unexposed) rats (found the platform as fast). However, the story did not end here. After the rats had learned to locate the platform, in a last session, the platform was removed and rats were released one at a time into the pool. We observed that unexposed rats, after being released into the pool, would swim around circling the area where the platform was once located, whereas RFR-exposed rats showed more random swimming patterns.

To understand this, let us consider another analogy. If I am going to sail from the west coast of the United States to Australia. I can learn to read a map and use instruments to locate my position, in latitude and longitude, etc. However, there is an apparently easier way: just keep sailing southwest. But, imagine, if I sailed and missed Australia. In the first case, if I had sailed using maps and instruments, I would keep on sailing in the area that I thought where Australia would be located hoping that I would see land. On the other hand, if I sailed by the strategy of keeping going southwest, and missed Australia, I would not know what to do. Very soon, I would find myself circumnavigating the globe.

Thus, it seems that unexposed rats learned to locate the platform using cues in the environment (like using a map from memory), whereas RFR-exposed rats used a different strategy (perhaps, something called ‘praxis learning’, i.e., learning of a certain sequence of movements in the environment to reach a certain location. It is less flexible and does not involve cholinergic systems in the brain).

Thus, RFR exposure can completely alter the behavioral strategy of an animal in finding its way in the environment.

…What is significant is that the effects persist for sometime after RFR exposure. If I am reading a book and receive a call from a mobile phone, it probably will not matter if I cannot remember what I has just read. However, the consequence would be much serious, if I am an airplane technician responsible for putting screws and nuts on airplane parts. A phone call in the middle of my work can make me forget and miss several screws. Another adverse scenario of short-term memory deficit is that a person may overdose himself on medication because he has forgotten that he has already taken the medicine.

Lastly, I like to briefly describe the experiments we carried out to investigate the effects of RFR on DNA in brain cells of the rat. We [Lai and Singh 1995, 1996; Lai et al., 1997] reported an increase in DNA single and double strand breaks, two forms of DNA damage, in brain cells of rats after exposure to RFR. DNA damages in cells could have an important implication on health because they are cumulative. Normally, DNA is capable of repairing itself efficiently. Through a homeostatic mechanism, cells maintain a delicate balance between spontaneous and induced DNA damage. DNA damage accumulates if such a balance is altered. Most cells have considerable ability to repair DNA strand breaks; for example, some cells can repair as many as 200,000 breaks in one hour. However, nerve cells have a low capability for DNA repair and DNA breaks could accumulate. Thus, the effect of RFR on DNA could conceivably be more significant on nerve cells than on other cell types of the body.

Cumulative damages in DNA may in turn affect cell functions. DNA damage that accumulates in cells over a period of time may be the cause of slow onset diseases, such as cancer. …Cumulative damage in DNA in cells also has been shown during aging. Particularly, cumulative DNA damage in nerve cells of the brain has been associated with neurodegenerative diseases, such as Alzheimer’s, Huntington’s, and Parkinson’s diseases.

Since nerve cells do not divide and are not likely to become cancerous, more likely consequences of DNA damage in nerve cells are changes in functions and cell death, which could either lead to or accelerate the development of neurodegenerative diseases. Double strand breaks, if not properly repaired, are known to lead to cell death. Indeed, we have observed an increase in apoptosis (a form of cell death) in cells exposed to RFR (unpublished results).

However, another type of brain cells, the glial cells, can become cancerous, resulting from DNA damage. This type of response, i.e., genotoxicity at low and medium cumulative doses and cell death at higher doses, would lead to an inverted-U response function in cancer development and may explain recent reports of increase [Repacholi et al., 1997], decrease [Adey et al., 1996], and no significant effect [Adey et al., 1997] on cancer rate of animals exposed to RFR.

Understandably, it is very difficult to define and judge what constitute low, medium, and high cumulative doses of RFR exposure, since the conditions of exposure are so variable and complex in real life situations.

Interestingly, RFR-induced increases in single and double strand DNA breaks in rat brain cells can be blocked by treating the rats with melatonin … [Lai and Singh, 1997]. Since it is a potent free radical scavenger, this data suggest that free radicals may play a role in the genetic effect of RFR. [Lai and Singh, 1998].

Work in the Laboratory of Neurochemistry at the Barrow Neurological Institute principally concerns molecules critically involved in such signaling called nicotinic acetylcholine receptors (nAChR). nAChR act throughout the brain and body as “molecular switches” to connect nerve cell circuits involved in essential functions ranging from vision and memory to the control of heart rate and muscle movement.

Defects in nAChR or their loss cause diseases such as myasthenia gravis and epilepsy and can contribute to Alzheimer’s and Parkinson’s diseases and schizophrenia.

nAChR also happen to be the principal targets of tobacco nicotine. …nicotine-like medicines show promise in the treatment of diseases such as attention deficit/hyperactivity disorder (ADHD) and Tourette’s syndrome and in alleviation of anxiety, pain, and depression, suggesting involvement of nAChR in those disorders.

…We have shown that numbers and function of diverse nAChR subtypes can be influenced by many biologically active substances, ranging from steroids to local anesthetics, and by agents acting on the extracellular matrix, the cytoskeleton, on second messenger signaling, and at the nucleus. We also have shown that chronic nicotine exposure induces numerical upregulation of many diverse nAChR subtypes via a post-transcriptional process that is dominated by effects on intracellular pools of receptors or their precursors.

Some current studies are testing our hypothesis that chronic nicotine exposure, as occurs with habitual use of tobacco products, disables nAChR and the nerve cell circuits they subserve, thereby contributing to long-lasting changes in brain and body function. [Lukas, 1999]

Now, notice in the above account how tricky they were when they said that nicotine …” That is jargon for “it increases the number of receptors” as well as the amount of acetylcholine. But, of course, the AMA wouldn’t let them get away with any of their work if they weren’t adding that they have a hypothesis that “habitual use of tobacco products… disables acetylcholine.” Never mind that in the beginning they are proposing it as a therapeutic drug for some of the very problems that have risen to almost epidemic numbers in the present time.

Let’s say it again: Research shows, however, that daily infusions of nicotine actually INCREASE the number of acetylcholine receptors by up to 40 %. Some researchers, such as the above, brush this finding off by saying “regardless, their function diminishes.” But that is not empirically observed. Most people who smoke find a “set point,” and once they have reached it, it does not take more and more and more to satisfy it.

How does nicotine act?

There are two major types (or classes) of acetylcholine receptors in the body, and they are commonly named by the other drugs which bind to them: nicotine and muscarine. Muscarinic acetylcholine receptors (mAChRs) can bind muscarine as well as ACh, and they function to change the metabolism…

Acetylcholine acts on nicotine acetylcholine receptors to open a channel in the cell’s membrane. Opening such a channel allows certain types of ions (charged atoms) to flow into or out of the cell. …When ions flow, there is an electrical current, and the same is true in the nervous system. The flowing of ions, or the passing of current, can cause other things to happen, usually those “things” involve the opening of other types of channels and the passing of information from one neuron to another.

Nicotinic AChRs are found throughout the body, but they are most concentrated in the nervous system (the brain, the spinal cord, and the rest of the nerve cells in the body) and on the muscles of the body (in vertebrates).

We say that nicotine acts like ACh at the receptors to activate them, and both substances are called agonists. The opposite type of drug, something that binds to the receptors and does not allow them to be activated is called an antagonist.

…When a substance comes into the body that can interfere with ACh binding to muscle nAChRs, that chemical can cause death in a relatively short time (because you use muscles to do things like breathe). A class of chemicals in snake and other poisonous venoms, neurotoxins, do exactly that. If you are bitten by a krait or a cobra, for example, and enough venom gets into the blood, there will be enough of their neurotoxin in your body to shut down the diaphragm muscle expands your lungs. Without that muscle functioning, the person ceases to breathe and dies of asphyxiation.

One of the reasons we know so much about these receptors is precisely that–plants and people have used substances [acetylcholine antagonists] which cause paralysis and asphyxiation for a long time. Plants use them to prevent being eaten by herbivores. Animals use similar substances to paralyze their prey. At least one human neuromuscular disease is related to nAChRs, and that is myasthenia gravis…

So, as you can see, nAChRs are important to life. …All known nicotinic receptors do share some common features. They are composed of 5 protein subunits which assemble like barrel staves around a central pore. …When the ligand (ACh or nicotine) binds to the receptor, it causes the receptor complex to twist and open the pore in the center. [Pugh]

Did you notice that it says that “animals use similar substances [acetylcholine antagonists] to paralyze their prey? We have to wonder about the oft reported conditions of mental paralysis associated with interactions with psychopaths.

Alcohol is a great pretender and can fool at least four types of receptors. It blocks the acetylcholine receptors… However, unlike nicotine which also binds to the acetylcholine receptors, alcohol doesn’t do anything useful while there. It simply sits there and blocks the ability to think. It also acts like cocaine in that it blocks the dopamine reuptake, flooding the brain with “feeling good.” Alcohol stimulates the release of endorphins, thus resembling morphine and heroin to a greatly lessened extent, and it modifies and increases the efficiency of the seretonin receptors.

Neuroscientist, Dr. Joseph LeDoux, professor of Science at New York University Center for Neuroscience has examined the way the brain shapes our experiences and our memories. His studies have unraveled the workings of emotions in general. He discovered that many neural pathways “bypass” the higher thinking parts of the brain.

The brain mechanisms that generate a given mental state, or what we choose, for the sake of convenience to call emotion, also give rise to certain measurable physiological states, such as pulse rates or brain waves, as well as observable behaviors such as running away or smiling. “Feelings,” by contrast, are a conscious, subjective labeling of the individual’s state. One person may say “I feel excited,” and another may say “I feel afraid,” and both will exhibit the same physiological symptoms and characteristic brain waves. So, trying to work backward is problematical. Dr. LeDoux writes:

…Fear is pervasive. …Fear is a good emotion to study [because] it is at the root of many psychiatric problems. The so-called anxiety disorders – panic attacks, obsessive-compulsive disorder, post-traumatic stress disorder – make up about half of all the psychiatric conditions that are treated every year, not including substance-abuse problems.

…The brain system that generates fear behavior evolved to help animals stay alive and has been preserved for millions of years, across a variety of species. The way that we act when we’re afraid – the way the body responds – is very similar to the way that other animals act when they’re afraid, even though we aren’t reacting to the same things. A rat would never be sent into a panic attack by the news that the stock market had crashed, and a human is not,, ordinarily, afraid of a cat. But the way our body responds to the news of a stock market crash is very similar to the way the rat’s body responds when it sees a cat. This is critically important, because it means that we can study the behavior of other animals, and the processes in their brains, to learn how the human fear system works.
…[We study fear with behavior tools] techniques and methods for studying such specific behavior… And we also need good neuroscience tools, method that allow us to study what is going on in the brain when the animal is behaving in a fearful way.

One important behavior tool is known as classical fear conditioning, which is a version of what Pavlov described as the conditioned reflex. The process of classical conditioning involves pairing, or associating, an innocuous stimulus – a sound or a flash of light, something that is essentially meaningless in itself – with something that is meaningful to the animal. In the case of Pavlov’s dogs, the meaningful stimulus was food; the meaningless stimulus was the bell. Food is not a useful stimulus if we’re interested in studying fear, however. So, using laboratory rats as subjects, we might pair a sound with, for instance, a mild foot shock. (We keep the shock as weak as possible to allow the experiments to be performed, and we administer it as infrequently as is feasible.)

On the basis of these kinds of pairings, the sound becomes something that the rat learns is associated with danger. Thus when the rat hears the sound, it reacts immediately: It freezes in anticipation of danger. This is a conditioned reflex, as is Pavlov’s dogs’ salivating at the sound of the bell, in anticipation of food.

An animal in the wild usually doesn’t have the luxury of trial and error in learning what’s dangerous; it doesn’t get to practice until it gets things right. If it’s lucky enough to escape once, it had better remember the sight of the predator, the smell of the predator, the sound of the predator, and so forth. In the laboratory, we need to apply the shock with the sound only once if it is sufficiently aversive.

When something like this occurs – the sound that’s been paired with the shock – it activates a variety of responses that are identical to those that would occur in a real-life situation. Television tapes of the bombing during the 1996 Olympic Games in Atlanta, for example, reveal that when the bomb went off the first thing that happened was that everyone flinched; this was the startle reflex. But then the next thing they did was freeze: They just hunkered down and held still for about two seconds. That’s evolution buying us a little time… Predators respond to movement… So we freeze when we’re in a dangerous situation, because our old evolutionary fear system detects danger and responds to it in an automatic way.

…In a situation of danger, a variety of physiological responses occur. Blood is redistributed to the body parts that are most in need (the muscles). This results in changes in blood pressure and heart rate. In addition, the hypothalamic-pituitary-adrenal, of HPA, axis is activated, releasing stress hormones. In addition, the brain activates the release of natural opiate peptides, morphine-like substances that block the sensation of pain. Called hypoalgesia, this reaction is an evolutionary carryover that allows a wounded animal to keep going. It’s often seen in wartime, where wounded soldiers don’t react to their injuries until they’re off the battle field. All of these things happen in the rat when it perceives a natural threat such as cat, or when it hears the sound that’s been paired with the shock. And all of these fear responses are easily measured. […]

Once we have conditioned the animal to respond to a sound – or that the sound produces freezing behavior, changes in blood pressure, heart rate, and so forth – the next step is to trace how the sound, coming into the ear, reaches the parts of the brain that produce these responses in the body. The strategy is to make a lesion in a certain part of the brain to determine whether damage to that area interferes with the fear conditioning. If it does, we then inject the tracer substance there to see which areas that part of the brain communicates with. Then we systematically make lesions in each of those downstream areas to see which one interferes with the fear conditioning, inject tracer substance at that point, look to see where it goes, and so on. We can then record electrical activity to see how cells in the area respond. In this way, we can walk our way, point by point, through whatever pathway of the brain we want to study…

Years of research by many workers have given us extensive knowledge of the neural pathways involved in processing acoustic information, which is an excellent starting point for examining the neurological foundations of fear. The natural flow of auditory information – the way you hear music, speech, or anything else – is that the sound comes into the ear, enters the brain, goes up to a region called the auditory midbrain, then to the auditory thalamus, and ultimately to the auditory cortex. Thus, in the auditory pathway, as in other sensory systems, the cortex is the highest level of processing. […]

We then did experiments with rats that had amygdala lesions… We found that the amygdala lesion prevented conditioning from taking place.

…So the amygdala is critical to this pathway. It receives information about the outside world directly from the thalamus, and immediately sets in motion a variety of bodily responses. We call this thalamo-amygdala pathway the low road because it’s not taking advantage of all the higher-level information processing that occurs in the neocortex, which also communicates with the amygdala.

…Say that a hiker is walking through the woods and sees something on the ground. The image gets to the thalamus, which sends a very crude template to the amygdala; the amygdala, in turn, activates the heart rate, gets the muscles tense and ready to go. At the same time, the stimulus is making its way through the cortex, which is slowly building up a complete representation of – a snake. Now, the thalamus doesn’t know if it’s a snake or just a stick that looks like a snake, but as far as the amygdala is concerned in this situation you’re better off treating the stick as a snake than your are treating a snake as a stick. The subcortical brain is over generalizing for the opportunity to stay alive in the presence of the snake. By getting the amygdala going instantly, it buys you time. If the object turns out to be a stick instead of a snake, nothing’s lost; you can turn the fight-or-flight system off. But if it turns out to be a snake, you’re ahead of the game: You’ve activated the amygdala, and your body is ready to respond effectively.

The low road, or the thalamo-amygdala pathway, is a quick and dirty system. Because it doesn’t involve the cortex at all, it allows us to act first and think later. Or, rather, it lets evolution do the thinking for us, at least at the beginning, buying us time.

The cortex – the high road – also processes the stimulus, but it takes a little longer. You need the cortex for high-level perception in order to distinguish one kind of music from another… or to distinguish between two speech sounds But you don’t need the cortex to carry out some of the emotional learning involved in the fear system. Thus we can have emotional reactions to something without knowing what we’re responding to – even as we start responding to it. In other words, we’re dealing with the unconscious processing of emotion. This is a neurological demonstration of at least part of what Freud was trying to get at when he talked about the unconscious.

…What we’re saying is that unconscious emotions are probably the rule rather than the exception.

We all know that there are many times in normal, day-to-day experience when we don’t understand where our emotions are coming from – why we feel happy, sad, afraid. For example, let’s say you’re in a restaurant having a meal with a friend and you have a terrible argument at the table, which happens to be covered with a red-and-white checkered tablecloth. The next day you’re walking down the street and you have this gut feeling that the person walking toward you is someone you don’t like. You’ve never seen the person before, but you know you don’t like him. We often hear about “gut feelings” and people say “you have to trust your gut.” But maybe in this case the reason you feel you don’t like this person is simply that he’s wearing a red-and-white checkered tie. This visual input is going in through your low road, activating your amygdala and causing you to have an unpleasant reaction to the person. You might attribute your reaction to the way this person looks or walks or acts, but in fact it’s just the low road …the unconscious activation of the amygdala.

Some of the time …these low road reactions are useful. Certainly that was the evolutionary goal: to protect us from danger. But these can also be harmful, or at least counterproductive. As in the case of the red-and-white checkered tie/tablecloth, an unconscious response may not be revealing some sort of inner truth but may instead be doing nothing more than reviving past emotional learning. “Listening to your gut” …might simply mean you are responding to past learning. […]

Let’s say, for example, that you regard all snakes as dangerous, but you know that you needn’t fear a snake in the zoo as much as you might a snake that you happened upon in the woods. Ordinarily, your hippocampus and cortex would recognize the context (are you in the woods or at the zoo?), and you would react appropriately to the sight of a snake. But if you had a hippocampal lesion, you might have trouble suppressing a strong fear reaction even at the zoo.

Another important player in the fear response is the prefrontal cortex. In rat studies, as well as in human experiments, when you give the sound over and over again, without the unpleasant event occurring, it eventually loses its ability to elicit the emotional fear reactions. This process is called extinction. But if the medial part of the prefrontal cortex is damaged, emotional memory is difficult to extinguish. So, for example, a rat that has a lesion in the prefrontal cortex tends to continue to respond to the sound as if it were still associated with the unpleasant event’ the learned response is resistant to extinction.

However, it’s important to know that even without damage to the prefrontal cortex, fear memories are hard to extinguish completely. Many studies show, for example, that weeks after a rat has ceased to react to a sound that had been paired with a shock, it might suddenly react fearfully to the sound again. Of if the animal goes back into the chamber where it had the conditioning experience, the fear behavior can be reactivated. Stress can reactivate extinguished fears in humans as well. A patient with a phobia can be treated, apparently successfully; then something happens – say the patient’s mother dies – and the phobia comes back.

What certain types of therapy can do – and what the extinction process does – is train the prefrontal cortex to inhibit the output of the amygdala. This training doesn’t eliminate the unconscious fear; it simply holds it in check.

Therapists find this both depressing and informative; they now understand that fear memories can’t be completely eliminated, but at least they know what battle they’re up against. …I don’t know of any animal that can’t be conditioned …and in any animal that has an amygdala, that structure seems to be involved in fear conditioning. The fear system, therefore, is probably a very basic, fundamental learning mechanism that’s built into the brain.

In this sense then, we’re emotional lizards. We’re running around with an amygdala that’s designed to detect danger and respond to it. This system is very efficient, and it hasn’t changed much in terms of how it works. What has changed, of course, are the kinds of things that will turn it on, the things that humans [are taught and conditioned] to respond to that have the same effect on us that seeing a cat has on a rat. [LeDoux, States of Mind, 1999]

Now, all animals have the fear-learning mechanism which enables them to survive. They can detect danger and respond to it appropriately. But these animals don’t have what we call fearful feelings the same way that human beings can “feel afraid.” When the basic “fear program” system is activated in a brain that also has self-consciousness, a new phenomenon occurs: subjective feelings. Feelings of fear are what happen in consciousness when the activity generated in the subcortical neural system involved in detecting danger is perceived by certain systems in the cortex, especially the “working memory.”

A conscious feeling of fearfulness is not necessary to trigger an emotional fear response. The low road can take care of this just fine. That is, we can produce responses to danger without being consciously afraid, as when we jump back up onto the curb to avoid being hit by a car. IN a situation like that, as people so often say, we don’t “have time to be afraid.” …At other times we will first have some kind of response in our body and only later be able to name what the feeling was: anxious, sad or angry. In many cases, though, even if we can say that we feel anxious, we don’t know what generated those feelings. Indeed, we see this again and again in the various disorders of the fear system, such as panic attacks and phobias.

Why is it so difficult to eliminate such fears? Once the amygdala is turned on, it can influence information processing in the cortex from the earliest stages onward, but only the later stages of cortical processing affect the amygdala. In other words, even though communication goes two ways, it’s not equally effective in both directions. In general, the projections from the amygdala to the cortex are much stronger than vice versa. If we think of the routes from the amygdala to the cortex as superhighways, then those from the cortex to the amygdala are narrow back roads. Once the emotions are activated, they can influence the entire working of the cortex, whereas the cortex is very inefficient at controlling the amygdala. So, using thinking to overcome emotion is like using a back road or side street from the cortex, while the amygdala is bombarding the cortex with input via the superhighways. [LeDoux, 1999]

But thinking with the cortex, it turns out, is basically a way to rewire your brain. It is like working on the back roads to develop them into the commanding interstate system of the brain they were meant to be. Research shows that changes in the brain are the result of learning experiences, and it seems that learning – acquiring knowledge – is the path of rewiring the synaptic connections in the brain.

It seems that the key to this is the fact that learning, hard thinking and pondering, requires that certain brain chemicals – usually acetylcholine – be squirted out at just the right place and in the right quantities. It is becoming clear that the molecules of memory are blind to the kind of memory – whether it is conscious or unconscious – that is occurring. What determines the quality of different kinds of memories is not the molecules that do the storing but the systems in which those molecules act. If they act in the hippocampus, the memories that get recorded are factual and accessible to our consciousness. If the chemicals are acting in the amygdala, they are emotional and mostly inaccessible to conscious awareness.

So, what happens is that even if we don’t know what has triggered a given emotional response until after the fact, we do have an awareness that we are “feeling” a certain way. This awareness is called our “working memory.”

Working memory, or awareness, involves the frontal lobes of the brain just above and behind the eyebrows. This is what we use when we want to remember a new phone number just long enough to dial it, or to remember what we went to the kitchen for long enough to get it! It is also the place where many different kinds of information is held simultaneously while we are comparing one thing to another. We can have all kinds of things going on there at once. We can look at something, hold this image in working memory along with the memory of something that we have pulled out of long term memory which we wish to compare it to; sounds, smells, and even the ongoing physiological input from our system as we are considering this: does it make us feel peaceful, happy, sad, afraid?

All of these elements come together simultaneously. However, this working memory can only do one thing at a time, even if that one task is multi-factored. A classic example is when you try to remember a new phone number and someone asks you a question before you get to dial it. The number flies out the window as you answer the question and you have to go back and look it up again.

It seems that this “working memory,” or “awareness,” is – if not consciousness itself – at least a window to it.

It is in working memory that “conscious feelings” occur. In working memory, three things come together to create conscious feeling: present stimuli, activation of the amygdala in some way and activation of conscious memory in the hippocampus.

Present stimuli might include standing inside a church. This would arouse the amygdala so that the unconscious memories of the many experienced in church – the flooding of the receptors with neurochemicals; and this would activate conscious memory of the last time you were in church, or several memorable times will pass through the mind. When all these things come together in working memory, with the body now activated with chemistry and past history, this is perceived as “feeling.”

The same thing can occur in any kind of encounter as we have already described. Something that is present now will turn on the chemicals which will arouse conscious memories that are related to those chemicals, and then the present moment will be interpreted in those same terms.

Since what we are looking at here is the fact that unconscious, chemical imprints, have a much greater ability to influence thinking than vice versa, we realize that we are face to face with an age-old debate between reason and emotion, logic and passion, knowledge and faith.

When you are aroused emotionally whether by fear or pleasure or sexual attraction, it is a cold hard fact that emotion dominates thinking.

Philosophers going all the way back to Plato have endlessly analyzed this fundamental schism. The body fills us with passions and desires and fears and fancies and foolishness and fairy tales made up to justify these chemical reactions. Plato opined that the true philosopher was one who could master his emotions by the use of reason. Socrates said “Know thyself,” by which he meant that we had to understand our emotions in order to be able to control them.

The vast majority of philosophers and philosophical writers throughout man’s recorded history have believed that in order to be truly human – as opposed to just an animal – we must activate reason. Descartes didn’t say “I FEEL, therefore I am.” Thinking seems to be the distinctly human thing that humans do which separates them from animals.

And it is our emotions and LACK of thinking, lack of control of those emotions, that make us susceptible to psychopaths.

There is, at present, such an imbalance between the amygdala’s input to the cortex and the very sparse control of the cortex over the amygdala. Even though thoughts can readily trigger emotions by activating the amygdala, it is very difficult to willfully turn off emotions.

As it happens, the cortical connections to the amygdala are actually far greater in primates than in other animals. It seems that more balanced cortical pathways are the evolutionary trend. It is my opinion that we will develop them or perish. A more harmonious integration of emotion and thinking would allow us to both know our TRUE feelings, and why we have them, and to be able to use them more effectively.

Not long ago I read the following article:

Brain cells work differently than previously thought: Nicotine helps to spark creativity
http://laura-knight-jadczyk.blogspot.com/2007/08/lets-all-light-up.html

which tells us:

Increasingly, studies are beginning to show that complex information processing, and perhaps consciousness itself, may result from coordinated activity among many parts of the brain connected by bundles of long axons. Cognitive problems may occur when these areas don’t communicate properly with each other. […]

Using nicotine, they stimulated the axon to determine how it would affect a signal the brain cell sent to the cortex. Without applying nicotine, about 35 percent of the messages sent by the brain cell reached the cortex. But when nicotine was applied to the axon, the success rate nearly doubled to about 70 percent.

Nicotine DOUBLES the efficiency of our thinking. Hmmm… I think that makes it pretty clear why the PTB (Powers That Be) wish to stamp out smoking. After all, as one comment to the article mentioned, “if our immunity to emotional manipulation and psychopathic propaganda is directly proportional to the cortical control we can exert over the knee-jerk emotional reactions programmed into the amygdala. If smoking can DOUBLE the effective communication between the cortex and other parts of the brain, then what does that say about efforts to do away with smoking in the general population? Can’t have any of the hysterical sheeple accidentally waking up and thinking rationally about their actions.”

This prompted me to write a post on the topic here:

Let’s All Light Up!
http://laura-knight-jadczyk.blogspot.com/2007/08/lets-all-light-up.html

I really don’t think that many people can read this with an open mind and then follow the research, follow the money, and follow the psychopathic trends in society that accompany the anti-smoking brain-washing, but for those who can, for those who can break out of the psychopathic brain-washing, getting free of this nonsense is a big first step toward freedom.

Psychopaths don’t want you to smoke because it just might assist you in resisting their manipulations.