The word fear comes from the Old English word faer (Oxford English Dictionary, 1933), which meant "sudden calamity or danger". It is currently defined as "an agitated foreboding often of some real or specific peril" (Webster’s Third International Dictionary, 1981) and as "the possibility that something dreaded or unwanted may occur" (Standard College Dictionary, 1963). These definitions underscore several connotations to the word fear; it points to the possible occurrence of an "unwanted" or calamitous event; the event has not yet occurred (that is, it is in the future); the individual is concerned (agitated foreboding) about the event. Fear, then refers to the appraisal that there is actual or potential danger in a given situation. It is a cognitive process as opposed to an emotional reaction.

Anxiety, on the other hand is defined as a "tense emotional state" (Funk & Wagnalls, 1963) and is often marked by such physical symptoms as tension, tremor, sweating, palpitation and increased pulse rate. The term anxiety comes from the Latin word anxius, and its usage dates back to as early as 1525. The Latin term was defined as a condition of agitation and distress. The stem of anxius - anx – comes from another Latin word, angere, which means to "choke" or to "strangle". The word anxius, probably referred to choking frequently experienced by anxious individuals (Lewis, 1970). We here this term used a lot in golf. This has a direct relation to stress and the HPA.

Phobia refers to a specific kind of fear and is defined as an "exaggerated and often disabling fear" (Webster’s Third International Dictionary, 1981). A phobia is also characterized by an intense desire to avoid the feared situation, and evokes anxiety when one is exposed to this situation. The word is derived from the Greek word phobos for "flight".

Panic is defined as a "sudden overpowering fright…accompanied by increasing or frantic attempts to secure safety" (Webster’s Third International Dictionary, 1981). The word, which was in use as early as 1603, derives from the name of the Greek deity Panikos, the god of woods and shepherds, who was regarded as the cause of panic among the Persians at marathon and, by the Greeks, as the cause of any sudden, groundless fear.

The professional athletes struggling with a Focal Dystonia will experience two or more of these physical and emotional experiences at the same time thus making top athletic performance impossible.

Anxiety may be distinguished from fear in that the former is an emotional process while fear is a cognitive one. Fear involves the intellectual appraisal of a threatening stimulus; anxiety involves the emotional response to that appraisal. When a person has anxiety he experiences a subjectively unpleasant emotional state characterized by unpleasant subjective feelings such as tension or nervousness, and by physiological symptoms like heart palpitations, tremor, nausea and dizziness. A fear is activated when a person is exposed, either physically or psychologically, to the stimulus situation he considers threatening. When the fear becomes activated, he experiences anxiety. Fear then is the appraisal of danger, anxiety is the unpleasant feeling state evoked when fear is stimulated. In addition to anxiety a variety of symptoms referable to the autonomic and the somatic nervous systems may be provoked concurrently. In a putting "yipping" case the fear would be the "possibility of missing the short putt" because the stroke might fall apart (physical), to go with the embarrassment of missing a short one (psychological), then this will activate anxiety that will in effect cause all the fears to become reality.

A phobia refers to a specific object of fear. Initially a person is afraid of missing the short putt. When in the situation, he is acutely afraid of consequences (other people’s thoughts, embarrassment, inability to perform etc.). When phobia or fear is activated, the individual’s reaction may range from mild anxiety to panic. The objects of phobias can range from small to large – the main quality of a phobia is that it involves the appraisal of a high degree of risk in a situation that is relatively safe. So the same person with the fear of missing a short putt will perceive this shot as "dangerous". However, he does not experience anxiety until he finds himself in that situation. A player might say: "I might stand over a short putt and not be able to take the putter back; this will embarrass me because I am a professional golfer, and I am not supposed to do this". The person who perceives this threat as overwhelming may have a panic attack.

The concept of danger arises from the possible consequences. Before he sets foot on the course this fear is latent, once in the presence of the association, the fear become activated, and all the unpleasant affective and physiological symptoms associated with panic attacks are aroused. Thus panic is an intense, acute state of anxiety associated with the other dramatic physiological, motor, and cognitive symptoms. The physiological correlates of panic are an intensified version of those of anxiety – that is rapid pulse, dizziness, cold and profuse sweating and tremor. In addition, one has a sense of impending catastrophe, pervasive inhibitions, and an overwhelming desire to flee or get help. This is what is called the stage of the full blown yip!

Anxiety is often looked at as a performance inhibitor, however very few experts have actually gone out to research and understand its influence from a psychological and physiological perspective in golf. Anxiety is related to a certain level of stress that either makes us perform well, inconsistent or "choke".

In people with anxiety-related disorders, fear comes to organize and control the person’s life to the extent of severe functional impairment. High levels of anxiety inhibit and distort rational cognitive processing. Cognitive interventions with these people often include educating them about the physiological symptoms of anxiety such as the racing heart, shortness of breath, and sweaty palms. These people are taught that feelings of dread are secondary to autonomic symptoms and should not be taken as seriously as they feel. A focus on understanding normal biological processes usually redirects the client away from catastrophic attributions of serious illness.

The boost of cortical processing from psycho-education is combined with exposure and response prevention. Exposure and response prevention means that the client faces the feared stimulus, without being allowed to retreat back to the "safety" environment. Exposure is usually systematic, gradual, and paired with relaxation training used to aid in the down regulation of effective arousal. This process combines increased cortical processing (thought) with the result of exposure (affect), allowing fear circuitry to integrate with cortical circuitry in order to permit inhibition, habituation, and increased conscious control (Cozolino, 2002).

How does this translate into what is going on in the brain during sports intervention? Research has demonstrated that disorders of anxiety and depression correlate with changes in metabolic balance within the brain. For example, symptoms of depression correlate with changes in activation in the frontal cortex – lower levels of activation in the left and higher levels in the right (Baxter et al., 1985; Field, Healy, Goldstein, Perry, & Bendell, 1988) have found. Alternately, the imbalance in functioning may be due to dysregulation among different regions within the frontal cortex (Brody et al., 2001).

Symptoms of obsessive-compulsive disorder correlate with heightened activation in the medial portions of the frontal cortex and a subcortical structure called the caudate nucleus (Rauch et al., 1994). Posttraumatic flashbacks and states of high arousal correlate with higher levels of activation in right-sided limbic and medial frontal structures. Importantly, high arousal also correlates with decreased metabolism in the expressive language centers of the left hemisphere (Rauch et al., 1996).

There is an increasing awareness that neural networks throughout the brain are stimulated to grow and organize by interaction with the social environment. Early relationship becomes neurally encoded in networks of sensory, motor, and emotional learning to form what dynamic therapists call inner objects. These inner objects have the power to soothe or dysregulate, depending on the quality of our attachment experiences with significant others. These unconscious memories organize our inner worlds both when we are alone and when we are in the proximity of others. Given the essential social organization of the brain, at some level we always experience ourselves in context of others.

In line with this, differentiation needs to be understood. Differentiation is the development of autonomy – a balance between the recognition of the needs of self and others. Anxiety is the enemy of differentiation that is the more frightened people are, the more dependent and primitive they become in their interaction with others and their environment (Bowen, 1978).

When individuals become anxious and this processing regression occurs, family members try – unconsciously and consciously – to shape the family in a manner so as to reduce their own anxiety. The primal responses to anxiety is quite common in sport, this is part of what people perceive as "choking".

The amygdala is a central neural hub of emotional experience, suggesting that it may be involved with some of the more unusual human experiences. Electrical stimulation of the amygdala results in a wide variety of bodily sensations (Halgren, Walter, Cherlow, & Crandall, 1978). Feelings of anxiety, déjà vu, and memory like hallucinations have also been reported with the stimulation of the amygdala (Chapman, Walter, Markham, Rand, & Crandall, 1967; Penfield & Perot, 1963; Weingarten, Cherlow, & Holmgren, 1977). Because of its low threshold, subtle seizure activity may trigger the amygdala to activate normally inhibited sensory and emotional memories that then break into conscious awareness (Sarter & Markowitsch, 1985). The primitive memories may also become activated in states of stress and posttraumatic arousal (Van der Kolk & Greenberg, 1987). Individuals under stress may become particularly vulnerable to the intrusion of powerful memories of early childhood (Cozolino, 1997).

The amygdala is located within the limbic system and beneath the temporal lobes on each side of the brain. It is well developed at birth and has a significant role in the networks involved with emotional learning (Brodal, 1992). Portions of the amygdala (the basolateral areas) have evolved in tandem with the expansion of the cerebral cortex in humans (Stephan & Andy, 1977). The amygdala’s neural connectivity supports its participation in the integration of the different senses with a special emphasis on vision (van Hoesen, 1981). The amygdala functions as an organ of appraisal for danger, safety, and familiarity in approach-avoidance situations (Sarter & Markowitsch, 1985).

The amygdala’s direct neural connectivity with the hypothalamus (Amaral, Veazy & Cowan, 1982) and limbic-motor circuits allows it to trigger rapid action. The power of phobias and flashbacks is greatly enhanced by the involvement of immediate and intense somatic activation provided by this direct connectivity. Thus, the amygdala is one of the key components of affective memory, not just in infancy but also throughout life (Ross, Homan, & Buck, 1994). In the fully developed brain, the amygdala enhances hippocampal processing of emotional memory by stimulating the release of norepinephrine and glucocorticoids via other brain structures (McGaugh, 1996; McGaugh et al., 1993). Through these chemical messages, the hippocampus is put on notice that what is being experienced is important to remember.

The hippocampus is noted for its late maturation, with the myelination of cortical-hippocampal circuits continuing into late adolescence (Benes, 1989). Research suggests that sustained stress results in excessive exposure of the hippocampus to glucocorticoids, released in the response to acute stress (Sapolsky, 1987). Prolonged high levels of glucocorticoids can result in dendritic degeneration, increased vulnerability to future neurological insult, inhibited hippocampal functioning, and cell death (Wantanabe, Gould, & McEwen, 1992). Given that chronic stress correlates with decreased hippocampal volume, and that so many of us suffer from it, it might be a good time to look at this from a nutritional protective standpoint.

The amygdala has a central role in the emotional and somatic organization of experience, whereas the hippocampus is vital for conscious, logical, and cooperative social functioning. The amygdala and the hippocampus play opposite roles in an attention-directing process. By accentuating small differences among inputs, the amygdala heightens awareness of specific aspects of the environment (attention) whereas the hippocampus inhibits responses, attention, and stimulus input habitation (Douglas, 1967; Kimble, 1968; Marr, 1971). The amygdala is involved with generalization, the hippocampus with discrimination (Sherry & Schacter, 1987). The amygdala will make us jump at the sight of a spider, whereas the hippocampus will allow us to remember that this particular spider is not poisonous, so we shouldn’t worry. Flashbacks from traumatic experiences likely reside in amygdaloid memory networks. Focal Dystonia ("Yips" victims in golf), describe these "freeze modes" as powerful, multisensory, often triggered by associative stress, and experienced as if they were occurring in the present. These flashbacks also have the characteristic of being stereotyped and repetitive, suggesting that they are not subject to the assimilating and contextualizing properties of hippocampal memory networks (Jacobs & Nadel, 1985).

The behavior of all organisms is based on approaching what is life sustaining and avoiding what is dangerous. The proper integration and balance between right and left hemisphere functioning allows us to experience a healthy mixture of positive and negative emotional experiences, as well as to regulate and manage anxiety. The left hemisphere is bias toward anxiety, suspiciousness, and negativity keeps the body alert to danger. Right hemisphere biased neural processing, measured in a variety of ways, and has been shown to correlate with low self-esteem (Persinger & Makarec, 1991). The same phenomena holds true for anxiety. Primates with extreme left frontal activity are more fearful and defensive, and have higher levels of stress hormones, than do those with activity biased toward the right hemisphere (Kalin, Larson, Shelton, & Davidson, 1998). The neural circuitry involved in fear and anxiety, although biased toward the left hemisphere, involves both hemispheres and all levels of the triune brain. The most primitive subcortical fight or flight circuitry, shared with our reptilian ancestors, interacts with the most highly evolved association areas of the cerebral cortex (Cozolino, 2002). This might explain in golf dystonias like "yipping", why an experienced golfer misses short putts that beginner golfers will never miss. The connection between every kind of anxiety and the core biological mechanisms of physical survival supports the philosophical notion that all anxiety, at its core may be the fear of death (Tillich, 1974). This explains why accumulative associatively learned and developed anxiety through all the senses of the nervous system might lead to competitive meltdown, because like the proper positive things are learned through the associative process, so is the negativity and thus anxiety.

Some anxieties appear to be hard wired, specific to primates, and linked to both our present and past survival needs. We know now that the amygdala plays a central role in the expression and regulation of anxiety and fear. Anxiety and fear are the conscious emotional aspects of the body’s ongoing appraisal of what is dangerous and life threatening. Anxiety can be triggered by countless conscious or unconscious cues and has the power to shape our behaviors, thoughts, and feelings. At its most adaptive, anxiety encourages us to step back from the edge of a cliff, check the road twice before crossing it.

The Mayo Clinic is undertaking a study of the "yips" in golf – the mysterious affliction in putting manifested by freezing over the putt, shaky hands, and a stabbing stroke. Previous researchers have classified yips as an occupational focal hand dystonia, a type of movement disorder apparently caused by degeneration of neural circuitry following decades of the same hand movement.

In order to fully understand this phenomenon we need to look at the physiological and psychological associations that lead to this problem. It also needs to be understood that this problem has a very strong physiological base and the body needs to be replenished by nutrients to get back to optimal performance. However before the explanation is given to replenish the abused organs, lets continue to look at the processes that cause this depletion.

These earlier putting studies are in line with modern neuroscience, in which occupational focal hand dystonia is only imperfectly understood (Hochberg et al., 1990; Wake Forest Neurosurgery, 2001), but is no longer considered to be psychological in origin (e.g., Abbruzzesse et al., 2001; Adler, 2000; Hallet, 1998; Hochberg et al., 1990; Sheehy and Marsden, 1982). Classed as a movement disorder along with Parkison’s Disease, cortico-basal degeneration (CBD), and various forms of spasticity (Dystonia Medical Research Foundation, 2001; We Move, 2001), focal hand dystonia has been linked with:

Sensorimotor degradation of hand-finger neurons in the sensory cortex (blurring of the fine sensory discrimination of finger and hand proprioception underlying movement control) (Abbruzzesse et al., 2001; Byl et al., 2000).

Basal ganglia dysfunction in the release of prepotent motor programs by inhibition of inhibition (Ibanez et al., 1999; Reilly at al., 1992; Tinazzi et al., 1999; Toro et al., 2000).

Imbalanced forearm muscle inhibition patterns (Nakashima et al. 1989).

Furthermore, occupational focal dystonias are not restricted to the hands (e.g., "auctioneer’s jaw", "writers cramp": Scolding et al., 1995).

The emerging picture is of a complex loop of brain centers integrating perception, emotion, and movement that is subject to disruption at varying points with resulting movement deficits that can be quite similar. For example, vestibular dysfunction contributes to spasmodic torticollis ( a related dystonia; Munchau et al., 2001); cervical spinal lesions can produce dystonia like deficits in hand movements without involvement of cerebral circuits (Uncini et al., 1994); and cerebellar degeneration results in excess cortical activation in motor control (Liepert et al., 2000). Focal hand dystonia is considered mostly intractable, but limited relief can be gained from periodic injections of the hand muscles with botulinum toxin A. In addition brain surgery with thalamotomies (lesions of basal-cortico motor control loop at a point in the thalamus) has been effective

(Kelly, 2001; Mempel et al., 1986). However not many golfers want to take up this option for their affliction in missing crucial putts under pressure.

The Mayo Clinic team includes Dr. Crews from the department of Exercise Science at Arizona State University (Crews, 2001). The Mayo Clinic position on the yips apparently builds upon other studies by Dr. Crews on "choking" under pressure in golf and on attentional patterns in putting (Crews and Landers, 1993). Choking is generally understood to refer to anxiety-sponsored increases in arousal level that lead to performance deficit, typically associated with failure in intense situations or in high pressure competition. The 1996 experience of Greg Norman at the Masters in losing a final round six-shot lead to Nick Faldo prompted NBC program Dateline to bankroll a study of choking in golf by Dr. Crews and others. This research consisted of an EEG study of ten amateur golfers with an average golfing experience of five years, and handicaps ranging from 11.5 to 26. The task was a trial of 20 five foot putts for baseline, followed by a second trial of putts on condition that the golfers who improved won $300 while the golfers who performed worse than baseline would have to pay $100. Five did better and five did worse (Linder et al.; 1998; Abrahams, 2001).

Basing her analysis of choking upon EEG patterns, Dr. Crews concluded that successful golfers had increased cortical activity just like unsuccessful golfers, but the activation was spread evenly over both hemispheres of the brain, whereas activation for unsuccessful golfers concentrated in the left (dominant) hemisphere (Abrahams, 2001).

Dr. Crews interpreted the increased left-brain EEG activity as anxiety-related and employment of right-brain processes. In keeping with this analysis of handling pressure, Dr. Crews teaches "right brain" golf by encouraging golfers to use imagery, relaxation techniques, and target focus as ways to promote right-brain activation and therefore hemispheric balance. This research was awarded the First Annual Golf Science award from the Golf Magazine and the World Scientific Congress on Golf.

The concept of anxiety and physiological research methodology followed in the Mayo Clinic study is closely similar to that utilized by Dr. Crews in her "choking" studies (Smith et al., 2000). And the behavioral aspects of anxiety are also similarly identified (heart rate increase and higher level of cortical excitation associated with anxiety).

Compensatory golf techniques (long putters, fat grips, grip style or position change, grip pressure adjustment, "sidesaddle" putting, reliance upon non-dominant hand, reliance upon shoulders rather than hands for stroke, etc.)

Neuromuscular re-educated (New swings and postures)

Sport Psychology cognitive therapies

Biofeedback

Relaxation therapy

Mental imagery

Thought-control (e.g., meditation, mindfulness, positive self-talk, self hypnosis, neurolinguistic programming)

Anxiolytic pharmacology (beta-blockers and tranquilizers)

The Mayo Clinic study affords a detailed look at the current understanding of the yips among golfers and golf scientists. However, the phenomena under examination must be observed separately by well-crafted experimental protocols for a deeper understanding of the controlling neurophysiolocigal processes. Without this deeper understanding, effective therapy will likely remain elusive.

The unfortunate problem with a lot of this research and investigation is that the experts in each field do not combine the sciences to understand the whole problem. Psychologists want to handle the problem with behavior modification and positive affirmation modalities. They want to include the techniques of relaxation that are effective in certain other pressure situations but not in cases of focal dystonia (yips). At this point you need to make physiological, neurological and psychological changes to stay ahead of the problem. The body at this point (yipping stage) is in "fight or flight mode" and is completely depleted from a lot of nutrients because of the physiological drain and strain it has been put under. Because of this "fight or flight" issue the brain is in

primal mode and no consciously manipulated thought process (like positive thinking) will make a difference.

Stress, in specific distress and eustress in the professional world of golf are the underlying bases for the development of "Focal Dystonia". This disorder has a neuropsychological basis and forces golfers not to be able to control their motor behaviors under severe pressure, as discussed in-depth.

Today, stress refers to the undue pressures of living in a fast-paced society. Hans Selye, who began his research in the 1930’s, was the first to describe biological stress and explain its effects on health. In his classic book The Stress of Life, originally published in 1955 and revised and reprinted in 1978, he defines stress as the "nonspecific response of the body to any demand." Nonspecific in this case, refers to any event or stimulus, whether it is external (such as a touch or a noise) or internal (such as emotion). Fundamentally stress is the wear and tear of living. Some people are prepared through genetic favor to handle it better.

The modern expression "stressed out", although overused and vague, refers to a state of anxiety, worry, or exhaustion that has resulted from difficult or challenging experiences. The term implies the existence or potential rise of unpleasant symptoms.

Stress, by itself, saps energy. When we are to deal with life’s challenges calmly and efficiently, we expend energy at a lower rate than if we were dealing with the challenges and experiencing stress. Under stress we become exhausted much quicker than we do otherwise, and recover energy a lot slower. Certain stress creates symptoms such as digestive upset, insomnia, fatigue and muscle tension. These symptoms reflect the disruption of energy and consequent disruptions of body systems.

Ancestral vital energy is supplemented by food, water, air, and perhaps other natural sources, such as stress and Mother Earth herself. Vital foods impart this energy as well. Some wild foods or super foods, such as nettles, dandelion, yellow dock greens, and green foods like spirulina and wheat grass juice is especially rich in energy.

Maintaining strong digestion ensures that we receive vital energy from food. Dr Bernard Jensen was a big believer in the health of the bowel; he felt all diseases start in the bowel (Jensen, 1981).

Since the term stress is often used quite loosely, many confusing and contradictory definitions of it have been formulated; hence, it will be useful to add a few remarks stating clearly what it is not (Selye, 1984):

Whatever the problem, it can only be met through one of two basic reaction forms: actively – through fight, or passively – through flight. The stress-producing factors, technically called stressors are different, yet they all elicit essentially the same biological stress response. Stress is the nonspecific response of the body to any demand made upon it (Selye, 1974). From the point of view of its stress producing or stressor activity, it is immaterial whether the agent or situation we face is pleasant or unpleasant; all that counts is the intensity of the demand for readjustment or adaptation.

The process of stress on a physiological level is as follows: The adrenals are endocrine glands situated just above each kidney. They consist of two parts, the outer layer (or cortex) and the inner core (or medulla). The cortex produces hormones that are called corticoids, whereas the medulla secretes adrenalin and related hormones, all of which play important roles in the response to stress. The thymus (a large lymphatic organ in the chest) and the lymph nodes (such as can be felt in the groins and armpits) form a single system usually referred to as the thymicolymphatic apparatus, which is mainly involved in immune defense reactions (Selye, 1976).

It has become evident through all types of research that the same set of organ changes caused by the glandular extracts were also produced by cold, heat, infection, trauma, hemorrhage, nervous irritation, and many other stimuli. Thus in all forms of stress the body basically reacts in the same way. This reaction was first described in 1936 as a "syndrome produced by various nocuous agents, and subsequently became know as general adaptation syndrome (G.A.S.) also known as biological stress syndrome (Selye, 1974). Its three stages – the alarm reaction (1), the stage of resistance (2), and the stage of exhaustion (3). After the initial alarm reaction, the body becomes adapted and begins to resist, the length of the resistance period depending upon the body’s innate adaptability and the intensity of the stressor. Lastly exhaustion will ensue.

The focal dystonia problem area in golf makes this behavior a very visible one in "yip" cases. First the golfer starts feeling trepidation about a short putt, then with extensive, associative exposure to the same anxiety this resistance will result in the body to fight "decelerating the stroke" (body doesn’t want to allow the stroke to happen, wants to put a block on the behavior or fight it) or flight "accelerating the stroke" (body wants the action to be dealt with as quickly as possible to get rid of anxiety by rapid flight.) At this point no conscious manipulation (mechanical thoughts about the stroke) will be helpful, the brain has gone "instinctive" and your logical mind means nothing. "Fear is fear at this point, whether it is a short putt or something more life threatening, the body sees them as the same. When the body’s self-preservation kicks in, you know the stress is at its fullest destructive potential. Finally you have the stage of exhaustion, following the long-continued exposure to the same stressor, to which the body had become adjusted, but now they are irreversible, just like the "yips" in golf. Once you have them, you have them! Your system is drained by this associative anxiety and needs to be recharged with the proper neurological disassociations (mechanical postures) and the proper nutrients to recharge the body and the organs. The process of adaptation should now start.

Our reserves of adaptation energy could be compared to an inherited fortune, from which we can make withdrawals, but there is no proof that we can make deposits in this case. Complete restoration is completely impossible, because every biologic activity leaves some irreversible "chemical scar". It is now generally recognized that the emergency discharge of adrenalin represents only one aspect of the acute phase of the initial alarm reaction. At least equally important in the maintenance of homeostasis is the hypothalamus-pituitary-adrenal-cortical axis.

This axis is a coordinated system consisting of the hypothalamus (a brain region at the base of skull) that is connected with the pituitary gland (hypophysis), which regulates adrenocortical activity (Crick, 1994). The stressor excites the hypothalamus through pathways not yet fully identified, to produce a substance that stimulates the pituitary to discharge the hormone ACTH (for adrenocorticotrophic) hormone in the blood. ACTH in turn induces the external, cortical portion of the adrenal to secrete corticoids. These elicit thymus shrinkage, simultaneously with any other changes, such as atrophy of the lymph nodes, inhibition of inflammatory reactions, and production of sugar (a readily available source of energy) (Selye, 1976).

Walter Cannon designated in 1932 the "emergency adrenalin secretion" in response to fear or rage. In his classic book, The Wisdom of the Body, he summarized his lifework on the distinct mechanisms which maintain the normalcy of sugar, protein, fat, calcium, oxygen, and temperature of the blood, as well as many other individual specific adaptive mechanisms. These are all the things of vital essence in sports performance enhancement as well.

As we can see, a certain amount of stress is needed to tune you up for sports action, to perform at your top level in golf or any sport. This is especially true for eustress, which is enjoyable in itself and actually gives purpose to life. On the other hand we need to learn the limits of our endurance before we exceed them dangerously.

The physiological benefits of exercise and playing sports are well documented. Public interest has centered on the role endorphin plays in mood-state changes (Hopson, 1988) and lately there is some scientific evidence to support such a link. Perhaps the

reason we pump up our endorphin with exercise is because it makes us feel calm – an inner reward for being fit. This was previously called the "runners high", but we should like rename it "athletic calm". This supports the concept that a healthy body houses a healthy mind. However, endorphins may act similarly to the exogenous opioids; the obligatory athlete may have learned to self-titrate his or her endorphins, and thus mood states, and that discontinuing pulsatile activity could lead to an endogenous dysphoric withdrawal state that could only be alleviated by the hedonistic pleasures of exercised induced endorphin (Begel & Burton, 2000). Thus in short we might get addicted to feeling competitive and the stress levels will wear and tear at the body pretty dramatically. Endorphins have been an important of human evolution – the human species functioned best when physically fit – a state that endorphin may have helped facilitate. There are many neurochemicals that affect moods and human performance; it just so happens that endorphin is one of the few for which such information is known.

Earlier the HPA was mentioned; let’s look at it a little more closely to understand exactly what it does and how it is effected by stress. The hypothalamic-pituitary-adrenal axis also can be called "stress axis" is the classic example of the stimulatory system, with it myriad actions, reactions, and feedback loops (Herman, Prewitt & Cullinan, 1996). It is also an example of a system that can be over activated with maladaptive outcomes. Normally, the HPA axis functions as a pulsatile system for management of stress and control of energy production. Glucocorticoids (cortisol) are the end result, which have widespread multifunction catabolic stimulatory effects, including the release of glucose from the liver for energy availability.

The physiology of the HPA stress response is the outcome of sequential and parallel processing of relevant stimulus attributes on both positive and negative effect, which upon researching a certain threshold at the hypothalamic paraventricular nucleus (PVN), then activates the HPA system (Begel & Burton, 2000). There would appear to be two overall approaches to activating this system. The primary "systematic" high-priority system demands immediate response via unimpeded input to the PVN region – such as from major blood loss or serious respiratory distress. When this happens, all stops are pulled, and the body instantly goes into a profound stress-response mode (Herman et al., 1996).

The second "processive or neurogenic" stress response system requires a series of active processing by the brain to determine if the stress has enough relevance to cause activation of the PVN. This requires indirect routing of the stimulatory message, such as pain or stress, via the cortex, prefrontal cortex, hippocampus, amygdala, and septum.

The locus coeruleus can release massive amounts catecholamines, mostly noradrenaline, which can give the effect of a full blown panic-phobic reaction and subsequently indirectly activate the PVN. Stressor stimulation mediated through the dorsal raphe nucleus (serotonin) is a modest excitator to the PVA-HPA (Morgan, 1986). In addition various fluid and electrolyte shifts and blood-pressure changes can cause a sudden release of various peptides, one being angiotensin II, which has indirect effects on the PVN-HPA. This multisystem modulation of stress-filtering is a variable requirement prior to activating the PVN. There may be an additional final screening within the limbic system before final loading of the PVN. But once loaded, the PVN activates the HPA, and the systematic stress response is irrevocably on its way (Herman et al., 1996).

The HPA system is but one aspect of the limbic system’s role in stress integration. Limbic outflow goes to many regions of the brain, the PVN to HPA system being but one. The final relays insure proper control of the degree of the HPA response, and in part is prone to habituation by repeated exposures – cellular learning. Athletes, by their repeated training are exposing their PVA-HPA to stress management learning, even at a cellular level. The closer the training can simulate the true stress of competition, the more optimum the adaptation would be to stress. Normally cortisol levels fluctuate over a 24 hour period, part of the cardiac rhythms, reaching a 40-fold peak up to 150 ng/mL in the morning, and dropping to near zero by late afternoon. Under severe stressful circumstances cortisol levels may rise to 400 ng/mL (Morgan, 1985). Therefore depending on the time of the stressor, the effect may be more or less magnified. However due to the fact the stress response levels are so much greater than normal fluctuations, the stressor-outcomes are probably not much blunted by the time of day. If enough stress is placed on a person time of day is irrelevant.

However after a major stressor event, the body tries to return to a normal baseline. Initially, part of the stressor signal will cause a somewhat delayed response of B-endorphin (Begel & Burton, 2000). This in effect has an inhibitory effect on the HPA-axis. The athlete with robust (cellular training) release of endorphin probably has an advantage in managing his stressor-modulating counter-response. This is something found in the top athletes of each sport, like Nicklaus, Woods, Jones, Hogan and Watson in golf. Secondly the very presence of elevated cortisol will have negative feedback effect upon further activation with the hypothalamus. Thus, the body is stressed, it responds, and then it calms itself down.

This nicely designed stimulatory system starts to maladapt if the stress is continuous. Prolonged activation of the hypothalamus will in time lead to a failure of the negative feedback such that the HPA axis becomes tonically stimulated, resulting in continuous high levels of glucocorticoids. This in turn can lead into multiple end-organ and muscular disorders like focal dystonia in golf. Thus a golfer being exposed to the same fear on a golf course every time he plays will activate the HPA through the PVA, and with extensive associative exposure the body learns this stressor (short putt, out of bounce fence, chip shots, driving, long irons etc.). This stressor then becomes a fear, then, phobia with enough exposure, however the entire problem stems from the HPA. It is ironic that the part of the body that is there to "help" you cope better under pressure is also the one that hurts you with excessive use.

For the athlete controlling PVN and HPA responses is tricky. Insufficient stressor activation might lead to poor competitive response. Yet an over activity of the pressure response system may also lead to poor performance or worse, like "yipping or focal dystonia". Unfortunately there are no simple tests that can be used to titrate on-line the stressor responses, nor are there any guidelines as to what response levels are optimums. In addition, some athletic activities, such as golf require a calm mental-physical state, however the demands on the body are almost as great as weight lifting if you weigh up how much more time you are exposed to fears and anxieties on a golf course. Many golfers have unwittingly learned how to gauge their stress levels in order to facilitate their personal best performance. This usually takes many practice sessions and various levels of competitive play in order to know how hard to push and when to back off and foster a calmer mood.

Recent studies have suggested that a host of other neurochemicals, such as serotonin and gamma-amino-butyric-acid (GABA), are felt to have a profound influence on moods, and thus presumably on athletic behavior. However, the details are currently unknown. All these neurochemicals affect each other; action on the part of one will affect another. It would appear that the neuro-psycho-biological-soup that influences our behavior is somewhat like a child’s mobile, a ripple at one end can send repercussions rattling all through the system. To compound the confusion, it is likely that we are currently only looking at a very small portion of what we should. This is why we need to nourish the brain and body properly for optimal sports performance.

Among the most generally used and reliable measures of stress are the blood levels of adrenalines, corticoids, ACTH and a drop in blood eosinophils.

Self-observable Signs

General irritability

Pounding of the heart, as an indication of high blood pressure (often due to stress)

Dryness of throat and mouth

Impulsive behavior, emotional instability

The overpowering urge to cry or run and hide

Inability to concentrate

Feelings of unreality, weakness and dizziness

Fatigue and loss of energy

"Floating anxiety" not sure what we are afraid of

"Keyed up" feeling, emotional alertness

Trembling and nervous ticks

Easily startled by sounds, hate noise

High pitched, nervous laughter

Stuttering and other speech difficulties

Grinding of teeth

Insomnia

Hypermotility or hyperkinesia, the inability to sit still, always moving parts of the body

Sweating

The frequent need to urinate

Diarrhea, indigestion, queasiness in the stomach, even vomiting

Migraine headaches

Premenstrual tension

Pain in the neck or lower back

Loss of appetite

Increased smoking

Increased used of legally and illegal drugs

Nightmares

Neurotic behavior
Psychoses
Accident prone

Because diet is likely to be closely linked with stressful events, what we eat has a huge impact on body chemistry and ultimately on health. Under stress, we tend to choose foods that are not the best for us; with care and consideration, however we can learn to use food in support of healing and good health. We know that a number of important neurotransmitters, which affect mood and mechanisms for coping with stress, are built from amino acid molecules found in protein foods. An example is serotonin, made by the body from the amino acid L-tryptophan, found in soy, dairy products and meats. This neurotransmitter is essential in coping with anxiety, depression and insomnia.

All cells, organs, and systems of the body are governed by the principle that continual overuse or use in one direction to the exclusion of others will break down the body’s normal, self-regulated state of health. Experimenting with foods as sources of amino acids as a part of a normal, healthy diet is an excellent way to work toward overcoming the effects of stress. In natural food stores, many amino acids are available in pure form as a supplement.

The amino acid GABA, is not found in food, it is known to calm the brain and can help issues of anxiety, depression and hypertension. Glycine is found in turkey, wheat germ, carrot, cottage cheese, celery and almonds. It is a sedative to the brain and can help in depression disorders. Leucine is found in wheat germ, milk, avocado, yogurt, chicken, almonds, walnuts and cheese. It promotes protein synthesis and slows the effects of stress; it is great to help low energy levels resulting from severe stress. L-Tryptophan can be found in soy, pinto, mung beans, tempeh, tofu and lentils. It influences serotonin concentration in the brain; it is good for pain, insomnia and depression (Hobbs, 1944).

In the classic herbalism of the early twentieth century, any herb that affected the nervous system in any way was called a nervine. Nervines can be divided into six subcategories.

Sedative nervines. The calmatives, they reduce anxiety and have a calming effect on the central nervous system. These herbs are frequently used in formulas for nervousness, sleeplessness, and mild anxiety. Examples are valerian, hops, kava-kava and lavender.
Analgesic nervines. They help to reduce nerve or muscle pain, although they can be useful for any kind of pain. Typically, these herbs will not work so well or so quickly as aspirin, but a well designed formula containing some of these herbs can be helpful in reducing pain and promoting healing with few side effects. Examples include valerian, St. John’s wort and Jamaican Dogwood. Stimulating nervines. These stimulate and raise the tone of the sympathetic nervous system and also raise the sympathetic tone. Small amounts of these herbs combined in a formula can enhance mental and physical performance and reduce fatigue. Examples are rosemary, kola nut, ephedra, coffee and tea.
Tonic nervines. Nourish the nervous system and should be taken for extended periods of time – at least three months – in order to help nourish and support the function of the nervous system. Examples include wild oats, passion flower, celery, and sea vegetables such as nori and wakame.
Psychotropic nervines. It enhances intuition and could aid in understanding about the meaning of unconscious images. Examples are Kava-kava and mugwort.
Soporific nervines. Is a great aid in all the sleeping processes. Examples St. John’s wort and California poppy.

Over the past two decades, it has become clear that the pituitary and hypothalamic hormones are involved in brain activity and have an effect on behavior (Hoffer & Walker, 1994). Nutrients and the right kinds of foods for the mind are vital. A neurotransmitter is the chemical language sent between cells in the human brain. These neurotransmitters allow the brain cells to talk to each other. Deficiency in neurotransmitter function results in depression, lifelessness, moods, irritability, sleeplessness, anxiety, brain fog, cravings and addictions. Depleted supplies of these "feel good" neurotransmitters make it difficult for you to feel happy, on track, focused and motivated. Neurotransmitter deficiencies can be caused through genetics, stress, and diets low in amino acids and through alcohol and drug abuse.

Two key amino acids are necessary to make the other neurotransmitters. Phenylalanine is an essential amino acid that makes you feel happy and motivated. Glutamine is a conditionally essential amino acid that can keep you calm, focused and in control. Both are very important in optimum sports performance. The body cannot convert Phenylalanine form other nutrients, it must depend on outside sources and specific supplements to acquire sufficient amounts. Since amino acids from meat, eggs, and dairy sources cannot readily be utilized by the brain, it is necessary to take supplements which also contain co-factors that help them across the blood brain barrier. The Rhodiola rosea extract has been shown to influence learning and memory, by supporting the neurotransmitters and affecting the brain chemistry. Tests using Rhodiola showed the quality of the task performed was dependent on fatigue levels. When Rhodiola was administered, it effectively increased a person’s resistance to fatigue, enhanced back muscle strength, hand strength and improved coordination. All of which are vital for sports performance enhancement in golf.

Neurotransmitter support is necessary for the brain function at top performance. Memory loss may be nothing more than amino acid deficiency, causing a short circuit. When athletes compete, they maximize their brain activity to keep focused. Poor diets and low amino acid levels will prevent this. No matter what we do, our thinking process determines the outcome of our actions. With good neurotransmitter support we can make choices that can keep us at peak performance.

According to a study out of University of Health Sciences in Bethesda, the University of Michigan Medical School in Ann Arbor, and the USDA Human Nutrition Research Center in Beltsville, Maryland, trace mineral levels are altered by stress.

Plasma levels of zinc, iron, copper, selenium, and selected blood proteins such as ferritin were monitored and dietary intakes were measured in 66 men before, during, and after a five day period of physical and psychological stress called "Hell Week". Physical stress included simulated combat exercises, and an obstacle course, aerobic workouts; psychological stresses included performance anxiety, verbal confrontations, and no-win situations.

The results of this study showed dietary intake of minerals during the stressful period greater than the Recommended Dietary Allowance (RDA), Zinc intake averaged 23.6 mg (RDA = 15 mg), iron intake averaged 35.4 mg (RDA = 10 mg), copper intake averaged 3.0 mg (RDA = 70 mcg). Despite adequate dietary intake, plasma levels of minerals decreased by 33%, 44%, 12%, and 9%, respectively. In addition, mineral carrying proteins increased as much as 59%, suggesting increased removal of trace minerals from tissue stores. Although the trace mineral alterations were transient, they required seven days without further stress plus adequate dietary intake to return to their former levels. The results of this study show that the physical and psychological stress in healthy adults produces alterations in trace mineral status characteristic of an acute-phase response (deficiency) despite otherwise adequate dietary intake.

Recent discoveries have proven beyond a doubt that our brain and immune systems are interlinked. Our thoughts affect our cellular level. The field of "Psychoneuroimmuneology" is a blossoming discipline which studies the mind-body connection. We experience stress on three levels: physical, environmental, and mental/emotional (Lipski, 1996). Stress plays a major role in many digestive problems. Like any professional or competitive golfer will tell you that they all have had diarrhea from "nerves" before a big event. The ‘butterflies" that people feel in their stomach when they are nervous happen to all of us. Continued stress in our body, mind or meanings affects the whole body’s ability to heal and perform. If the body is using most of its energy to put out fires, it has less time for maintenance and repair. Because the digestive tract repairs and replaces itself every few days, it is one of the first places where our bodies alert us that all is not well. Athletes with digestive-related problems can benefit from stress management tools. Mental stress is one of the greatest challenges to our immune systems, putting pressure on nearly every organ and system in the body. Let’s look at the "Quick Ideas" for stress management (Lipski, 1996):

Eat healthy foods

Develop better communication skills

Exercise regularly

Spend time outdoors

Each day should have pleasure and relaxation

Meditate

Realize that you are not perfect

Think creatively

Go at your own pace

Think of solutions, not problems

Prioritize

Keep journals

Live one day at a time
Play and laugh

Spend time with family and friends

Be flexible

View problems as opportunities to grow

Plan for chaos

Set priorities

Breathe deeply

Plan ahead

Learn to say "No"

Unplug your phone

Make lists

Take long showers or baths

Drive 10 mph slower

Take on day per week to relax

Be loving and caring and trust people have good intensions

It is an unfortunate fact that 80% of illnesses can be traced back to stress (Ramazanov & Suarez, 1999). The Academy for Family Physicians reports about two-thirds of all office visits are prompted by stress. Stress is a silent killer, with little resistance mounted against it. Unlike bacteria, viruses and even cancer, which our immune system can counteract and destroy, stress suppresses immunity and destroys our resistance to other forms of attack. A study conducted in 1991 and published in Psychological Science, showed that certain detrimental effects on stress (such as increasing the number of suppressor T-cells) are only seen in people who are overly sensitive to stress. For thousand of years, people all around the world have been using adaptogens (things that help the body deal with stress).

Rhodiola rosea is probably the least-known adaptogen in the West and yet maybe the most impressive of all. It has been shown to normalize the immune system and glucocorticoid hormone levels in a positive way, bringing them into balance. The main targets of Rhodiola rosea are stress related molecules called neurotransmitters. These include serotonin, dopamine, epinephrine, norepinephrine as well as other active molecules in the brain. Serotonin is one of the most actively investigated chemicals in the body, specifically as it relates to its role in brain function.

The brain however is only a small part of serotonin’s arena of effect. This ubiquitous chemical participates in many processes throughout the body, including smooth muscle contraction, temperature regulation, appetite, pain perception, behavior, blood pressure and respiration. Although the amount of serotonin in the brain is relatively small, when compared to other parts of the body, its importance in brain function cannot be underestimated. Serotonin is clearly implicated in the etiology of treatment of many disorders, particularly those of the central nervous system, including anxiety, depression, obsessive compulsive disorder, schizophrenia, stroke, obesity, pain, hypertension, vascular disorders, migraine and nausea. Serotonin cannot cross the blood brain barrier; therefore the biosynthesis of brain serotonin that takes place in the brain is due to its precursor amino acid, called tryptophan. This is actively transported in the brain through the foods we eat. Scientists have found the Rhodiola rosea enhances the level of serotonin in the brain. Additionally, research points to Rhodiola as playing an important role in the biosynthesis and preservation of serotonin and neurotransmitters. Rhodiola’s ability to help the body adapt to stress may lie in its ability to enhance serotonin levels (Ramazanov & Suarez, 1999).