Summary of Creatine
How could anyone forget a back-from-the-dead Irene becoming head of a major international crime organization engaging in brainwashing, kidnappings and murder? She mumbles and pauses about as much as he does. Their primary function is to stimulate the pituitary gland to produce more Growth Hormone. Rosalie is already boring me. Do not forget to take Tamoxifen and HCG after the cycle, otherwise you can have big problems with your balls and natural Testosterone production.
The misc.fitness.weights FAQ Table of Contents
Therefore, unbound cortisol may be significantly increased and available to the tissues in patients with anorexia nervosa. One would expect the higher levels of cortisol measured in these patients to suppress adrenocorticotropic hormone ACTH. The observation that a new circadian rhythm at the higher cortisol level is established suggests that a new set point is determined by the hypothalamic-pituitary-adrenal axis.
Hourly mean cortisol level derived from averaging the level in samples taken 20 minutes before the hour, on the hour, and 20 minutes after the hour in 10 patients with anorexia nervosa, compared with 6 normal controls matched for age and sex. Circadian rhythm remains intact in anorexia nervosa, but at a higher level. Cortisol secretion and metabolism in anorexia nervosa.
N Engl J Med Despite their marked cachexia, patients with anorexia nervosa have clinical and metabolic signs suggestive of hypothyroidism. These include constipation, cold intolerance, bradycardia, hypotension, dry skin, prolonged ankle reflex, low basal metabolic rate, and hypercarotenemia. Serum levels of thyroxine T 4 , triiodothyronine T 3 , and thyroid-stimulating hormone TSH in patients with anorexia nervosa are significantly lower than in normal persons, particularly the level of T 3.
T 3 appears to increase with weight gain, but T 4 and TSH remain low, and all three hormones are lower than in controls. In anorexia nervosa, as in starvation, the peripheral deiodination conversion of T 4 is diverted from formation of the active T 3 to production of reverse T 3 , an inactive metabolite. Low T 4 euthyroidism has been seen in seriously ill patients, 99 , in whom studies indicate there is a unique dysfunctional state of deficient T 4 binding with a normal free T 4 availability to peripheral tissue sites.
Presumably, a similar mechanism may be operative in anorexia nervosa. Another study showed that the T 4 and T 3 response to thyroid-releasing hormone TRH is subnormal, although the TSH response is normal, suggesting chronic understimulation of the thyroid, as occurs in hypothalamic hypothyroidism.
Other parameters of pituitary-hypothalamic function have been studied. In general, basal GH levels are significantly higher than normal in anorexia nervosa but respond normally to one or more provocative stimuli. The enhanced GH secretion in anorexia nervosa may be caused by a heightened frequency of secretory pulses superimposed on augmented tonic GH secretion. When anorexics are compared with subjects of normal weight and with obese subjects, the enhancement of GH secretion appears to reflect a complex hypothalamic dysregulation of GH release, as opposed to simply a malnutrition-induced impairment of the production of insulin-like growth factor I.
TRF-stimulated prolactin levels are also normal, although the time of peak prolactin is delayed. In addition to the endocrine abnormalities described, a number of other physiologic changes strongly suggest a hypothalamic dysfunction. One of the most impressive is the disorder of thermoregulation reported in this condition.
For instance, in the cold, no shivering or vasoconstriction occurs, and core temperature continues to fall. In the heat, no vasodilation occurs, and eventually the core temperature rises with no stabilization. The rate of change of core temperature per hour also correlates with the percent below ideal body weight. These responses, including shivering, vasoconstriction, and vasodilation, indicating loss of central temperature, are dysfunctional in the anorexic.
The thermosensitive neurons in the anterior hypothalamus which mediate vasomotor responses and its interconnectives with a motor center for shivering in the posterior hypothalamus may be affected. Studies of thermoregulatory responses to a given metabolic heat load resulting from exercise in anorexia nervosa indicate that the altered response may involve other mechanisms.
In particular, the low sweating capacity seen in this syndrome and the loss of body fat, which reduces thermal insulation, alter the ambient temperatures over which the body temperature can be maintained during exercise.
Patients with anorexia nervosa also appear to have abnormalities of water conservation that are diagnostic of partial diabetes insipidus. This was judged by the ability to concentrate the urine maximally after 15 hours of dehydration and a further response to exogenous vasopressin. A further increase in urine osmolarity after administration of exogenous antidiuretic hormone was seen in the majority of patients with anorexia nervosa and was diagnostic of partial diabetes insipidus.
The altered behavior patterns in this syndrome are also distinctive and include preoccupation with food and hyperactivity. Sometimes periods of gorging bulimia alternate with starvation and food avoidance. Altered food intake, combined with activity changes, has been seen in hypothalamic tumors and has been documented in rats with lesions of the ventromedial nucleus of the hypothalamus. These lesions have led investigators to conclude that the ventromedial nucleus can inhibit food intake and promote activity, as seen in anorexia nervosa.
Other behavioral changes include a perceptual distortion in which patients with anorexia nervosa perceive themselves to be too fat. This body image misperception can be quantitated by the use of a special apparatus consisting of two movable lights equidistant from a central point.
The subject can move the lights until they appear to approximate what she perceives to be specific body dimensions or even a piece of wood. Experiments of this nature have shown that there is a direct association between the degree of the perceptual disorder and that of malnutrition and that patients with anorexia nervosa consistently overestimate body and other dimensions.
This suggests that when the patient is severely underweight, the illness tends to be self-perpetuating, and that weight gain in itself is an important goal to break this vicious cycle. Other investigators have found, however, that these abnormalities are complexly determined and can be demonstrated in nonanorectic persons in their teens and in obese subjects. Generally, the prognosis is thought to be better in those patients whose self-reported estimates are more or less accurate after restoration of weight and are no longer influenced by an ordinary carbohydrate meal.
Gross overestimation of body widths is associated with premorbid obesity, bulimia and vomiting. Studies have also been performed to evaluate the behavior disorder seen in anorexia as well as the perceptual abnormality. Anorexic behavior scales have been devised to aid in differentiating persons with anorexia nervosa from those who have secondary amenorrhea due to other causes. The scale may consist of a psychologic profile that is self-administered or administered by a doctor, nurse, or clinical psychologist.
One study indicated that the anorectic behavior scale was very useful and accurate in distinguishing healthy female subjects from those with anorectic behavior. These scales may therefore be useful in the early diagnosis of anorexia nervosa, particularly in patients presenting with only secondary amenorrhea and little or no weight loss. In contrast to the perceptual disorder, the degree of anorectic behavior does not always correlate with the malnutrition, suggesting that the anorectic behavior is more pronounced in the better-nourished patients.
Along with the behavioral disorder, objective changes in the brain have been demonstrated by computed tomography. Enlargement of the cortical sulci and subarachnoid spaces, as well as cerebral atrophy, has been demonstrated in a small number of cases, with reversal of the atrophy with weight gain in one.
Gray matter volume deficits, unilateral temporal lobe hypoperfusion, and various localized brain dysfunctions appear to persist despite weight recovery. Anorexia nervosa continues to be a perplexing syndrome, most likely psychogenic in nature. The large preponderance of girls from upper socioeconomic backgrounds who are affected at or near puberty suggests the importance of environmental influences. The fact that the amenorrhea may precede the development of the full-blown syndrome has often been emphasized, although in most studies amenorrhea has most often coincided with the onset of food restriction.
Some of the metabolic changes—including lowered metabolic rate, a decrease in attainable oxygen uptake and maximal aerobic power V O 2 max , an increase in cortisol which stimulates gluconeogenesis and decreases peripheral glucose utilization , and a decrease in gonadotropins with a loss of fertility —are appropriate adaptations to starvation. On the other hand, the early development of amenorrhea and behavioral symptoms also suggests a primary hypothalamic syndrome.
The abnormalities of gonadotropin release and activity are associated with the medial central hypothalamus; those of thermoregulatory control, with the anterior and posterior hypothalamus; and those of water conservation, with the supraoptic area. The involvement of all these areas suggests a lesion too diffuse to be anything but perhaps metabolic.
Although anorexia nervosa may be a primary hypothalamic syndrome, it is much more likely that this dysfunction is a result of the diffuse metabolic changes associated with starvation Table 4.
The association of psychologic and neuroendocrine changes in patients with anorexia nervosa has led investigators to speculate that abnormalities of neurotransmission may be involved in the pathogenesis of the syndrome. Excessive dopamine and norepinephrine in particular have well-documented effects on behavior and appetite. These peptides have been isolated from other areas than the brain, including the gut, and it is not unreasonable to consider that the messages mediated by these neuropeptides may play a role in the alterations seen in anorexia nervosa.
Evidence also indicates that some estrogens are formed in the brain and that their synthesis is favored in anorexia nervosa; an example is the catechol estrogen, 2-hydroxyestrone. Catechol estrogens may have the potential for interacting with both the catecholamine and the estrogen-mediated system in the central nervous system, thereby influencing dopamine and norepinephrine synthesis.
The striking incidence of anorexia nervosa in professional ballet dancers suggests that the chronic dieting behavior followed by persons in this profession to achieve a thin body image may be important in the pathogenesis of anorexia nervosa. A number of investigators have been interested in the concept that anorexia nervosa occurs as a continuum of chronic dieting behavior.
Weight loss-related amenorrhea and exercise-induced amenorrhea have similar endocrine profiles, suggesting that all three entities have similar hypothalamic mechanisms.
The fact that some of these activities are fertile breeding ground for the development of anorexia nervosa is becoming evident. Recent research indicates that excessive exercise is an integral aspect of the disorder in its acute phases. Findings on comorbidity of excessive exercise and anorexia nervosa highlight the detrimental effects of combining strenuous physical activity with immoderate dieting. Bulimia, although more common in slightly older age groups, is also generally a condition of young women and is often related to previous anorectic behavior.
Bulimics gorge themselves and use artificial means to purge themselves of calories. These means include vomiting and abuse of laxatives or diuretics. Gorging episodes may alternate with periods of severe food restriction. The bulimic's weight may fluctuate, but usually not to dangerously low levels. There is often a history of other impulsive behaviors, such as alcohol or drug use, and features of this disorder are not unlike those seen with drug addiction.
Depression is also common. Stealing and shoplifting, as well as unrestrained promiscuity, may be part of the syndrome, in contrast to the restrictive anorectic, who remains generally asexual. The patients tend to be older than anorectics, usually between 17 and 25 years of age.
A separate condition, known as bulimia nervosa, has been described in which the bulimic behavior evolves from the completely restricting, anorexia nervosa-type pattern. Bulimics have a wide variety of medical problems that may be superimposed on the anorectic syndrome. These include severe tooth decay, parotid enlargement, stomach rupture, metabolic alkalosis, carpopedal spasm, hypercarotenemia, and pancreatitis.
These persons may also have adequate estrogen secretion and present with an anovulatory syndrome. This type of problem may be difficult to diagnose because the menstrual disorders and the amenorrhea can develop even when the weight remains normal.
The behavior is often chronic, and increased anxiety, irritability, depression, and poor social functioning are common. A number of neurologic problems have been seen in association with bulimia, including Huntington's chorea, schizophrenia, and seizure disorders associated with a postictal phenomenon. Bulimic behavior has also been described after amygdalectomy, with frontal lobe tumors, and after prefrontal lobotomy. Bilateral destruction of the ventromedial hypothalamus has been associated with hyperphasia and obesity and has been a sequela to encephalitis.
Bulimia can also be seen in association with hypersomnia in cases of Kleine-Levin syndrome and in patients with parkinsonism, who have been reported to improve in their eating patterns after treatment. Furthermore, bulimia may have an organic cause; hypothalamic diseases may be associated with excessive appetite and lack of satiety inhibition. An underlying neurophysiologic dysfunction may be present in patients with bulimia.
Electroencephalographic abnormalities have been reported in response to bulimic behavior. The association of neurologic abnormalities raises the intriguing possibility of underlying neuroendocrine dysfunction as a cause of both the nutritional and the menstrual disorder. A high incidence of substance abuse and alcoholism is seen in association with eating disorders, particularly bulimia.
Some data suggest that diagnosis of one of these disorders in women is an indicator for close monitoring and counseling for both. Management and therapy for these syndromes is still a subject of wide debate.
Treatment includes various combinations of psychotherapy, including family therapy, psychoanalysis, and, occasionally, drug therapy. Chlorpromazine, insulin therapy, tricyclic antidepressants, cyproheptadine, L -dopa, and metoclopramide have all been considered but have met with only transitory or no success. It is disconcerting to both physician and patient that, despite impressive studies on the cause and psychogenesis of anorexia nervosa, few specific or new therapeutic modalities are available.
Emphasis has been placed on early diagnosis and the recognition of anorectic behavior, so that the patient may be treated before the full-blown syndrome sets in.
Because amenorrhea in the early part of the disease process is usually the first symptom that causes the patient to seek help, gynecologists should be particularly attentive to a history of dieting and weight loss in their young patients. Behavioral modification is used with some success, although opinions on its efficacy vary.
Some workers maintain that the inclusion of psychotherapeutic measures and family therapy improves the late prognosis by more specifically correcting the psychopathology of anorexia nervosa.
The first essential goal is to restore the patient's weight to normal. This can be accomplished by a variety of methods. Management has included hospitalization, forced fluids, and nasogastric feedings. The latter should be regarded with some caution because of the decreased motility of the gut seen in this syndrome. Dietary therapy is important, because response to psychotherapy is improved with nutritional rehabilitation. Recent research highlights the dangers associated with refeeding in severely malnourished patients.
Gradual dietary intervention should proceed only in combination with close monitoring of cardiac status and phosphorus, serum, and electrolyte levels. This improved muscle performance allows high levels of physical activity concomitant with sustained malnourishment. Generally, with weight gain, all of the metabolic parameters revert to normal.
There is evidence that in some cases the perceptual disorder and the preoccupation with food persist. This is generally associated with a poorer prognosis. A poorer prognosis is also associated with bulimia. Abnormally low levels of serum albumin and a low weight at initial examination may predict a lethal prognosis.
A chronic course may be predicted by high serum creatinine and uric acid concentrations. Ongoing research suggests that bulimia in particular may respond to antidepressant therapy. Environmental influences, such as a poor parental relationship and a lower socioeconomic status, also appear to play a role. Electrolyte imbalance, sepsis, and aspiration have all been reported. In general, the prognosis tends to be worse among men, and when the condition does develop it appears to be within the context of overwhelming psychopathology or premorbid massive obesity.
In male patients, it is particularly important to exclude the rare tumors of the hypothalamus that mimic anorexia nervosa. Recovery from anorexia nervosa can take several years. Patients with a restriction-type anorexia nervosa and low serum creatinine levels tend to recover earlier, whereas patients exhibiting purging behavior in combination with social disturbances may have a lower chance of recovery.
After 10 to 15 years, most patients should have achieved normal weight and regular menstruation. Recovery time may range from 57 to 79 months after treatment commencement, depending on the definition of recovery.
More long-term follow-up studies should eventually help improve the chances of recovery. The resumption of normal cyclic menses depends first on the return to normal weight. Ninety percent of standard body weight may be a reasonable target weight for treatment because it appears to be an average weight for the resumption of menses. Resumption of menses does not appear to depend on amount of body fat, but rather on restoration of hypothalamic-pituitary-ovarian function.
For those who do not have return of menstrual function, fertility may be restored by induction of ovulation. Agents such as clomiphene citrate or human menopausal gonadotropins can induce ovulation in almost all cases.
The patient should have an evaluation to rule out other causes of amenorrhea, such as pituitary tumors or ovarian failure, before induction of ovulation; with these causes definitely eliminated, the patient can be reassured of future fertility.
Research indicates that cyclic menstrual function can be restored in weight-related hypothalamic amenorrhea e. These therapeutic modalities hold much promise for the future, because weight loss-related amenorrheas represent a group of disorders that respond particularly well to this form of therapy. These and other therapeutic modalities will soon be available to treat the deficiencies that remain after the illness is cured.
Despite the return of weight, some patients continue to have permanent problems. Preoccupation with food and persistent dieting behavior are not uncommon in weight-recovered patients. Recent work suggests, however, that estrogen replacement does not restore bone mass in women with anorexia nervosa. As would be expected, a severe nutritional deficiency with prolonged hypoestrogenism places patients with eating disorders at risk for osteoporosis.
Severe skeletal complications, such as collapse of the femoral head and hip fracture, have been reported in young patients. Occasionally the hydrox-yvitamin D level is low, but values for dihydroxycholecalciferol 1,25 OH 2 D are normal. Further study of this syndrome, particularly in its early stages, may lead to a greater understanding of its evolution. Until then, recognition of the disorder depends on a number of factors, both psychiatric and metabolic, the first being weight loss.
It is generally contended that the weight loss is secondary to a psychologic disturbance and that the physiologic changes are also secondary.
The ensuing malnutrition produces a distinctive syndrome seen only in starvation. How common is anorexia nervosa? Br J Psychiatry The epidemiology of anorexia nervosa. Prevalence and prognosis in anorexia nervosa. Aust N Z J Psychiatry Therapy-oriented diagnosis of secondary amenorrhea. Sociocultural influences on eating disorders in professional female ballet dancers. Int J Eat Disord 4: A theory of activity-based anorexia. Int J Eat Disord 3: Anorexia nervosa in black adolescents.
J Am Acad Child Psychiatry 1: Askevold F, Heiberg A: Two cases in discordant MZ twins. Roland JM, Bhanji S: Anorexia nervosa occurring in patients with diabetes mellitus. Postgrad Med J Development of Cushing's disease in patient with anorexia nervosa. J Endocrinol Invest 7: Clinical and metabolic features of anorexia nervosa. Am J Obstet Gynecol Excessive weight loss and food aversion in athletes stimulating anorexia nervosa.
Willi J, Grossmann S: Epidemiology of anorexia nervosa in a defined region of Switzerland. Am J Psychiatry The incidence of bulimia in freshman college students. Int J Eat Disord 2: Psychiatric diagnosis in a university population. A survey of a college population. Self-induced vomiting and bulimia nervosa: Br Med J The bulimic syndrome in normal weight individuals: Int J Eat Disord 1: Bulimarexia and related serious eating disorders with medical complications.
Ann Intern Med Acute pancreatitis associated with bulimia. J Clin Gastroenterol 6: Diagnostic criteria for use in psychiatric research. Arch Gen Psychiatry Psychologic antecedents of anorexia nervosa. In Vigersky R ed: Anorexia Nervosa, p 1. Testing the hypothesis of the multidimensional model of anorexia nervosa in adolescents.
Clinical and therapeutic aspects of anorexia nervosa: A study of 30 cases. J Psychosom Res 9: Demographic and clinical features in 94 cases. Hypercarotenemia in hypothalamic amenorrhea. The hypercarotenemia in anorexia nervosa: A comparison of vitamin A and carotene levels in various forms of menstrual dysfunction and cachexia. Am J Clin Nutr Anorexia nervosa and salivary gland enlargement. Int J Psychiatry Med Case report of cardiovascular abnormalities in anorexia nervosa.
Silverman JA, Krongad E: A cause of pericardial effusion? A complication, a concomitant, or a cause of an anorexia nervosalike syndrome. J Am Acad Child Psychiatry Biochemical and ultrasonic abnormalities of the pancreas in anorexia nervosa. Dig Dis Sci Nordgren L, von Scheele C: Hepatic and pancreatic dysfunction in anorexia nervosa: A report of two cases.
Luthi M, Zurbrugg RP: Anorexia nervosa, high sweat electrolytes and indication to partial exocrine pancreatic insufficiency. Helv Paediatr Acta A case of subcutaneous emphysema, pneumomediastinum and pneumoretroperitoneum associated with functional anorexia.
Br J Clin Pract Kwashiorkor-like zinc deficiency syndrome in anorexia nervosa. Acta Derm Venereol Hypothermia in a patient with anorexia nervosa.
Bulimia nervosa complicated by deficiency of vitamin K-dependent coagulation factors. Acid-base and electrolyte disturbances in anorexia nervosa. Treatment of undernutrition and electrolyte disturbances in anorexia nervosa. Acta Psychiatr Belg Sheridan PH, Collins M: Potentially life-threatening hypophosphatemia in anorexia nervosa. J Adolesc Health Care Limb circulation in anorexia nervosa. Acta Paediatr Scand Somatomedin activity and growth hormone secretion: Changes related to body weight in anorexia nervosa.
Hematological changes in anorexia nervosa are correlated with total body fat mass depletion. Int J Eat Disord Bowers TK, Eckert E: Leukopenia in anorexia nervosa: Lack of increased risk of infection. Arch Intern Med An immunological assessment of patients with anorexia nervosa. Immunocompetency in anorexia nervosa. Anorexia nervosa presenting as reversible hypoglycaemic coma. J R Soc Med Death from complications of ruptured gastric ulcer. Can J Psychiatry Acute vascular compression of the duodenum in anorexia nervosa.
Br J Surg Superior mesenteric artery syndrome in anorexia nervosa: Cause or complication of anorexia nervosa? Can Psychiatr Assoc J Rib fractures and anorexia nervosa. J Adolesc Health Care 4: Osteopenia in hypoestrogenic young women with anorexia nervosa.
Osteoporosis in women with anorexia nervosa. I have done a lot of research and experimentation over 20 years to figure out what works for me in the gym.
My journey to fast muscle gains started when I finally found the book that helped me crack the hardgainer label I had given myself for years. I started lifting weights at age It highlighted all the errors I was making in training and how to fix them based on scientific research. I want to share with you not just what works for me, but what I also did wrong over the years. In doing so, it is my hope you will recognize some part of yourself in my muscle journey and learn from the path I have walked in trying to build my ultimate physique.
Western Cancer wrote a great article on the origin of somatotypes — ectomorph, mesomorph, and endomorph. While the origins of these body type classifications may be less than scientific by 21st century standards, there is no questioning the wise generalization of body types they attempt to describe. No matter how much you close your eyes and try to wish it away, you are your genes.
Your genetic profile—bone density, muscle fiber type composition, height, limb length, tendon insertion points, skeletal structure, etc.
When it comes to those former body type classifications, I now like to think of them in terms of muscle fiber type composition and proportion — i. They can actually mimic, be turned into, or switched from, a type I or a type IIb muscle fiber depending on the type of training you do. So in one way, Western Cancer was right.
That said, you are limited by your overall muscle fiber type composition, and thus, how much potential it has to be modified by training and diet. Some guys will be bursting with type IIa miracle fibers that naturally just blow up and become huge with little fat gain and basic training regimens.
The guy that just grows walking into the gym. Other guys will take forever to grow because their overall muscle fiber type is for endurance type I ectomorphs and will forever be dominated by a more lean and athletic build instead of big and beefy.
Then you have the guys that can naturally lift huge weights and thus gravitate to power lifting where they find tremendous success type IIb mesomorphs. Shedding fat is almost impossible for them without God-like discipline and submission to a very strict diet and exercise regimen. I think you can see where this is going. The science of muscle fiber types is now explaining why men on the same training program get different results.
Each body is different in its muscle fiber type composition and proportion, and thus a single training program is not going to work for every man. Your goal in training is to find out which muscle fibre type dominates your body as a whole and perhaps even within each muscle group and then optimize your training to develop ALL your muscle fiber types to their maximum genetic potential.
You want to get big? You are going to have to train hard and be prepared to make pain your friend.