[Editor's note:  af]

Grandfather’s Homemade ‘KettleBell’ Weights

You can’t buy these! -     But you can buy the one to the right→

Introduction:  ©aof 2010

My father, Olof Karl-Erik Forsberg, was born in Javle Sweden and later resided in a small town near there called Krylbo.( about 3 hours north by train from Stockholm)… When I was six, the whole family, went to visit his father and sister who still lived in that small town.

I can remember (later on) seeing my father at 52 years of age, hanging from a rope holding on with only his front teeth and later picking up a chair by biting on it.

All of this was the result of healthy eating and proper exercise.

Both my father and his father explained to me how they made what are called “kettlebells” – This is sort of like a dumb bell but different because of its structure. It only caught on in The United States recently and is used in weight training.

Here’s what they did:

The process: (as I can remember it)

Now I’m talking 1890 to 1916 and at that time, many people got their milk from local farmers, and they were often over a mile away. It (the milk) was carried in metal containers, one on either end of a wooden pole across a persons shoulders.

They used the tinned milk containers after they broke so much they wouldn’t hold milk, as a cast for making the lead ‘kettle bells’. These empty vessels were put on top of a small platform made out of wood under which was cold water or oil. After heating the lead to a melting point in a fire, it was poured carefully into the casts.

Now before the lead hardened, a one inch flexible steel cable (with the ends splayed out) was inserted into the molten lead in two places. It was about 14 inches in length and later wrapped with leather for friction and holding power.

The only protection they had was a welding face mask, and a leather apron with leather gloves covered with asbestos particles. Leather appears to be the choice material for handling hot objects even today.

• Yeah, I know what you’re thinking: asbestos, lead fumes…Well, my granddad lived to be 99 years old and died peacefully while taking a nap after dinner\supper. And when he was 92, I had a 1 ½ hour bike ride with him in the country. Not bad.

As soon as the metal appears to have hardened – you test (poke) it with a metal rod – it was quickly placed into the water or oil mix. What this does is give the ‘kettlebell’ a ‘case hardening’. Now all that was left is to break away the casing. And Voila! – You’ve got your very own homemade weight ready to be used in training. The ‘kettlebells’ that I saw and used were 40, 60, and 80 pounds – not absolutely sure because everything over there is in metric.

A heavy cloth which I think was burlap was placed around both the handle and the ‘kettle bell’ itself to make it a Exercising was done in an  8’ x 8’ box filled with sand, having about ½ foot of sand in it, over which was placed an ample amount of hay. They had plenty of hay, too.

• The actual workouts were made to not be monotonous because the athlete exercising was obeying commands from one of his fellow athletes. He didn’t know in what direction, for how long, or how fast he would be required to work with the weights.      This was done on purpose to boost adrenaline.

I don’t know if you know what rings are, but my Dad liked them. If you’ve ever followed the Olympics, you know what they looks like. This type of gymnastic exercise requires a lot of strength in wrists, forearms, shoulders, lats, and upper chest muscles.

Here’s the six pack ab part of it. As you raise yourself up on the rings and kick your feet out so that your body forms a 90 degree angle, strong stomach muscles are important. You really need to burn fat off in that area, and that’s where these ‘kettlebells’ came into their own in our weight training.

The advantage to having the flexible shaft attached to the weight is that it forces you to re-balance all the time as you are lifting.

The weight training took place in a farmers’ barn which was also arranged so that some could walk on a high wire – about 22 to 26 feet off the ground. Now to get up to that high wire they used a wide board over a wooden barrel, so that when someone jumped on one side of the plank the gymnast on the other side flew right up = just like you see in the circus.

Using a ladder was discouraged and was considered as being ‘a girly mon’ – quote from Arnold S. There were no real safety nets. If you fell – too bad…didn’t get any sympathy if you did fall, either.

We also manufactured smaller, similar looking weights that were more rectangular at about 20 pounds each. The length and width for these was determined by the size and measurements of the person using them. These ‘kettlebells’ didn’t use lead, but were simply burlap bags filled with clay with a lead rod placed in the center for added weight. The clay helped it mold to your body, and would give a little when you move.

These smaller ‘kettlebells’ were then wrapped to your body and tied with a heavy twine, to secure the weights in place.

Try this:

Construct 4 of these things and the strap one to each forearm, calf, and thigh – for the whole day…and if you were pitching hay – which all the farmers had to do – tape one more onto the pitch fork.

If you use this in boxing training, you will really get super strong and lightning fast.

• All the food we consumed was organic and freshly picked (usually by yourself) from the ground. No junk food like we have here. And at the time, I never thought that this was a weight loss program. ©aof 2010.

[Editor's note: "Far - FrÅn en Viking til en annan." af]

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[Editot's note:   af]

An eating disorder is characterized by abnormal eating habits that may involve either insufficient or excessive food intake to the detriment of an individual’s physical and emotional health. The causes of eating disorders are complex and not yet fully understood. Eating disorders are estimated to affect 5-10 million females and 1 million males in the United States. Although not yet classified as separate disorder, binge eating disorder is the most common eating disorder in the US affecting 3.5% of females and 2% of males according to a study by Harvard affiliated McLean Hospital. Bulimia nervosa was the second most common followed by anorexia nervosa

Statistics

• Eating disorders affect all socioeconomic levels.
• 40% of 9- and 10-year-old girls are already trying to lose weight.
• Girls with ADHD are 5.6 times more likely to develop bulimia and 2.7 times more likely to develop anorexia nervosa.
• Women who were raised in foster care are 7 times more likely to develop bulimia nervosa.
• Binge eating is the most common eating disorder in the US affecting 3.5% of females and 2% of males, followed by bulimia nervosa and anorexia nervosa.
• Females with anorexia nervosa have a higher suicide rate than those with any other mental health disorder and the general population up to 60 times higher according to one study.
• Anorexia nervosa has the highest mortality rate of any psychiatric disorder.
• Anorexia nervosa, although usually reported in white adolescent females, affects all races and age groups
• The mortality rate for anorexia nervosa is 4.0%, bulimia nervosa is 3.9% and “eating disorder not otherwise specified” (EDNOS) which includes binge eating disorder is placed at 5.2%.
• Males account for 5%-10% of anorexia nervosa cases and 10%-15% of bulimia nervosa cases.
• An optimum healthy weight is calculated using the Body Mass Index

Biological

• Genetic: Numerous studies have been undertaken that show a possible genetic predisposition toward eating disorders as a result of Mendelian inheritance.
• Epigenetics: Epigenetic mechanisms are means by which genetic mutations are caused by environmental effects that alter gene expression via methods such as DNA methylation; these are independent of and do not alter the underlying DNA sequence. They are heritable, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission due to epigenetic mechanisms has been implicated in various eating disoders.

“We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders.”

• Biochemical: Eating behavior is a complex process controlled by the neuroendocrine system of which the Hypothalamus-pituitary-adrenal-axis (HPA axis) is a major component. Dysregulation of the HPA axis has been associated with eating disorders, such as irregularities in the manufacture, amount or transmission of certain neurotransmitters, hormones or neuropeptides and amino acids such as homocysteine, elevated levels of which are found in AN and BN as well as depression.
  • serotonin: a neurotransmitter involved in depression also has an inhibitory effect on eating behavior.
  • norepinephrine is both a neurotransmitter and a hormone; abnormalities in either capacity may affect eating behavior.
  • dopamine: which in addition to being a precursor of norepinephrine and epinephrine is also a neurotransmitter which regulates the rewarding property of food.
• leptin and ghrelin: leptin is a hormone produced primarily by the fat cells in the body; it has an inhibitory effect on appetite by inducing a feeling of saiety. Ghrelin is an appetite inducing hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity, both hormones and their respective effects have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.
• immune system: studies have shown that a majority of patients with anorexia and bulimia nervosa have elevated levels of autoantibodies that affect hormones and neuropeptides that regulate appetite control and the stress response. There may be a direct correlation between autoantibody levels and associated psychological traits.
• infection: PANDAS, is an abbreviation for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections. Children with PANDAS “have obsessive-compulsive disorder (OCD) and/or tic disorders such as Tourette syndrome, and in whom symptoms worsen following infections such as “strep throat” and scarlet fever.” (NIMH) There is a possibility that PANDAS may be a precipitating factor in the development of anorexia nervosa in some cases, (PANDAS AN).
• lesions: studies have shown that lesions to the right frontal lobe or temporal lobe can cause the pathological symptoms of an eating disorder.
• tumors: tumors in various regions of the brain have been implicated in the development of abnormal eating patterns.
• brain calcification: a study highlights a case in which prior calcification of the right thalumus may have contributed to development of anorexia nervosa.
• somatosensory homunculus: is the representation of the body located in the somatosensory cortex, first described by renowned neurosurgeon Wilder Penfield. The illustration was originally termed “Penfield’s Homunculus”, homunculus meaning little man. “In normal development this representation should adapt as the body goes through its pubertal growth spurt. However, in AN it is hypothesized that there is a lack of plasticity in this area, which may result in impairments of sensory processing and distortion of body image”. (Bryan Lask, also proposed by VS Ramachandran)
• Obstetric complications: There have been studies done which show maternal smoking, obstetric and perinatal complications such as maternal anemia, very pre-term birth (32<wks.), being born small for gestational age, neonatal cardiac problems, preeclampsia, placental infarction and sustaining a cephalhematoma at birth increase the risk factor for developing either anorexia nervosa or bulimia nervosa. Some of this developmental risk as in the case of placental infarction, maternal anemia and cardiac problems may cause intrauterine hypoxia, umbilical cord occlusion or cord prolapse may cause ischemia, resulting in cerebral injury, the prefrontal cortex in the fetus and neonate is highly susceptible to damage as a result of oxygen deprivation which has been shown to contribute to executive dysfunction, ADHD, and may affect personality traits associated with both eating disorders and comorbid disorders such as impulsivity, mental rigidity and obsessionality. The problem of perinatal brain injury, in terms of the costs to society and to the affected individuals and their families, is extraordinary. (Yafeng Dong, PhD)

Psychological

Eating disorders are classified as Axis I disorders in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV) published by the American Psychiatric Association. There are various other psychological issues that may factor into eating disorders, some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 “clusters”, A, B and C. The causality between personality disorders and eating disorders has yet to be fully established. Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.

Some develop them afterwards. The severity and type of eating disorder symptoms have been shown to affect comorbidity. The DSM-IV should not be used by laypersons to diagnose themselves, even when used by professionals there has been considerable controversy over the diagnostic criteria used for various diagnoses, including eating disorders. There has been controversy over various editions of the DSM including the latest edition, DSM-V, due in May 2013.

Personality traits

There are various childhood personality traits associated with the development of eating disorders. During adolescence these traits may become intensified due to a variety of physiological and cultural influences such as the hormonal changes associated with puberty, stress related to the approaching demands of maturity and socio-cultural influences and perceived expectations, especially in areas that concern body image.

Many personality traits have a genetic component and are highly heritable. Maladaptive levels of certain traits may be acquired as a result of anoxic or traumatic brain injury, neurodegenerative diseases such as Parkinson’s disease, neurotoxicity such as lead exposure, bacterial infection such as Lyme disease or viral infection such as Toxoplasma gondii as well as hormonal influences. While studies are still continuing via the use of various imaging techniques such as fMRI; these traits have been shown to originate in various regions of the brain such as the amygdala and the prefrontal cortex Disorders in the prefrontal cortex and the executive functioning system have been shown to affect eating behavior.

Personality Traits
The Big Five personality traits	The “Big Five” also referred to as the “Five-Factor Model” are five broad factors (dimensions) of personality, that are based upon empirical research. A mnemonic device to remember them is the acronym “OCEAN”. Two of the tests to measure the Big Five are the “Big Five Inventory” and the IPIP (International Personality Item Pool ) an abbreviated form is the “IPIP-NEO”. The BFI and the IPIP-NEO are available free online for noncommercial purposes. Online test
1. Openness to Experience/Intellect	Composed of two related but separable traits, Openness to Experience and Intellect. Behavioral aspects include having wide interests, and being imaginative and insightful, correlated with activity in the dorsolateral prefrontal cortex. Considered primarily a cognitive trait.
2. conscientiousness	Scrupulous, meticulous, principaled behavior guided or conforming to one’s own conscience. Associated with the dorsolateral prefrontal cortex. Anorexics are noted to have higher levels of conscientiousness.
3. extroversion	Gregarious, outgoing, sociable, projecting one’s personality outward. The opposite of extroversion is introversion. Extroversion has shown to share certain genetic markers with substance abuse. Extroversion is associated with various regions of the prefrontal cortex and the amygdala.
4. agreeableness	Refers to a compliant, trusting, empathic, sympathetic, friendly and cooperative nature.
5. neuroticism	“Refers to an individual’s tendency to become upset or emotional” (Hans Eysenck) “Neuroticism is the major factor of personality pathology” (Eysenck & Eysenck, 1969). Neuroticism has a been linked to serotonin transporter (5-HTT) binding sites in the thalamus: as well as activity in the insular cortex.
self esteem (low)	A “favorable or unfavorable attitude toward the self” (Rosenberg, 1965). An individual’s sense of his or her value or worth, or the extent to which a person values, approves of, appreciates, prizes, or likes him or herself” (Blascovich & Tomaka, 1991).
harm avoidance	A tendency towards shyness, being fearful and uncertain, tendency to worry. Neonatal complications such as preterm birth have been shown to affect harm avoidance. Those with BED, AN, and BN exhibit high levels of harm avoidance. The volume of the left amygdala in girls was correlated to levels of HA, in separate studies HA was correlated with reduced grey matter volume in the orbito-frontal, occipital and parietal regions.
novelty seeking	Impulsive, exploratory, fickle, excitable, quick-tempered, and extravagant. Associated with addictive behavior.
perfectionism	“I don’t think needing to be perfect is in any way adaptive” (Paul Hewitt, PhD) Socially prescribed perfectionism – “believing that others will value you only if you are perfect.” Self-oriented perfectionism – “an internally motivated desire to be perfect. Perfectionism is one of the traits associated with obsessional behavior and like obsessionality is also believed to be regulated by the basal ganglia.
alexithymia	The inability to express emotions. “To have no words for one’s inner experience” (Rený J. Muller PhD).In studies done with stroke patients, alexithymia was found to be more prevalent in those who developed lesions in the right hemisphere following a cerebral infarction. There is a positive association with post-traumatic stress disorder (PTSD), childhood abuse and neglect and alexithymia. Utilizing psychometric testing and fMRI, studies showed positive response in the insula, posterior cingulate cortex (PCC), and thalamus.
rigidity	Inflexibility, difficulty making transitions, adherence to set patterns. Mental rigidity arises out of a deficit of the executive functions. Originally termed frontal lobe syndrome it is also referred to as dysexecutive syndrome and usually occurs as a result of damage to the frontal lobe. This may be due to physical damage, disease (such as Huntington’s disease) or a hypoxic or anoxic insult.
impulsivity	Risk taking, lack of planning, and making up one’s mind quickly (Eysenck and Eysenck). A component of disinhibition. Abnormal patterns of impulsivity have been linked to lesions in the right inferior frontal gyrus and in studies done by Antonio Damasio author of Descartes Error, damage to the ventromedial prefrontal cortex has been shown to cause a defect in real-life decision making in individuals with otherwise normal intellect. Those who sustain this type of damage are oblivious to the future consequences of their actions and live in the here and now.
disinhibition	Behavioral disinhibition is an inability or unwillingness to constrain impulses, it is a key component of executive functioning. Researchers have emphasized poor behavioral inhibition as the central impairment of ADHD. It may be symptomatic of orbitofrontal lobe syndrome, a subtype of frontal lobe syndrome which may be an acquired disorder as a result of traumatic brain injury, hypoxic ischemic encephalopathy (HIE), anoxic encephalopathy, degenerative diseases such as Parkinson’s, bacterial or viral infections such as Lyme disease and neurosyphilis. Disinhibition has been consistently associated with substance abuse disorders, obesity, higher BMI, excessive eating, an increased rate of eating, and perceived hunger.
obsessionality	Persistent, often unwelcome, and frequently disturbing ideas, thoughts, images or emotions, rumination, often inducing an anxious state. Obsessionality may result as a dysfunction of the basal ganglia.

Child maltreatment

Child abuse which encompasses physical, psychological and sexual abuse, as well as neglect has been shown by innumerable studies to be a precipitating factor in a wide variety of psychiatric disorders, including eating disorders. Children who are subjugated to abuse may develop a disordered eating pattern in an effort to gain some sense of control or for a sense of comfort. Or they may be in an environment where the diet is unhealthy or insufficient. Child abuse and neglect can cause profound changes in both the physiological structure and the neurochemistry of the developing brain. Children who, as wards of the state, were placed in orphanages or foster homes are especially susceptible to developing a disordered eating pattern. In a study done in New Zealand 25% of the study subjects in foster care exhibited an eating disorder (Tarren-Sweeney M. 2006). An unstable home environment is detrimental to the emotional well-being of children, even in the absence of blatant abuse or neglect the stress of an unstable home can contribute to the development of an eating disorder.

Social isolation

Social isolation has been shown to have a deleterious effect on an individuals’ physical and emotional well-being. Those that are socially isolated have a higher mortality rate in general as compared to individuals that have established social relationships. This effect on mortality is markedly increased in those with pre-existing medical or psychiatric conditions, and has been especially noted in cases of coronary heart disease. “The magnitude of risk associated with social isolation is comparable with that of cigarette smoking and other major biomedical and psychosocial risk factors.” (Brummett et al.)

Social isolation can be inherently stressful, depressing and anxiety provoking. In an attempt to ameliorate these distressful feelings an individual may engage in emotional eating in which food serves as a source of comfort. The loneliness of social isolation and the inherent stressors thus associated have been implicated as triggering factors in binge eating as well.

Parental influence

Parental influence has been shown to be an intrinsic component in developing the eating behaviors of children. This influence is manifested and shaped by a variety of diverse factors such as familial genetic predisposition, dietary choices as dictated by cultural or ethnic preferences, the parents’ own body shape and eating patterns, the degree of involvement and expectations of their children’s eating behavior as well as the interpersonal relationship of parent and child. This is in addition to the general psychosocial climate of the home and the presence or absence of a nurturing stable environment.

It has been shown that maladaptive parental behavior has an important role in the development of eating disorders. As to the more subtle aspects of parental influence it has been shown that eating patterns are established in early childhood and that children should be allowed to decide when their appetite is satisfied as early as the age of two. A direct link has been proven between obesity and parental pressure to eat more.

Coercive tactics in regard to diet have not been proven to be efficacious in controlling a child’s eating behavior. Affection and attention have been shown to affect the degree of a childs’ finickiness and their acceptance of a more varied diet.

Peer pressure

In various studies such as one conducted by The McKnight Investigators, peer pressure was shown to be a significant contributor to body image concerns and attitudes toward eating among subjects in their teens and early twenties.

Eleanor Mackey and co-author, Annette M. La Greca of the University of Miami, studied 236 teen girls from public high schools in southeast Florida. “Teen girls’ concerns about their own weight, about how they appear to others and their perceptions that their peers want them to be thin are significantly related to weight-control behavior,” says psychologist Eleanor Mackey of the Children’s National Medical Center in Washington and lead author of the study. “Those are really important.”

Dieting among adolescents was also reported to being influenced by peer behavior, with many of those individuals on a diet reporting that their friends also were dieting. The number of friends dieting and the number of friends who pressured them to diet also played a significant role in their own choices.

Cultural pressure

There is a cultural emphasis on thinness which is especially pervasive in western society. There is an unrealistic stereotype of what constitutes beauty and the ideal body type as portrayed by the media, fashion and entertainment industries. “The cultural pressure on women to be thin is an important predisposing factor for the development of eating disorders” (Bryan Lask, PhD).

In men

There has been an increasing rate of males suffering from various eating disorders including anorexia nervosa. There is a perceived stigma attached, as eating disorders are generally viewed as primarily affecting women. Among men the rates of eating disorders are higher in the gay and bi-sexual communities (Feldman & Meyer, 2007), yet it also affects heterosexual men.

Despite the perceived stigma, some high profile male celebrities have publicized their struggles with eating disorders such as actor Dennis Quaid, who struggled with what he called “manorexia” for which he sought treatment. Quaid said his problems began when he went on a diet to lose forty pounds to play Doc Holliday in the movie “Wyatt Earp” in 1994. Billy Bob Thornton has also struggled with anorexia, once losing 59 lbs. Thomas Holbrook, MD, is Clinical Director of the Eating Disorders Program at Rogers Memorial Hospital in Oconomowoc, Wisconsin despite being a psychiatrist specializing in eating disorders, he suffered from anorexia nervosa with compulsive exercising. At one time the 6-ft-tall psychiatrist weighed just 135 lbs. “I was terrified,” he says, “of being fat.” His story has been chronicled in various publications including USA Today and People Magazine.

Signs of Anorexia-bulimia

Anorexia nervosa (AN) is divided into two subtypes: restrictive, which doesn’t engage in purging behavior; and purging type which does. Bulimia nervosa is divided into two subtypes: purging and the less common; non purging. There is a tendency for diagnostic “crossover” in which symptoms change over time between the restricting and binge eating/purging anorexia nervosa subtypes and bulimia nervosa. While anorexics are often underweight or below average body weight, bulimics range from a normal weight to even slightly above average weight.

Possible Signs of Anorexia Nervosa and Bulimia Nervosa
weight loss	an obvious, rapid, dramatic weight loss
Russell’s sign	scarring of the knuckles from placing fingers down throat to induce vomiting.
lanugo	soft fine hair grows on face and body
obsession	with calories, fat content
preoccupation	with food, recipes, cooking, may cook elaborate dinners for others but not eat themselves
dieting	despite being thin or dangerously underweight
fear	of gaining weight or becoming overweight
rituals	cuts food into tiny pieces, refuses to eat around others, hides or discards food
purging	uses laxatives, diet pills, ipecac syrup, water pills may engage in self induced vomiting, may run to bathroom after eating, to vomit to quickly get rid of the calories
exercise	may engage in frequent strenuous exercise
perception	perceives themselves to be overweight despite being told by others they are too thin
cold	becomes intolerant to cold, frequently complains of being cold due to loss of insulating body fat, body temperature lowers (hypothermia) in effort to conserve calories.
depression	may frequently be in a sad lethargic state
solitude	may avoid friends and family, become withdrawn and secretive
clothing	may wear baggy, loose fitting clothes to cover weight loss
cheeks	may become swollen due to enlargement of the salivary glands caused by excessive vomiting

Binge eating

Both bulimics and those with binge eating disorder (BED) engage in binge eating. Those with BED do not engage in any compensatory behavior, e.g. they do not purge, use laxatives or engage in compulsive exercise. The binge eating is caused by emotional upset and not by hunger. During these episodes, those affected with BED will consume thousands of calories at once, often in one sitting. Because of the lack of purging, those with BED tend to be overweight or obese, even though persons of normal or average weight can be affected.

Possible Signs of Binge Eating Disorder | Binge Eating in Bulimia Nervosa
rapid	eats at a rapid pace, much faster than normal
amount	eats a large amount of food at one sitting
powerless	feels powerless to stop eating
satiety	never feeling satisfied after eating
embarrassment	embarrassed over amount of food being eaten
secret	eats normally around others but binges in secret
hunger	eats even when not hungry
depression	frequently in depressed mood
hoarding	hoards food and hides empty food containers

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder to affect women. Though often associated with obesity it can occur in normal weight individuals. PCOS has been associated with binge eating and bulimic behavior.

Rumination syndrome

Rumination syndrome, is characterized by the repeated painless regurgitation of food following a meal which is then either re-chewed, re-swallowed or discarded. It is an under-diagnosed disorder possibly due to the fact that most physicians do not recognize the symptoms of the disorder. While often diagnosed in infants and developmentally disabled individuals, it also occurs in adults of normal intelligence. An accurate clinical diagnosis is critical in making an accurate diagnosis. The Rome III Consensus Criteria for rumination syndrome varies for infants, adolescents and adults.

Diabulimia

• Diabulimia, not currently a recognized medical condition, is the deliberate manipulation of insulin, including withholding shots, by individuals with Type 1 diabetes in an effort to control their weight. Insulin is an anabolic hormone that is involved in the metabolism of carbohydrates and lipids (fats).^] It helps the body maintain muscle mass, it also encourages fat retention.

The effects of withholding insulin can lead to severe complications, such as diabetic ketoacidosis. The long term effects can lead to the acceleration of diabetes related complications such as diabetic vasculopathy which may lead to limb amputation.

Food maintenance syndrome

Food maintenance syndrome is characterized by a set of aberrant eating behaviors of children in foster care it is “a pattern of excessive eating and food acquisition and maintenance behaviors without concurrent obesity”, it resembles “the behavioral correlates of Hyperphagic Short Stature” (Tarren-Sweeney M. 2006). It is hypothesized that this syndrome is triggered by the stress and maltreatment these children are subjected to.

Female athlete triad

Female athlete triad is a syndrome in which eating disorders/disordered eating behavior, amenorrhea/oligomenorrhea and decreased bone mineral density (osteoporosis and osteoenia) are present. Not all patients exhibit all three components of the triad; according to recent studies some may have only one or two which increases the difficulty of proper diagnosis and long-term morbidity. The full impact of this disorder may not be realized until menopause when the resultant bone loss is accelerated. The strict criteria for diagnosis have been amended by the American College of Sports Medicine in 2007. The diagnostic criteria are now ascertained on a continuous spectrum instead of the most severe presentation. Disordered eating has been replaced by “optimal energy availability” to “low energy availability with or without an eating disorder”. Amenorrhea has been replaced by a spectrum ranging from normal menstruation (eumenorrhea) to “functional hypothalmic amenorrhea”, in younger patients delayed primary menstruation may occur. Osteoporosis has been replaced by a spectrum ranging from optimal bone health to osteoporosis.

Diagnosis

The initial diagnosis should be made by a competent medical professional. “The medical history is the most powerful tool for diagnosing eating disorders”(American Family Physician). There are many medical disorders that mimic eating disorders and comorbid psychiatric disorders. All organic causes should be ruled out prior to a diagnosis of an eating disorder or any other psychiatric disorder is made.

According to an in depth study conducted by psychiatrist Richard Hall as published in The Archives of General Psychiatry:

• Medical illness often presents with psychiatric symptoms.
• It is difficult to distinguish physical disorders from functional psychiatric disorders on the basis of psychiatric symptoms alone.
• Detailed physical examination and laboratory screening are indicated as a routine procedure in the initial evaluation of psychiatric patients.
• Most patients are unaware of the medical illness that is causative of their psychiatric symptoms.
• The conditions of patients with medically induced symptoms are often initially misdiagnosed as a functional psychosis.

Medical

A consultation with a reputable medical professional who specializes in eating disorders is an indispensable part of both the diagnostic process and treatment. A complete medical and psychosocial history should be provided and a rational and formulaic approach to the diagnosis should be used. Neuroimaging using fMRI, MRI, PET and SPECT scans have been used to detect cases in which a lesion, tumor or other organic condition has been either the sole causative or contributory factor in an eating disorder. “Right frontal intracerebral lesions with their close relationship to the limbic system could be causative for eating disorders, we therefore recommend performing a cranial MRI in all patients with suspected eating disorders” (Trummer M et al. 2002), “intracranial pathology should also be considered however certain is the diagnosis of early-onset anorexia nervosa. Second, neuroimaging plays an important part in diagnosing early-onset anorexia nervosa, both from a clinical and a research prospective”.(O’Brien et al. 2001).

Without visible images of neuropathology, psychiatric disorders have been a fertile ground for stigma and bizarre propositions, as evidenced by etiologic theories involving “schizophrenogenic” and “refrigerator mothers”. Neuroimaging will clearly establish psychiatric disorders as being “medical”, thereby bringing these disorders into the mainstream in terms of public attitude and, perhaps more importantly, funding for treating these problems (Derryck H Smith, MD, Canadian Psychiatric Association). In addition to neuroimaging there are a variety of tests that may be performed to diagnosis and assess the effects of an eating disorder.

Medical Tests used in the Diagnosis and Assessment of Eating Disorders
Complete Blood Count (CBC)	a test of the white blood cells, red blood cells and platelets used to assess the presence of various disorders such as leukocytosis, leukopenia, thrombocytosis and anemia which may result from malnutrition.
urinalysis	a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for substance abuse, and as an indicator of overall health
ELISA	Various subtypes of ELISA used to test for antibodies to various viruses and bacteria such as Borrelia burgdoferi (Lyme Disease)
Western Blot Analysis	Used to confirm the preliminary results of the ELISA
Chem-20	Chem-20, also known as SMA-20, a group of twenty separate chemical tests performed on blood serum. Tests include cholesterol, protein and electrolytes such as potassium, chlorine and sodium and tests specific to liver and kidney function.
glucose tolerance test	Oral glucose tolerance test (OGTT) used to assess the bodies’ ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing syndrome, hypoglycemia and polycystic ovary syndrome
Secritin-CCK Test	Used to assess function of pancreas and gall bladder
Serum cholinesterase test	a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a test of liver function and to assess the effects of malnutrition
Liver Function Test	A series of tests used to assess liver function; some of the tests are also used in the assessment of malnutrition, protein deficiency, kidney function, bleeding disorders, Crohn’s disease
Lh response to GnRH	Luteinizing hormone (Lh) response to gonadotropin-releasing hormone (GnRH). Tests the pituitary glands’ response to GnRh, a hormone produced in the hypothalumus. Central hypogonadism is often seen in anorexia nervosa cases.
Creatine Kinase Test (CK-Test)	measures the circulating blood levels of creatine kinase, an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).
Blood urea nitrogen (BUN) test	urea nitrogen is the byproduct of protein metabolism first formed in the liver, then removed from the body by the kidneys. The BUN test is used primarily to test kidney function. A low BUN level may indicate the effects of malnutrition.
BUN-to-creatinine ratio	A BUN to creatinine ratio is used to predict various conditions. High BUN/creatinine ratio can occur in severe hydration, acute kidney failure, congestive heart failure, intestinal bleeding. A low BUN/creatinine can indicate a low protein diet, celiac disease rhabdomyolysis, cirrhosis of the liver.
echocardiogram	utilizes ultrasound to create a moving picture of the heart to assess function
electrocardiogram (EKG or ECG)	measures electrical activity of heart; can be used to detect various disorders such as hyperkalemia
electroencephalogram (EEG)	measures the electrical activity of the brain. Can be used to detect abnormalities such as those associated with pituitary tumors
Upper GI Series	test used to assess gastrointestinal problems of the middle and upper intestinal tract
Thyroid Screen TSH, T4, T3	test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3)
Parathyroid hormone (PTH) test	tests the functioning of the parathyroid by measuring the amount of(PTH) in the blood. Test is used to diagnose hypoparathyroidism. PTH also controls the levels of calcium and phosphorus in the blood (homeostasis).
barium enema	an x-ray examination of the lower gastrointestinal tract

Psychological

After ruling out organic causes and the initial diagnosis of an eating disorder being made by a medical professional, a trained mental health professional aids in the assessment and treatment of the underlying psychological components of the eating disorder and any comorbid psychological conditions. The clinician conducts a clinical interview and may employ various psychometric tests. Some are general in nature while others were devised specifically for use in the assessment of eating disorders. Some of the general tests that may be used are the Hamilton Depression Rating Scale and the Beck Depression Inventory.

Differential diagnoses

According to a recent report issued in The Journal of the American Medical Association (JAMA), anywhere from 40,000 to 80,000 deaths in the US are attributable to misdiagnosis in the hospital setting per year. Also in the US, deaths due to medical errors are higher than the numbers attributable to the 8th-leading cause of death. More people die in a given year as a result of medical errors than from motor vehicle accidents (43,458), breast cancer (42,297), or AIDS (16,516). These figures do not factor in those misdiagnosed outside the hospital setting or for individuals who present with psychiatric symptoms and receive contraindicated, i.e. wrong, mental health care predicated upon poor diagnostic procedure. In the Rosenhan experiment, eight individuals with no psychiatric history, amongst them a pediatrician, a psychiatrist and three psychologists presented false symptoms to gain admission to 12 different psychiatric hospitals; despite acting normally once admitted including openly taking notes, 11 of the hospitals diagnosed schizophrenia, prescribed medication and kept them from 7 to 52 days.

On average, 32,000 Americans commit suicide per year. 77% had seen a physician and 30% had received mental health counseling in the year prior. In England alone independent of the rest of the United Kingdom an average of four psychiatric patients die, many from suicide and another three suffer serious physical harm each day while under the care of the National Health Service.

• acute pandysautonomia is one form of an autonomic neuropathy, which is a collection of various syndromes and diseases which affect the autonomic neurons of the autonomic nervous system (ANS). Autonomic neuropathies may be the result of an inherited condition or they may be acquired due to various premorbid conditions such as diabetes and alcoholism, bacterial infection such as Lyme disease or a viral illness. Some of the symptoms of ANS which may be associated with an ED include nausea, dysphagia, constipation, pain in the salivary glands, and early saiety. It also affects peristalsis in the stomach. ANS may cause emotional instability and has been misdiagnosed as various psychiatric disorders including hysterical neurosis and anorexia nervosa.
• mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a rare genetic disorder characterized by gastrointestinal dysmotility, severe cachexia, progressive external ophthalmoplegia, post-prandial emesis (vomiting after eating), peripheral neuropathy, and diffuse leukoencephalopathy. Onset is prior to age 20 in 60% of cases. ” ‘Miss A’ was a 21-year-old Indian woman diagnosed as having treatment-resistant anorexia nervosa.” It was subsequently proven to be MNGIE.
• achalasia; there have been cases where achalasia, a disorder of the esophagus which affects peristalsis, has been misdiagnosed as various eating disorders including anorexia nervosa, bulimia nervosa, compulsive eating disorder and obesity related problems. It has been reported in cases where there is sub-clinical manifestation of anorexia nervosa and also in cases where the full diagnostic criteria of AN has been met.
• superior mesenteric artery syndrome: SMA syndrome “is a gastrointestinal disorder characterized by the compression of the third or transverse portion of the duodenum against the aorta by the superior mesenteric artery resulting in chronic partial, incomplete, acute or intermittent duodenal obstruction”. It may occur as a complication of AN or as a differential diagnosis. There have been reported cases of a tentative diagnosis of AN, where upon treatment for SMA syndrome the patient is asymptomatic.
• Lyme disease is known as the “great imitator”, as it may present as a variety of psychiatric or neurologic disorders including anorexia nervosa.
• “A 12 year old boy with confirmed Lyme arthritis treated with oral antibiotics subsequently became depressed and anorectic. After being admitted to a psychiatric hospital with the diagnosis of anorexia nervosa, he was noted to have positive serologic tests for Borrelia burgdorferi. Treatment with a 14 day course of intravenous antibiotics led to a resolution of his depression and anorexia; this improvement was sustained on 3 year follow-up.” Serologic testing can be helpful but should not be the sole basis for diagnosis. The Centers for Disease Control (CDC) issued a cautionary statement (MMWR 54;125) regarding the use of several commercial tests. Clinical diagnostic criteria has been issued by the CDC (CDC, MMWR 1997; 46: 531-535).
• Addison’s Disease is a disorder of the adrenal cortex which results in decreased hormonal production. Addison’s disease, even in subclinical form may mimic many of the symptoms of anorexia nervosa.
• Simmond’s disease (organic hypopituitarism) – “A 20-year-old Japanese man with a hypothalamic tumor which caused hypopituitarism and diabetes insipidus was mistakenly diagnosed as anorexia nervosa because of anorexia, weight loss, denial of being ill, changes in personality, and abnormal behavior resembling the clinical characteristics of anorexia nervosa”(Hotta, M. 1999)
• Celiac disease is an inflammatory disorder triggered by peptides from wheat and similar grains which cause an immune reaction in the small intestine. “Information on the role of the gastrointestinal system in causing or mimicking eating disorders is scarce.”(Leffler DA et al.)
• gastric adenocarcinoma is one of the most common forms of cancer in the world. Complications due to this condition have been misdiagnosed as an eating disorder.
• helicobacter pylori is a bacteria which causes stomach ulcers and gastritis and has been shown to be a precipitating factor in the development of gastric carcinomas. It also has an effect on circulating levels of leptin and ghrelin, two hormones which help regulate appetite. Upon successful treatment of helicobacter pylori associated gastritis in pre-pubertal children they showed “significant increase in BMI, lean and fat mass along with a significant decrease in circulating ghrelin levels and an increase in leptin levels” (Pacifico, L).”SUMMARY: H. pylori has an influence on the release of gastric hormones and therefore plays a role in the regulation of body weight, hunger and satiety,”(Weigt J, Malfertheiner P).
• gall bladder disease which may be caused by inflammation, infection, gallstones, obstruction of the gallbladder or torsion of the gall bladder. Many of the symptoms of gall bladder disease may mimic anorexia nervosa (AN). Laura Daly, a woman from Missouri, suffered from an inherited disorder in which the gall bladder was not properly attached; the resultant complications led to multiple erroneous diagnoses of AN. Upon performance of a CCK test, standard imaging techniques are done with the patient lying prone, in this instance it was done with the patient in an upright position. The gall bladder was shown to be in an abnormal position having flipped over the liver. The gallbladder was removed and the patient has since recovered. The treatment was performed by William P. Smedley, MD, FACS in Pennsylvania.
• colonic tuberculosis misdiagnosed as anorexia nervosa in a physician at the hospital where she worked. “This patient, who had severe wasting, was misdiagnosed as having anorexia nervosa despite the presence of other symptoms suggestive of an organic disease, namely, fever and diarrhea”(Madani, A 2002).
• Crohn’s disease: “We report three cases of young 18 to 25 year-old girls, initially treated for anorexia nervosa in a psychiatric department. Diagnosis of Crohn’s disease was made within 5 to 13 years.”(Blanchet C, Luton JP. 2002) “This disease should be diagnostically excluded before accepting anorexia nervosa as final diagnosis”. (Wellmann W et al.)
• insulinomas, are (pancreatic tumors) that cause an overproduction of insulin causing hypoglycemia. Various neurological deficits have been ascribed to this condition including misdiagnosis as an eating disorder.
• hypothyroidism, hyperthyroidism, hypoparathyroidism and hyperparathyroidism may mimic some of the symptoms of, can occur concurrently with, be masked by or exacerbate an eating disorder.
• multiple sclerosis (Encephalomyelitis disseminata) is a progressive autoimmune disorder in which the protective covering (myelin sheath) of nerve cells is damaged as a result of inflammation and resultant attack by the body’s own immune system. In its initial presentation MS has been misdiagnosed as an eating disorder.
• cestodes (tapeworm) infestations can affect various regions of the human body including the gastrointestinal and neuroendocrine systems. While most of those infected are asymptomatic, infestations can cause psychiatric symptoms, epilepsy, weight gain or loss and Megaloblastic anemia, which itself can cause neuropsychiatric symptoms.
  • Cysticercosis is an infection caused by the larval stage of the pork tapeworm (Taenia solium). The larval stage of T. solium can create cysts in various regions of the body including the brain (neurocysticercosis). Hypothalimic cysticercosis has been associated with obesity. Cysts may form in the bile and pancreatic ducts causing full or partial obstruction; some of the symptoms may include weight loss, anorexia, or increased appetite.

There are multiple medical conditions which may be misdiagnosed as a primary psychiatric disorder. These may have a synergistic effect on conditions which mimic an eating disorder or on a properly diagnosed ED. They also may make it more difficult to diagnose and treat an ED.

• Lupus: 19 psychiatric conditions have been associated with systemic lupus erythematosus (SLE), including depression and bipolar disorder.
• Toxoplasma seropositivity: even in the absence of symptomatic toxoplasmosis, toxoplasma gondii exposure has been linked to changes in human behavior and psychiatric disorders including those comorbid with eating disorders such as depression. In reported case studies the response to antidepressant treatment improved only after adequate treatment for toxoplasma.
• neurosyphilis: It is estimated that there may be up to one million cases of untreated syphyilis in the US alone. “The disease can present with psychiatric symptoms alone, psychiatric symptoms that can mimic any other psychiatric illness”. Many of the manifestations may appear atypical. Up to 1.3% of short term psychiatric admissions may be attributable to neurosyphilis, with a much higher rate in the general psychiatric population. Neurosyphilis like Lyme disease has been given the appellation the “great imitator” for it may present in various ways such as depression and chronic alcoholism. (Ritchie, M Perdigao J,)
• dysautonomia: a term used to describe a wide variety of autonomic nervous system (ANS) disorders may cause a wide variety of psychiatric symptoms including anxiety, panic attacks and depression. Dysautonomia usually involves failure of sympathetic or parasympathetic components of the ANS system but may also include excessive ANS activity. Dysautonomia can occur in conditions such as diabetes and alcoholism.

There are separate psychological disorders which may be misdiagnosed as an eating disorder.

• Emetophobia is an anxiety disorder characterized by an intense fear of vomiting. A person so afflicted may develop rigorous standards of food hygiene, such as not touching food with their hands. They may become socially withdrawn to avoid situations which in their perception may make them vomit. Many who suffer from emetophobia are diagnosed with anorexia or self-starvation. In severe cases of emetophobia they may drastically reduce their food intake.
• phagophobia is an anxiety disorder characterized by a fear of eating, it is usually initiated by an adverse experience while eating such as choking or vomiting. Persons with this disorder may present with complaints of pain while swallowing.
• Body dysmorphic disorder (BDD) is listed as a somatoform disorder that affects up to 2% of the population. BDD is characterized by excessive rumination over an actual or perceived physical flaw. BDD has been diagnosed equally among men and women. While BDD has been misdiagnosed as anorexia nervosa, it also occurs comorbidly in 39% of eating disorder cases. BDD is a chronic and debilitating condition which may lead to social isolation, major depression and suicidal ideation and attempts. Neuroimaging studies to measure response to facial recognition have shown activity predominately in the left hemisphere in the left lateral prefrontal cortex, lateral temporal lobe and left parietal lobe showing hemispheric imbalance in information processing. There is a reported case of the development of BDD in a 21 year old male following an inflammatory brain process. Neuroimaging showed the presence of a new atrophy in the frontotemporal region.

Treatment

Treatment varies according to type and severity of eating disorder. Usually more than one treatment option is utilized. Some of the treatment methods are:

• Cognitive behavioral therapy (CBT): CBT is an evidence based approach. The basic premise is that a person’s thoughts cause their feelings and behaviors not external stimuli like other people, situations or events in a person’s life. The idea is to change how a person thinks and reacts to a situation even if the situation itself does not change. CBT has been shown to be efficacious in the treatment of bulimia nervosa.
  • Acceptance and commitment therapy: a type of CBT, has shown promise in the treatment of AN. Participants experienced clinically significant improvement on at least some measures; no participants worsened or lost weight even at 1-year follow-up.
  • Dialectical behavior therapy is a form of CBT developed by Marsha M. Linehan, PhD.
  • Cognitive Remediation Therapy (CRT): CRT is an evidenced-based treatment that has shown positive results in the treatment of the neurocognitive deficits seen in schizophrenia and psychotic disorders. CRT is a set of cognitive drills or compensatory interventions designed to enhance cognitive functioning. It has been shown that those with AN have deficits in cognition such as cognitive inflexibility. CRT is being evaluated for use in the treatment of AN as a primary therapy or as an adjunct to CBT. Via the use of fMRI CRT has been proven to effect physiological change in the brain, particularly the prefrontal cortex.
• Family therapy: various forms of family therapy have been proven to work in the treatment of adolescent AN including “conjoint family therapy” (CFT), “separated family therapy” (SFT) and Maudsley Family Therapy “Eisler’s cohort show that, irrespective of the type of FBT, 75% of patients have a good outcome, 15% an intermediate outcome…”.
  • Maudsley Family Therapy: The Maudsley model of family-based treatment for anorexia nervosa, was developed in the 1980s (Dare, 1985), it utilizes a variety of family therapy models and is designed for use with adolescents 18 and under who are living with their families. It is an evidence based approach designed as an aggressive intervention within three years of the onset of anorexia nervosa and bulimia nervosa.
• Behavioral therapy: focuses on gaining control and changing unwanted behaviors.
• Interpersonal psychotherapy (IPT): “The current treatment of IPT was developed by the late Gerald Klerman and Myrna Weissman in the 1980s as a means of operationalising the interpersonal approach to psychotherapy for a series of treatment studies in depression conducted in the United States. Since that time it has been modified for a variety of other indications including Dysthymia, Bulimia Nervosa, Substance Misuse, Somatization and depression in a variety of clinical settings. Preliminary studies in Anorexia Nervosa, Bipolar Disorder, PTSD and some anxiety disorders are underway. In each adaptation the fundamentals of the treatment manual are adhered to, however different components are emphasized.” (International Society for Interpersonal Psychotherapy)
• Art therapy: is the therapeutic use of art. The American Art Therapy Association describes art therapy “as a belief that individuals can resolve conflicts, develop interpersonal skills, and gain self-esteem and insight through the creative process of artistic self-expression”.
• Nutrition counseling
• Medical nutrition therapy: Medical nutrition therapy (MNT), also referred to as nutrition therapy, is the development and provision of a nutritional treatment or therapy based on a detailed assessment of a person’s medical history, psychosocial history, physical examination, and dietary history.
• Medication: there are currently medications developed for use in obesity treatment such as Orlistat. To date there are none specifically designed for use in either anorexia or bulimia nervosa although olanzapine has shown promise in various studies for its propensity to promote weight gain as well as the ability to ameliorate obsessional behaviors concerning weight gain. The Endocrine Research Project has conducted studies with cortisol supplements. Zinc supplements have been shown to be helpful as well.
• Self help and guided self help have been shown in various studies to be helpful in varying degrees including cost reduction for treatment in AN, BN and BED.
  • Self help groups: there are various support and self-help groups for eating disorders which may be helpful and can be used in conjunction with professional treatment. Both Eating Disorders Anonymous and Overeaters Anonymous are based on the traditional 12-step program pioneered in Alcoholics Anonymous. In some instances such as with BED, self help groups alone have been shown to be on par with individual therapy.
• Psychoanalysis is a non-evidence-based approach. While the psychoanalyst Hilde Bruch, the author of “The Golden Cage”, helped bring anorexa nervosa to the public consciousness, the discipline has fallen into disrepute. “Alice Eagly, the chairwoman of the psychology department at Northwestern University, explained why: Psychoanalysis is ‘not the mainstream anymore’ and so ‘we give it less weight.’ “

Psychoanalysis has been accused of having iatrogenic, i.e. harmful tendencies. Psychoanalysis is a great idea in personality, just as long as one is a male, who grew up in a two parent house, who had either a sister or female playmate at a very young age, with a great memory, and who has lots of money and no specific time frame in which one would like one’s psychological problems cured.” (Popkin, Nathan. NWU) “Psychoanalysis is a spurious, ineffective pseudoscience, Freud’s legacy continues to inform a ‘therapeutic’ tradition that destroys people’s lives.” (Frederick Crews). In 2004 The French Institute of Health and Medical Research (INSERM) issued an official government funded report on three separate therapeutic approaches. The report was highly critical of the efficacy of psychoanalysis.

Paying for treatment

Getting the proper diagnosis and treatment for an eating disorder is expensive. There are few studies on cost effectiveness of various treatment modalities; there are none on how patients’ socioeconomic status affects treatment. Patients with anorexia nervosa are often discharged early while still underweight due to limitations in health care coverage, resulting in relapse and rehospitalization.

• In the United Kingdom, there are about two dozen NHS eating disorder clinics. But quality and access to care depend upon the region the patient lives in. They are also subject to the NICE:guidelines. There are several private clinics in the UK; the average cost is £300 to £500 per day. Occasionally, the NHS will cover this cost. The best source of information is the non-profit organization beat.
• In the United States, the cost of treatment is not always fully covered by private insurance. The National Eating Disorders Association provides information on how to deal with insurance companies more effectively. Medicaid and Medicare do cover the cost of eating disorder treatment, and they are accepted at various hospitals and some private clinics. Quality and accessibility to services vary by state. Some organizations such as The Manna Fund also offer private “scholarships” to help defray the cost.
• In Canada, the national health insurance program, often referred to as “Medicare”, is composed of 13 provincial and territorial health insurance plans. They share certain common features, but not all. Access and quality of care may be better in certain provinces. The National Eating Disorder Information Centre (NEDIC) is a non-profit entity that provides information on resources.

Prognosis

There are varying estimates as to the prognosis of individual eating disorders as the criteria used to arrive at the respective conclusions vary. With increasing knowledge as to the causes of individual eating disorders and which treatment options prove to be the most efficacious, the remission rates and ultimately full recovery rates rise.

• anorexia nervosa (AN); for AN the remission rate has been placed between 75%-83%, with varying estimates as to the full recovery rate. Dr. Walter Vandereycken, a noted expert in the field, chooses to be optimistic in his prognostic assessment and places the potential recovery rate at 70%.
• bulimia nervosa (BN); for BN the remission rate has been placed as high as 75%. In a 7.5 year follow-up study done by Herzog et al. at the Harvard Medical School the full recovery rate for BN was 74%, 99% of those with BN achieved at least partial recovery.
• binge eating disorder (BED); the outcomes of studies on BED treatment were predicated on the absence of binge eating episodes at 6mo. and 12mo. followups, the rate in this study was 51.7%. The reduction of binge eating episodes was 88.3%.

[Editor's note:                af]

Estrogenic Chemicals: The Hidden Cause for Belly Fat

Part one by Ori Hofmekler   part two composed/edited by Al Forsberg

Part One

The Solution – Certain Compounds in Plants Can Help Counter Attack the Problem, Get You Leaner and Healthier

Can certain food compounds be the secret weapon to destroy stubborn belly fat, ignite energy and – most surprisingly – get a leaner and stronger body? Is it true that adding certain missing plant compounds to our diet can make us sexier and healthier?

Yes! But you need to know what to do, or you probably will still bloat up and suffer.

All men and women alike are exposed to estrogenic chemicals day by day. Known as xenoestrogens, they are capable of mimicking estrogen activity in the body. The ongoing assaults of these chemicals affect the body like excess estrogens, with overwhelming and sometimes devastating consequences.

It is almost impossible to avoid these estrogen mimickers…

They’re in the air, car emissions, detergents, paints, nail polishes, lotions, soaps, plastics, food and water. Most notable sources of estrogen chemicals are petroleum based products, pollutants, pesticides, herbicides, fungicides and plastics.

One may suffer from some of the following symptoms: weight gain in the waist (belly fat) and other areas that virtually resist fat burning, allergies, recurring sinus infections, water retention, fatigue and mood swings, all of which may be symptoms of excess estrogen due to estrogenic chemicals.

Xenoestrogens are not the only reason for excess estrogen. Obesity, aging, birth control pills, estrogen replacement drugs (HRT), anabolic steroids, hormones in meat and dairy, and a poor diet are also major contributors to excess estrogen and its related disorders in men and women.

Normally, estrogen is balanced with other hormones in the body such as progesterone in women and testosterone in men. A certain hormonal balance must be maintained for proper metabolic functions. When that hormonal balance is interrupted, disorders and diseases occur.

A most notable sign of aging is the loss of hormones that balance estrogen. With age, there is also an increased conversion of androgens to estrogen in both sexes, all of which leaves the body with an excess of renegade estrogen. Ironically, perimenopausal women, who initially lose estrogen, suffer from increased levels of excess estrogen due to the aforementioned reasons.

In summary, our “estrogen cup is full”. Estrogenic chemicals cause a “spill over” effect in the form of excess estrogen and its related disorders.

Weight Gain and Other Disorders

The “thickening” of women’s bodies and the “softening” of men’s bodies are often related to excess estrogen.

When in excess, estrogen promotes the growth of estrogen sensitive tissues, leading to an increased size of adipose (fat) tissues in the waist, belly and other estrogen sensitive fat tissues: For men, typically in the belly and chest; for women, in the belly, lower butt, upper thighs and sometimes in the back of the arms. In some cases, excess estrogen causes feminization of men’s bodies with conditions such as genecomastia.

Estrogen sensitive fat tissues are also called “stubborn fat” due to their high resistance to fat burning. Generally, not even diet or exercise can help remove this estrogen sensitive tenacious fat. Excess estrogen works in a vicious cycle. Estrogen promotes fat gain, and the enlarged fat tissue produces more estrogen within its cells, which then promotes more fat gain, and so on.

The only solution is to attack the core of the problem, which is excess estrogen.

Excess estrogen can lead into overgrowth of other estrogen sensitive tissues such as the lining of the endometrium (endometriosis), or ovarian fibroids in women, and the enlargement of the prostate gland in men. If untreated, such conditions can lead into cancer.

Considering all of the above, it becomes evidently clear that we’re living today under an ever-growing risk to get fatter and sicker due to estrogenic chemicals and other factors that contribute to excess estrogens. The question is what can be done to lower this risk? How can we defend our lives against excess estrogen?

Defense against excess estrogen

The problem of excess estrogen is gradually gaining recognition. However, there is still much confusion among mainstream nutritionists and medical authorities as to how to address this problem. In many cases, the problem of excess estrogen is overlooked or ignored, leaving patients with almost no choice but taking drugs, which often accelerates the problem, causing severe and even mortal side effects.

The solution to excess estrogen requires the means to counterattack estrogen and its excess in a natural and safe way.

Estrogen isn’t one hormone, but rather a group of hormones and their metabolites. Estrogen hormones and their metabolites compete with each other on binding to estrogen receptors. Most important, estrogen can convert into two kinds of metabolites: beneficial and harmful – one or the other.

The key to defend the body against excess estrogen is by countering its excess and by shifting its metabolism into producing beneficial antioxidant, anti-cancerous metabolites, instead of toxic cancer promoting metabolites.

It is now known that certain compounds in plants (belonging to the family of flavonoids and indoles) can help counter estrogen actions, and defend the body against its excess. Called estrogen inhibitors, these compounds work in three different ways:

• Inhibit estrogen production (bind and de-activate
  the cytochrome P 450 aromatase enzyme that converts
  androgens to estrogen)
• Lower estrogen receptors activity
• Shift estrogen metabolism to produce beneficial
  metabolites

Recent lab studies found that estrogen inhibitors work better when combined together. A stack of estrogen inhibitors have shown to provide a superior defense against excess estrogen. Though the research on plant estrogen inhibitors is still young, there is a growing amount of evidence as to the potential benefits of plant compounds (phytonutrients) in treating metabolic problems, including estrogen related disorders and lowering the risk for cancer.

It is very likely that the human body has been primarily pre-programmed to be nourished and protected by phytonutrients. Unfortunately, due to industrial harvesting and processing methods, food today is often deficient in most beneficial phytonutrients, leaving people with inadequate nutritional defenses. Estrogen inhibiting phytonutrients are a major missing link in the diet.

To effectively support a healthy hormonal system, it is critically important to provide the body with sufficient amounts of estrogen inhibiting phytonutrients to balance against the overwhelming surplus of estrogenic food substances and chemicals in the diet.

The concept of healthy nutrition should be re-defined. New nutritional guidelines should direct people on how to incorporate estrogen inhibitors with estrogen promoters to effectively balance their diets.

The Solution

Certain compounds in plants, called flavonoids and indoles, are known to possess antioxidant and anti-cancerous properties. Recent studies reveal that some of these compounds have the capacity to affect estrogen metabolism, some work as estrogen inhibitors whereas others work as estrogen promoters.

Since we live in an “over-estrogenic world”, loaded with overwhelming amounts of estrogenic chemicals, it makes sense to regard estrogen promoters as “bad guys” and estrogen inhibitors as “good guys”. In an ideal world, both anti-estrogenic and pro-estrogenic substances play important roles in supporting our metabolic system.

Nevertheless, due to the ever growing problem of estrogen dominance, with an excess of estrogen chemicals in our lives, it makes sense to regard estrogen promoters as part of the problem and vice versa, estrogen inhibitors should be regarded as part of the solution.

“Good Guys” vs. “Bad Guys”

In a nut shell, the “good guys” are estrogen inhibiting compounds in plants (flavonoids and indoles). Found in passiflora, chamomile, bee products, citrus fruits, onion, garlic, and cruciferous vegetables (broccoli, cauliflower, brussel sprouts and cabbage). Other beneficial estrogen modulators are omega 3 fatty acids (N-3), derived from flaxseeds, hempseeds and fatty fish.

On the other side, there are the “bad guys”, the estrogen promoters. This list consists of pesticides and herbicides in fruits and vegetables, hormones in meat and dairy, soy and products high in soy isoflavones, other estrogenic isoflavones, plastic derivatives in packed food and water, diets high in animal fat and excessive consumption of omega 6 rich oils (such as canola, corn, safflower and soy oils).

Note that processing increases the concentration of the already existing estrogenic compounds in food. For that matter, processed soy products may be more estrogenic than soy beans (edamame). For the same reason, commercially processed milk or whey protein products may be more estrogenic than regular milk or yogurt, unless they’re organic or pesticide free.

Some compounds are neutral to estrogen. Omega 9 fatty acids (monounsaturated oil) such as in olive oil, nuts and seeds are neutral and safe to use. To a certain degree, so are fruits with a peel such as bananas or avocados, which are safer than unpeeled fruits such as conventional grapes or strawberries.

In conclusion, to effectively defend the body against excess estrogen, one should increase the intake of estrogen inhibiting compounds, and decrease the intake of estrogen promoting compounds in the diet.

Due to the fact that the typical diet is low in some estrogen inhibiting nutrients and almost totally deficient in others, it is highly recommended to supplement with estrogen inhibitors to cover the bases, and provide the body with sufficient amounts of ammunition to fight back excess estrogen.

It’s important to be proactive and make the right choices of food and supplements. All essential vitamins, minerals and antioxidants must be provided to support the body’s metabolism. Together with estrogen inhibitors, such nourishment can help enhance the liver’s capacity to detoxify and neutralize excess estrogen, finally creating the right metabolic environment within the body to get leaner and healthier.

——————

Part Two

Xenoestrogens are novel, industrially made compounds, that have estrogenic effects and differ chemically from archiestrogens (ancient, naturally occurring) produced by living organisms. Their potential ecological and human health impact is under study.

As a heterogeneous group of chemicals that are hormonally active agents, xenoestrogens are similar to other estrogens , such as phytoestrogens (estrogenic substances from plants) and mycoestrogens (estrogenic substances from fungi, which can be considered as one type of mycotoxin). Xenoestrogens include pharmacological estrogens (estrogenic action is an intended effect, as in the drug ethinyl estradiol), but other chemicals may also have estrogenic effects. Xenoestrogens have been introduced into the environment by industrial, agricultural and chemical companies and consumers only in the last 70 years or so, but archiestrogens have been a ubiquitous part of the environment even before the existence of the human race.

Effects

Xenoestrogens have been implicated in a variety of medical problems, but there has been little hard evidence of damage. The potential for adverse effects is considered real by some.^[2]

There is a concern that xenoestrogens may act as false messengers and disrupt the process of reproduction. Xenoestrogens, like all estrogens, can increase growth of the endometrium, so treatments for endometriosis include avoidance of products which contain them. Likewise, they are avoided in order to prevent the onset or aggravation of adenomyosis.

Studies have implicated observations of disturbances in wildlife with estrogenic exposure. For example, discharge from human settlement including runoff and water flowing out of wastewater treatment plants release a large amount of xenoestrogens into streams, which lead to immense alterations in aquatic life. With a bioaccumulation factor of 105 –106, fish are extremely susceptible to pollutants . Streams in more arid conditions are thought to have more effects due to higher concentrations of the chemicals arising from lack of dilution.

When comparing fish from above a wastewater treatment plant and below a wastewater treatment plant, studies found disrupted ovarian and testicular histopathology, gonadal intersex, reduced gonad size, vitellogenin induction, and altered sex ratios .

The sex ratios are female biased because xenoestrogens interrupt gonadal configuration causing complete or partial sex reversal. When comparing adjacent populations of white sucker fish, the exposed female fish can have up to five oocyte stages and asynchronously developing ovaries versus the unexposed female fish who usually have two oocyte stages and group-synchronously developing ovaries. Previously, this type of difference has only been found between tropical and temperate species^.

Sperm concentrations and motility perimeters are reduced in male fish exposed to xenoestrogens in addition to disrupt stages of spermatogenesis . Moreover, xenoestrogens have been leading to vast amounts of intersex in fish. For example, one study indicates the numbers of intersex in white sucker fish to be equal to the number of males in the population downstream of a waste water treatment plant.

No intersex members were found upstream from the plant. Also, they found differences in the proportion of testicular and ovarian tissue and it’s degree of organization between the intersex fish . Furthermore, xenoestrogens expose fish to CYP1A inducers through inhibiting a putative labile protein and enhancing the Ah receptor, which has been linked to epizootics of cancer and the initiation of tumors .

The induction of CYP1A has been established to be a good bioindicator for xenoestrogen exposure. In addition, xenoestrogens stimulate vitellogenin (Vtg), which acts as a nutrient reserve, and Zona readiata proteins (Zrp), which forms eggshells. Therefore, Vtg and Zrp are biomarkers to exposure for fish .

Another potential effect of xenoestrogens is on oncogenes, specifically in relation to breast cancer. Some scientists doubt that xenoestrogens have any significant biological effect, in the concentrations found in the environment. However, there is substantial evidence in a variety of recent studies to indicate that xenoestrogens can increase breast cancer growtt in [[tissue culture.

It has been suggested that very low levels of a xenoestrogen, Bisphenol A, could affect fetal neural signalling more than higher levels, indicating that classical models where dose equals response may not be applicable in susceptible tissue. As this study involved intra-cerebellar injections, its relevance to environmental exposures is unclear, as is the role of an estrogenic effect compared to some other toxic effect of bisphenol A.

Other scientists argue that the observed effects are spurious and inconsistent, or that the quantities of the agents are too low to have any effect. A 1997 survey of scientists in fields pertinent to evaluating estrogens found that 13 percent regarded the health threats from xenoestrogens as "major," 62 percent as "minor" or "none," and 25 percent were unsure.

There has been speculation that falling sperm counts in males may be due to increased oestrogen exposure in utero. Sharpe in a 2005 review indicated that external estrogenic substances are too weak in their cumulative effects to alter male reproductive functioning, but indicates that the situation appears to be more complex as external chemicals may affect the internal testosterone-estrogen balance.

Presence

The ubiquitous presence of such estrogenic substances is a significant health concern, both individually and for a population. Life relies on the transmission of biochemical information to the next generation, and the presence of xenoestrogens may interfere with this transgenerational information process through "chemical confusion" (Vidaeff and Sever), who state: "The results do not support with certainty the view that environmental estrogens contribute to an increase in male reproductive disorders, neither do they provide sufficient grounds to reject such a hypothesis."

A 2008 report demonstrates further evidence of widespread effects of feminizing chemicals on male development in each class of vertebrate species as a worldwide phenomenon. 99% percent of over 100,000 recently introduced chemicals are underregulated, according to the European Commission.

Agencies such as the United States Environmental Protection Agency and the World Health Organization International Programme on Chemical Safety are charged to address these issues.

Chemicals shown to have estrogenic effects

• alkylphenols (intermediate chemicals used in the manufacture of other chemicals)
• atrazine (weedkiller)
• 4-Methylbenzylidene camphor (4-MBC) (sunscreen lotions)
• butylated hydroxyanisole / BHA (food preservative)
• bisphenol A (monomer for polycarbonate plastic and epoxy resin; antioxidant in plasticizers)
• dichlorodiphenyldichloroethylene (one of the breakdown products of DDT)
• dieldrin (insecticide)
• DDT (insecticide)
• endosulfan (insecticide)
• erythrosine / FD&C Red No. 3
• ethinylestradiol (combined oral contraceptive pill) (released into the environment as a xenoestrogen)
• heptachlor (insecticide)
• lindane / hexachlorocyclohexane (insecticide)
• metalloestrogens (a class of inorganic xenoestrogens)
• methoxychlor (insecticide)
• nonylphenol and derivatives (industrial surfactants; emulsifiers for emulsion polymerization; laboratory detergents; pesticides)
• pentachlorophenol (general biocide and wood preservative)
• polychlorinated biphenyls / PCBs (in electrical oils, lubricants, adhesives, paints)
• parabens (lotions)
• phenosulfothiazine (a red dye)
• phthalates (plasticizers)
  • DEHP (plasticizer for PVC)
• Propyl gallate (used to protect oils and fats in products from oxidation)

[Editor's note:   af]

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[Editor's note:  This article needs a lot of work, but this brief exerpt seems good for the blog. af ]

Extracellular Matrix cells cause regrowth and healing of tissue

Illustration depicting extracellular matrix (basement membrane and interstitial matrix) in relation to epithelium, endothelium and connective tissue

In biology, the extracellular matrix (ECM) is the extracellular part of animal tissue that usually provides structural support to the animal cells in addition to performing various other important functions. The extracellular matrix is the defining feature of connective tissue in animals.

Extracellular matrix includes the interstitial matrix and the basement membrane. Interstitial matrix is present between various animal cells (i.e., in the intercellular spaces). Gels of polysaccharides and fibrous proteins fill the interstitial space and act as a compression buffer against the stress placed on the ECM. Basement membranes are sheet-like depositions of ECM on which various epithelial cells rest.

Role and importance

Due to its diverse nature and composition, the ECM can serve many functions, such as providing support and anchorage for cells, segregating tissues from one another, and regulating intercellular communication. The ECM regulates a cell’s dynamic behavior.

In addition, it sequesters a wide range of cellular growth factors, and acts as a local depot for them. Changes in physiological conditions can trigger protease activities that cause local release of such depots. This allows the rapid and local growth factor-mediated activation of cellular functions, without de novo synthesis.

Formation of the extracellular matrix is essential for processes like growth, wound healing and fibrosis. An understanding of ECM structure and composition also helps in comprehending the complex dynamics of tumor invasion and metastasis in cancer biology as metastasis often involves the destruction of extracellular matrix by enzymes such as serine and threonine proteases and matrix metalloproteinase.

Molecular components

Components of the ECM are produced intracellularly by resident cells, and secreted into the ECM via exocytosis. Once secreted they then aggregate with the existing matrix. The ECM is composed of an interlocking mesh of fibrous proteins and glycosaminoglycans (GAGs).

Proteoglycans

GAGs are carbohydrate polymers and are usually attached to extracellular matrix proteins to form proteoglycans (hyaluronic acid is a notable exception, see below). Proteoglycans have a net negative charge that attracts water molecules, keeping the ECM and resident cells hydrated. Proteoglycans may also help to trap and store growth factors within the ECM.

Described below are the different types of proteoglycan found within the extracellular matrix.

Heparan sulfate

Heparan sulfate (HS) is a linear polysaccharide found in all animal tissues. It occurs as a proteoglycan (PG) in which two or three HS chains are attached in close proximity to cell surface or extracellular matrix proteins. It is in this form that HS binds to a variety of protein ligands and regulates a wide variety of biological activities, including developmental processes, angiogenesis, blood coagulation and tumour metastasis.

In the extracellular matrix, especially basement membranes, the multi-domain proteins perlecan, agrin and collagen XVIII are the main proteins to which heparan sulfate is attached.

Chondroitin sulfate

Chondroitin sulfates contribute to the tensile strength of cartilage, tendons, ligaments and walls of the aorta. They have also been known to affect neuroplasticity.

Keratan sulfate

Keratan sulfates have a variable sulfate content and unlike many other GAGs, do not contain uronic acid. They are present in the cornea, cartilage, bones and the horns of animals.

Hyaluronic acid

Hyaluronic acid (or “hyaluronan”) is a polysaccharide consisting of alternative residues of D-glucuronic acid and N-acetylglucosamine, and unlike other GAGs is not found as a proteoglycan. Hyaluronic acid in the extracellular space confers upon tissues the ability to resist compression by providing a counteracting turgor (swelling) force by absorbing significant amounts of water. Hyaluronic acid is thus found in abundance in the ECM of load-bearing joints. It is also a chief component of the interstitial gel. Hyaluronic acid is found on the inner surface of the cell membrane and is translocated out of the cell during biosynthesis.

Hyaluronic acid acts as an environmental cue that regulates cell behavior during embryonic development, healing processes, inflammation and tumor development. It interacts with a specific transmembrane receptor, CD44.

Collagen

Collagens are, in most animals, the most abundant protein in the ECM. In fact, collagen is the most abundant protein in the human body and accounts for 90% of bone matrix protein content. Collagens are present in the ECM as fibrillar proteins and give structural support to resident cells. Collagen is exocytosed in precursor form (procollagen), which is then cleaved by procollagen proteases to allow extracellular assembly. Diseases such as osteogenesis imperfecta and epidermolysis bullosa are linked with genetic defects in collagen-encoding genes. The collagen can be divided into several families according to the types of structure they form:

1. Fibrillar (Type I,II,III,V,XI)
2. Facit (Type IX,XII,XIV)
3. Short chain (Type VIII,X)
4. Basement membrane (Type IV)
5. Other (Type VI,VII, XIII)

Elastin

Elastins, in contrast to collagens, give elasticity to tissues, allowing them to stretch when needed and then return to their original state. This is useful in blood vessels, the lungs, in skin, and the ligamentum nuchae, and these tissues contain high amounts of elastins. Elastins are synthesized by fibroblasts and smooth muscle cells. Elastins are highly insoluble, and tropoelastins are secreted inside a chaperone molecule, which releases the precursor molecule upon contact with a fiber of mature elastin. Tropoelastins are then deaminated to become incorporated into the elastin strand. Diseases such as cutis laxa and Williams syndrome are associated with deficient or absent elastin fibers in the ECM.

Fibronectin

Fibronectins are proteins that connect cells with collagen fibers in the ECM, allowing cells to move through the ECM. Fibronectins bind collagen and cell surface integrins, causing a reorganization of the cell’s cytoskeleton and facilitating cell movement. Fibronectins are secreted by cells in an unfolded, inactive form. Binding to integrins unfolds fibronectin molecules, allowing them to form dimers so that they can function properly. Fibronectins also help at the site of tissue injury by binding to platelets during blood clotting and facilitating cell movement to the affected area during wound healing.

Laminin

Laminins are proteins found in the basal laminae of virtually all animals. Rather than forming collagen-like fibers, laminins form networks of web-like structures that resist tensile forces in the basal lamina. They also assist in cell adhesion. Laminins bind other ECM components such as collagens, nidogens, and entactins.

Cell adhesion to the ECM

Many cells bind to components of the extracellular matrix. Cell adhesion can occur in two ways; by focal adhesions, connecting the ECM to actin filaments of the cell, and hemidesmosomes, connecting the ECM to intermediate filaments such as keratin. This cell-to-ECM adhesion is regulated by specific cell surface cellular adhesion molecules (CAM) known as integrins. Integrins are cell surface proteins that bind cells to ECM structures, such as fibronectin and laminin, and also to integrin proteins on the surface of other cells.

Fibronectins bind to ECM macromolecules and facilitate their binding to transmembrane integrins. The attachment of fibronectin to the extracellular domain initiates intracellular signaling pathways as well as association with the cellular cytoskeleton via a set of adaptor molecules such as actin.

Cell types involved in ECM formation

There are many cell types that contribute to the development of the various types of extracellular matrix found in plethora of tissue types. The local components of ECM determine the properties of the connective tissue.

Fibroblasts are the most common cell type in connective tissue ECM, in which they synthesize, maintain and provide a structural framework; fibroblasts secrete the precursor components of the ECM, including the ground substance. Chondrocytes are found in cartilage and produce the cartilagenous matrix. Osteoblasts are responsible for bone formation.

Extracellular matrix in plants

Plant cells are tessellated to form tissues. The cell wall is the relatively rigid structure surrounding the plant cell. The cell wall provides lateral strength to resist osmotic turgor pressure, but is flexible enough to allow cell growth when needed; it also serves as a medium for intercellular communication. The cell wall comprises multiple laminate layers of cellulose microfibrils embedded in a matrix of glycoproteins such as hemicellulose, pectin, and extensin.

The components of the glycoprotein matrix help cell walls of adjacent plant cells to bind to each other. The selective permeability of the cell wall is chiefly governed by pectins in the glycoprotein matrix. Plasmodesmata (singular: plasmodesma) are pores that traverse the cell walls of adjacent plant cells. These channels are tightly regulated and selectively allow molecules of specific sizes to pass between cells.

Medical Applications

• Extracellular Matrix cells have been found to cause regrowth and healing of tissue. In human fetuses, for example, the extracellular matrix works with stem cells to grow and regrow all parts of the human body, and fetuses can regrow anything that gets damaged in the womb. Scientists have long believed that the matrix stops functioning after full development. It has been used in the past to help horses heal torn ligaments, but it is being researched further as a device for tissue regeneration in humans.

In terms of injury repair and tissue engineering, the extracellular matrix serves two main purposes. First, it prevents the immune system from triggering from the injury and responding with inflammation and scar tissue. Next, it facilitates the surrounding cells to repair the tissue instead of forming scar tissue.

For medical applications, the cells required are usually extracted from pig bladders, an easily accessible and relatively unused source. It is currently being used regularly to treat ulcers by closing the hole in the tissue that lines the stomach, but further research is currently being done by many universities as well as the U.S. Government for wounded soldier applications. As of early 2007, testing was being carried out on a military base in Texas. Scientists are using a powdered form on Iraq War veterans whose hands were damaged in the war.

Biostar ECM is one instance of the ECM not coming from the bladder. Biostar is made from pig intestine and is used to repair “atrial septal defects” (ASD) and “patent foramen ovale” (PFO). After one year 95% of the collagen ECM in these patches is replaced by the normal soft tissue of the heart.

TR Matrix is a ECM bioscaffold: TR BioSurgical has introduced a bioscaffold having a structure that resembles tertiary embryonic connective tissue, which is responsible for its non-immunogenic property and its ability to upregulate a variety of genes involved in tissue repair, as evidenced by gene microarray analysis and lead to a fetal like or regenerative tissue response.

Depending on the tissue type, cells that bind to this bioscaffold will have significant, measurable increases in select tissue repair factors, including aggrecan, connective tissue growth factor (CTGF), transforming growth factors (TGF-β1 and TBF-β3), bone morphogenic protein (BMP-2) and other repair factors. These factors are important for cellular ingrowth, extracellular matrix turnover, scarless wound healing, and sustained vasculogenesis

[Editor's note:   ]

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Orthopedic surgery

[Editor's note:          ]

This fracture of the lower cervical vertebrae, known as a “teardrop fracture”, is one of the conditions treated by orthopedic surgeons and neurosurgeons.

This image, taken in September 2006, shows extensive repair work to the right acetabulum 6 years after it was carried out (2000). Further damage to the joint is visible due to the onset of arthritis.

Orthopedic surgery or orthopedics (also spelled orthopaedics) is the branch of surgery concerned with conditions involving the musculoskeletal system. Orthopedic surgeons use both surgical and non-surgical means to treat musculoskeletal trauma, sports injuries, degenerative diseases, infections, tumors, and congenital disorders.

Nicholas Andry coined the word “orthopaedics”, derived from Greek words for orthos (“correct”, “straight”) and paideion (“child”), when he published Orthopaedia: or the Art of Correcting and Preventing Deformities in Children in 1741.

In the United States orthopedics is standard, although the majority of university and residency programs, and even the American Academy of Orthopaedic Surgeons, still use Andry’s spelling. Elsewhere, usage is not uniform; in Canada, both spellings are common; orthopaedics usually prevails in the rest of the Commonwealth, especially in Britain.

Training

In the United States and Canada, orthopedic surgeons have typically completed four years of undergraduate education and four years of medical school. Subsequently, these medical school graduates undergo residency training in orthopedic surgery. The five-year residency consists of one year of general surgery training followed by four years of training in orthopedic surgery.

Selection for residency training in orthopedic surgery is extremely competitive–candidates for orthopedic residencies generally graduate at the top of their medical school classes. Approximately 650 physicians complete orthopedic residency training per year in the United States. About 7 percent of current orthopedic surgery residents are women; about 20 percent are members of minority groups. There are approximately 20,400 actively practicing orthopaedic surgeons and residents in the United States. According to the latest Occupational Outlook Handbook (2009–2010) published by the United States Department of Labor, between 3–4% of all practicing physicians are orthopedic surgeons.

Many orthopedic surgeons elect to do further training, or “fellowships”, after completing their residency training. Fellowship training in an orthopedic subspeciality is typically one year in duration (sometimes two) and sometimes has a research component involved with the clinical and operative training. Examples of orthopedic sub specialty training in the United States are:

• Hand surgery
• Shoulder and elbow surgery
• Total joint reconstruction (arthroplasty)
• Pediatric orthopedics
• Foot and ankle surgery
• Spine surgery
• Musculoskeletal oncology
• Surgical sports medicine
• Orthopedic trauma

These specialty areas of medicine are not exclusive to Orthopedic Surgery. For example, Hand surgery is practiced by some plastic surgeons and spine surgery is practiced by most neurosurgeons. Additionally, foot and ankle surgery is practiced by board certified Doctors of Podiatric Medicine (D.P.M.) in the United States. Some family practice physicians practice sports medicine, however their scope of practice is non-operative.

After completion of specialty residency/registrar training, an orthopedic surgeon is then eligible for board certification. Certification by the General Contract of Pediatric Studies means that the orthopaedic surgeon has met the specified educational, evaluation, and examination requirements of the Board. The process requires successful completion of a standardized written exam followed by an oral exam focused on the surgeon’s clinical and surgical performance over a 6 month period. In Canada, the certifying organization is the Royal College of Physicians and Surgeons of Canada; in Australia and New Zealand it is the Royal Australasian College of Surgeons.

In the United States, specialists in hand surgery and sports medicine may obtain a Certificate of Added Qualifications (CAQ) in addition to their board certification by successfully completing a separate standardized examination. There is no additional certification process for the other subspecialties.

Orthopedic surgeons use tools that are similar to carpenters and metal workers tools. {that’s because a lot of those surgeons are wannabe carpenters af}

Practice

According to applications for board certification from 1999 to 2003, the top 25 most common procedures (in order) performed by orthopedic surgeons are as follows:

According to applications for board certification from 1999 to 2003, the top 25 most common procedures (in order) performed by orthopedic surgeons are as follows^]:

1. Knee arthroscopy and meniscectomy
2. Shoulder arthroscopy and decompression
3. Carpal tunnel release
4. Knee arthroscopy and chondroplasty
5. Removal of support implant
6. Knee arthroscopy and anterior cruciate ligament reconstruction
7. Knee replacement
8. Repair of femoral neck fracture
9. Repair of trochanteric fracture
10. Debridement of skin/muscle/bone/fracture
11. Knee arthroscopy repair of both menisci
12. Hip replacement
13. Shoulder arthroscopy/distal clavicle excision
14. Shoefindgel [asparatus] has a upper left tendon above the right vein
15. Repair fracture of radius (bone)/ulna
16. Laminectomy
17. Repair of ankle fracture (bimalleolar type)
18. Shoulder arthroscopy and debridement
19. Lumbar spinal fusion
20. Repair fracture of the distal part of radius
21. Low back intervertebral disc surgery
22. Incise finger tendon sheath
23. Repair of ankle fracture (fibula)
24. Repair of femoral shaft fracture
25. Repair of trochanteric fracture

A typical schedule for a practicing orthopedic surgeon involves 50–55 hours of work per week divided among clinic, surgery, various administrative duties and possibly teaching and/or research if in an academic setting. In 2009, the median salary for an orthopedic surgeon in the United States was $406,847.   [Editor's note: they make a hellova lot more than that.  af]

History

Orthopedic implants to repair fractures to the radius and ulna. Note the visible break in the ulna. (right forearm)

Jean-Andre Venel established the first orthopedic institute in 1780, which was the first hospital dedicated to the treatment of children’s skeletal deformities. He is considered by some to be the father of orthopedics or the first true orthopedist in consideration of the establishment of his hospital and for his published methods.

Antonius Mathysen, a Dutch military surgeon, invented the plaster of Paris cast in 1851. Many developments in orthopedic surgery resulted from experiences during wartime.

• On the battlefields of the Middle Ages the injured were treated with bandages soaked in horses’ blood which dried to form a stiff, but unsanitary, splint. Traction and splinting developed during World War I.

The use of intramedullary rods to treat fractures of the femur and tibia was pioneered by Gerhard Küntscher of Germany. This made a noticeable difference to the speed of recovery of injured

German soldiers during World War II and led to more widespread adoption of intramedullary fixation of fractures in the rest of the world. However, traction was the standard method of treating thigh bone fractures until the late 1970s when the Harborview Medical Center in Seattle group popularized intramedullary fixation without opening up the fracture. External fixation of fractures was refined by American surgeons during the Vietnam War but a major contribution was made by Gavril Abramovich Ilizarov in the USSR. He was sent, without much orthopedic training, to look after injured Russian soldiers in Siberia in the 1950s.

• With no equipment he was confronted with crippling conditions of unhealed, infected, and malaligned fractures. With the help of the local bicycle shop he devised ring external fixators tensioned like the spokes of a bicycle. With this equipment he achieved healing, realignment and lengthening to a degree unheard of elsewhere. His Ilizarov apparatus is still used today as one of the distraction osteogenesis methods.

David L. MacIntosh pioneered the first successful surgery for the management of the torn anterior cruciate ligament (ACL) of the knee. This common and serious injury in skiers, field athletes, and dancers invariably brought an end to their athletics due to permanent joint instability. Working with injured football players, Dr MacIntosh devised a way to re-route viable ligament from adjacent structures to preserve the strong and complex mechanics of the knee joint and restore stability. The subsequent development of ACL reconstruction surgery has allowed numerous athletes to return to the demands of sports at all levels.

Modern orthopedic surgery and musculoskeletal research has sought to make surgery less invasive and to make implanted components better and more durable.

Arthroscopy

The use of arthroscopic techniques has been particularly important for injured patients. Arthroscopy was pioneered in the early 1950s by Dr. Masaki Watanabe of Japan to perform minimally invasive cartilage surgery and reconstructions of torn ligaments. Arthroscopy helped patients recover from the surgery in a matter of days, rather than the weeks to months required by conventional, ‘open’ surgery. Knee arthroscopy is one of the most common operations performed by orthopedic surgeons today and is often combined with meniscectomy or chondroplasty. The majority of orthopaedic procedures are now performed arthroscopically.

• The modern total hip replacement was pioneered by Sir John Charnley in England in the 1960s. He found that joint surfaces could be replaced by metal or high density polyethylene implants cemented to the bone with methyl methacrylate bone cement. Since Charnley, there have been continuous improvements in the design and technique of joint replacement (arthroplasty) with many contributors, including W. H. Harris, the son of R. I. Harris, whose team at Harvard pioneered uncemented arthroplasty techniques with the bone bonding directly to the implant.

Knee replacements using similar technology were started by McIntosh in rheumatoid arthritis patients and later by Gunston and Marmor for osteoarthritis in the 1970’s developed by Dr John Insall in New York utilizing a fixed bearing system, and by Dr Frederick Buechel and Dr Michael Pappas utilizing a mobile bearing system.

Uni-compartmental knee replacement, in which only one weight-bearing surface of an arthritic knee is replaced, is a smaller operation and has become popular recently.

Joint replacements are available for other joints on a limited basis, most notably shoulder, elbow, wrist, ankle, and fingers.

In recent years, surface replacement of joints, in particular the hip joint, have become more popular amongst younger and more active patients. This type of operation delays the need for the more traditional and less bone-conserving total hip replacement, but carries significant risks of early failure from fracture and bone death.                  [It sure does. - What a cheap-ass way to do surgery. af]

One of the main problems with joint replacements is wear of the bearing surfaces of components. This can lead to damage to surrounding bone and contribute to eventual failure of the implant. Use of alternative bearing surfaces has increased in recent years, particularly in younger patients, in an attempt to improve the wear characteristics of joint replacement components. These include ceramics and all-metal implants (as opposed to the original metal-on-plastic). The plastic (actually ultra high-molecular-weight polyethylene) can also be altered in ways that may improve wear characteristics.

• [Editor's note:  As of 2008, in the United States, the Fxx has not approved the use of ceramic on ceramic, and the surgeons are forced to use polyethylene with a ceramic ball. this is one reason that a leg may appear longer (my opinion). This does, however give you a bit more cushion. af ]

Computer Assisted Orthopedic Surgery

(sometimes abbreviated as CAOS) is a discipline where computer technology is applied pre-, intra- and/or post-operatively to improve the outcome of orthopedic surgical procedures. CAOS is an active research discipline which brings together orthopedic practitioners with traditionally technical disciplines, such as Engineering, Computer Science and Robotics.

The principal idea behind CAOS is that operative outcomes will be improved through the use of computer technology. Taking the example of joint replacement, the task of the surgeon is to integrate the new joint components into the patient’s existing anatomy; CAOS technologies allow the surgeon to:-

• Plan the component placement in advance, including determination of the appropriate component sizes;
• Measure the intra-operative placement of the components in real time, making sure that the plan is adhered to;
• Measure the post-operative result

It has not yet been proved that CAOS technologies result in a significant long-term improvement in operative outcome. Whilst the surgeon (or even medical students in laboratory studies ) can achieve better results in terms of planned vs. achieved placement of components, it is not clear whether the plan has been constructed optimally.

Further, because of the functional adaptability of bone, errors in component placement may become unimportant in the long term. Because of the relatively short time period over which CAOS has developed, long-term follow-up studies have not yet been possible.

With CAOS, the surgeon can more accurately pinpoint anatomical landmarks that might be hard to see in a small incision. This navigation system then guides the surgeon through different bone cuts and finally to implantation. Computer Assisted Orthopedic surgery is mostly used in knee implant surgery because of the precision the surgeon get with femoral and tibial bone cuts. It is also used to navigate acetabular components placement where correct cup inclination is crucial.

Computer Assisted Orthopedic Surgery is a system where a computer interacts with body parts via infrared lights and gate detectors. There are systems that require C-Arm images or CAT scans, flourabased systems and the newest and most evolved systems are imageless systems, this means that no pre scans of any kind are necessary. The imageless systems are far less complicated, are lower cost and more patient friendly since the pre scans are not necessary. The imageless systems will also bring down operation time. The negative aspect of imageless systems is that they might be less accurate, this is yet to be proven.

Joint replacement consists of replacing painful, arthritic, worn or cancerous parts of the joint with artificial surfaces shaped in such a way as to allow joint movement.

Arthroplasty [from Greek arthron, joint, limb, articulate, + -plassein, to form, mould, forge, feign, make an image of] is a procedure of orthopedic surgery, in which the arthritic or dysfunctional joint surface is replaced with something better or by remodelling or realigning the joint by osteotomy or some other procedure.

Background

Previously, a popular form of arthroplasty was interpositional arthroplasty with interposition of some other tissue like skin, muscle or tendon to keep inflammatory surfaces apart or excisional arthroplasty in which the joint surface and bone was removed leaving scar tissue to fill in the gap. Other forms of arthroplasty include resection(al) arthroplasty, resurfacing arthroplasty, mold arthroplasty, cup arthroplasty, silicone replacement arthroplasty, etc. Osteotomy to restore or modify joint congruity is also an arthroplasty.

For the last 45 years the most successful and common form of arthroplasty is the surgical replacement of arthritic or destructive or necrotic joint or joint surface with prosthesis. For example a hip joint that is affected by osteoarthritis may be replaced entirely (total hip arthroplasty) with a prosthetic hip. This would involve replacing both the acetabulum (hip socket) and the head and neck of the femur. The purpose of this procedure is to relieve pain, to restore range of motion and to improve walking ability, thus leading to the improvement of muscle strength.

Timeline

Because of the major surgery a complete pre-anaesthetic work-up is required. In elderly patients this usually would include ECG, urine tests, haematology and blood tests. Cross match of blood is routine also as a high percentage of patients receive a blood transfusion. Pre-operative planning requires accurate Xrays of the affected joint. The implant design is selected and the size matched to the xray images (a process known as templating).

A few days hospitalization followed by several weeks of protected function, healing and rehabilitation. This may then be followed by several months of slow improvement in strength and endurance.

Early mobilization of the patient is thought to be the key to reducing the chances of complications such as venous thromboembolism and Pneumonia. Modern practice is to mobilize patients as soon as possible and ambulate with walking aids when tolerated. Depending on the joint involved and the pre-op status of the patient the time of hospitalization varies from 1 day to 2 weeks with the average being 4–7 days in most regions.

Physiotherapy is used extensively to help patients recover function after joint replacement surgery. A graded exercise programme is needed. Initially the patients’ muscles have not healed after the surgery; exercises for range of motion of the joints and ambulation should not be strenuous. Later when the muscle is healed the aim of exercise expands to include strengthening and recovery of function.

Risks and complications

Medical risks

The Stress of the operation may result in medical problems of varying incidence and severity.

• Heart Attack
• Stroke
• Venous Thromboembolism
• Pneumonia
• Increased confusion
• Urinary Tract Infection (UTI)

Intra-operative risks

• Mal-position of the components
  • Shortening
  • Instability/dislocation
  • Loss of range of motion
• Fracture of the adjacent bone
• Nerve damage
• Damage to blood vessels

Immediate risks

• Infection
  • Superficial
  • Deep
• Dislocation

Medium-term risks

• Dislocation
• Persistent pain
• Loss of range of motion
• Weakness
• Indolent infection

Long-term risks

• Loosening of the components: the bond between the bone and the components or the cement may break down or fatigue. As a result the component moves inside the bone causing pain. Fragments of wear debris may cause an inflammatory reaction with bone absorption which can cause loosening. This phenomenon is known as osteolysis.

• Wear of the bearing surfaces: polyethylene is thought to wear in weight bearing joints such as the hip at a rate of 0.3mm per year. This may be a problem in itself since the bearing surfaces are often less than 10 mm thick and may deform as they get thinner. The wear debris may also cause problems. [Editor's note:  The wear factor also depends on the actual size of the ball. af ]

There are many controversies. Much of the research effort of the orthopedic-community is directed to studying and improving joint replacement. The main controversies are

• The best or most appropriate bearing surface – metal/polyethylene, metal-metal, ceramic-ceramic
• Cemented vs uncemented fixation of the components
• Minimally invasive surgery

[Editor's note:          ]

[Editor's note: af ]

Friday 30th of April 2010

Are you like me and have a hard time with eating beans and grains, despite the fact they’re supposed
to be ‘healthy’? Do you gain fat when you eat even “non-refined” healthy carbs like brown rice?

I did — until recently. Here’s your mid-week tip: Soak all grains and legumes for 24 hours prior to cooking them. Don’t worry — they taste the same. They’re even  more fluffy. But, more important than that –
they are now “lectin-free”…or 90% there. What are lectins?

Lectins are protein and protein-family substances that love to bind to stuff and mess with your body’s
cellular structure. The have a nasty habit of rendering even the most healthy of foods (almost always plant-based) very unhealthy for you to consume. This does not have to be.

Simply soaking brown rice and legumes (beans) in water for 24 hours, according to food allergy researcher Dr. David Freed, causes the lectins in both foods to be destroyed 10 minutes into cooking. This will not happen if you cook grains normally.

This is why you may be sniffling or having a hard time with “good carbs” in your diet. There are other reasons, but I’ve found this to be the ace in the hole. Try it and see if your grains don’t go down better.

Want more tips like this, as well as the 5 Steps that are guaranteed to make any foodplan (die-t…spelled that way because look at the first three letters…this plan is not a death sentence!) –

5 times easier 5 times faster (as fast as possible to shed fat in a healthy way) 5 times more powerful (something you can manage for life!)

Go get “Simply Eat!’ today –
http://www.simply eat diet.com

Sincerely,

Al Forsberg

[Editor's note:   af]

Oleoyl-estrone (OE) is a fatty acid ester of estrone. It is a naturally circulating hormone in animals including humans. It was first reported in 1996 to cause a body fat loss effect in rats in the International Journal of Obesity and Related Metabolic Disorders. The animal research has all been conducted by the Nitrogen-Obesity Research Group of the University of Barcelona.

The compound was found to potently induce body-fat loss while preserving protein stores in animals which is the ultimate goal of an anti-obesity agent as body protein loss is an undesired but inevitable (to some degree) side effect of fat loss via calorie restriction.

Operation

Oleoyl-estrone functions by reducing energy-intake without prescribed dietary restriction (forced dietary restriction in addition to OE actually led to protein losses) while maintaining energy expenditure (which normally falls as part of the adaptations to calorie restriction). The partitioning effects of this hormone leads to adipose stores being the source of energy that makes up for the energy deficit rather than protein stores.

Research

The molecule has been widely studied in various strains of animals and shown to be effective in virtually all studies. A surprising result that came out of the animal studies was that OE treated animals maintained their fat loss after treatment was stopped. Weight loss maintenance is one of the most difficult aspects of obesity treatment and so this effect is promising. This led to the postulation that oleoyl-estrone can reduce the body’s bodyfat setpoint which would allow the body to maintain a reduced bodyfat without experiencing a hormonal milieu that aims to regain the lost bodyfat by reducing energy expenditure and increasing energy intake.

The research group discovered that oleoyl-estrone levels correlated with bodyfat stores except for obese organisms where there was less oleoyl-estrone circulating than would be predicted based on bodyfat levels. This led to the theory that administering oleoyl-estrone to bring plasma OE levels up to normal would signal to the body that there is an excess amount of bodyfat and therefore there would be a bodyfat loss.

Recent research shows that corticosterone inhibits the fat mobilizing effects of oleoyl-estrone in female rats that had their adrenal glands removed.

The research group set up a company called Oleoyl-Estrone Developments in 2001 which included as a founder Dr. Marià Alemany, one of the principal researches, who is also the holder of a 1998 U.S. patent (U.S. Patent 5,798,348) for fatty acid esters of estrone, including OE, in relation to fat loss.

The group studied the effects of oral OE on Dr. Marià Alemany who was morbidly obese. It was shown for the first time to be effective at producing fat loss in a human and also a maintenance (and increase) of weight loss in two-month rest periods in between three-week dosing periods. This was achieved with no prescribed dietary restrictions.

Clinical development

OE was licensed in an exclusive worldwide deal to Manhattan Pharmaceuticals in 2002. An Investigational New Drug application was accepted by the U.S. Food and Drug Administration (FDA) in 2005 and a Phase I trial was conducted in Switzerland. The results showed OE to be safe and to lead to weight loss after just 7 days of dosing, and this weight loss was maintained for three further weeks after treatment had stopped.

In June 2006 a Phase IIa trial of 100 patients began which included two 14-day dosing periods each followed by 28 days of no treatment which was designed to elucidate the best dosing methods and in particular the maintenance of weight loss that had been shown. This trial was originally a single-centre trial in Switzerland, but in November 2006 it was announced that the trial had been expanded to two additional clinical sites in the USA. The results from this trial are expected in the first half of 2007.

An additional trial was commenced in October 2006 that is designed to investigate the efficacy of the drug in morbidly obese patients who had been designated as bariatric patient candidates. This trial, taking place in the USA, will recruit 24 patients and will dose OE for 30 days, without any break, and then have a follow-up 30 days after dosing has been completed. The results from this trial are also expected in the first half of 2007.

On July 10, 2007 Manhattan Pharmaceuticals announced that its phase 2a studies for oral oleoyl-estrone failed. The two studies demonstrated no clinically meaningful or statistically significant placebo adjusted weight loss.

[Editor's note: This is a post concerned to help people lose weight and belly fat. However, there are no clinical proofs that it works for fat loss, yet.  af]

[Editor's note: I hope this is not a duplicate article.  af  ]

7 Minute Science
The science behind brevity training
by Jon Benson, Author of 7 Minute Muscle

A few months ago I released a book whose title was more reminiscent of a line out of “There’s Something About Mary” than a serious work on fitness. “7 Minute Muscle” — yep, it’s getting more and more difficult to distinguish fact from parody.

Here’s the real irony:  Of the 27 testimonials I’ve received so far that I deem worthy of publishing on the web, over a dozen were from fitness professionals. I’m not talking about “doctors” with a gut as large as their paycheck. I’m speaking of men and women with both academic and real-world experience in the fitness and bodybuilding world.

There were exceptions of course. My friend John Berardi, while saying some nice things about the work, couldn’t endorse it due to the emphasis on shorter training sessions. That’s cool. Everyone has a different approach. But the overwhelming number of folks with consonants behind their names — those who read the book and applied the principles — had wonderful things to say.

There’s a reason for that:  The workout protocol is based on the science of hypertrophy as well as psychophysiology, the study of the mind/body connection.

I will delve into the mental aspects of the protocols in a later article. For now, since most of you are experienced, educated and (dare I say it) hard-core, let’s delve into the meat.

7 Minute Muscle is primarily a density-based training system. It demands varying rep ranges done within specific time periods. The protocol factors six of the primary variables of hypertrophy, or muscle growth:  Intensity, Load, Volume, Density, Time and Force. (Time includes rest intervals as well as the time required to perform a given task.)

A layman’s take on one of the basic laws of physics states that time and energy are interrelated. Doing the same amount of work in less time demands more energy, which translates into more power. While power is a factor in training, our interest is focused on forcing muscle growth and adaptation. This is also an element of time and energy. More energy expended in less time = more power.

If you break down the typical 3-4 set bench press routine, with reps starting at 12 and ending in the 4-6 range, with longer rest intervals between heavier sets, you’ll find that the aggregate weight lifted is “less” than a protocol like 7 Minute Muscle, which uses ‘less’ weight (easier on the joints) but demands more work in less time. In other words, X amount of repetitions done with Y amount of weight in just 5 minutes (phase 1 of our two-phase protocol) ends up being greater than your typical 3-4 set protocol, despite the fact that more weight is used in the latter.

Other routines, of course, utilize this factor of density. Vince Gironda’s infamous 8 sets of 8, EDT and so-forth. 7 Minute Muscle goes a bit further by varying rest, load factors and repetition range. Reps will vary from as low as one rep to as much as ten, and all of this is at the trainee’s discretion. They have only one objective: Increase the aggregate repetition count from one training session to the next. Since time is limited (broken down into two phases:  A Power Phase of no more than 5 repetitions and a Mass Phase of no more than 10 repetitions) the trainee is given a system that more accurately measure the seventh and most crucial factor of hypertrophy:  Progression.

More work in less time. Variable repetition ranges. Variable rest intervals. And all in seven minutes (for beginners.) Intermediate and advanced-level trainees are given 14 and 21-minute protocols if they wish to implement them. I myself rarely go beyond 14 minutes, as that is all that’s required to stimulate muscle growth.

I will cover health factors, cardiovascular work, ab training, and the science of mind and body in future articles. For now, give 7 Minute Muscle a shot. There’s nothing funny about it, except for the fact that you’ll be laughing all the way home from the gym as you finished your killer workout while your buddies were still warming up.

———

[ Ed. Note:  Jon Benson is the author of four best-selling fitness and nutrition books:  Fit Over 40, Simply Eat, The Every Other Day Diet and 7 Minute Muscle, as well as the year-long M-Power Audio Series. You can read more here  about the 7 Minute Muscle Program.

[Editor's note: Ya, I know, the title could use improvement, but it's 2:30 in the morning and I am tired  af   ]

Tendon

This text refers to picture at right.
One such tendon in the Human Body, the Achilles Tendon.
Latin	tendo
Dorlands/Elsevier	Tendon

A tendon (or sinew) is a tough band of fibrous connective tissue that usually connects muscle to bone and is capable of withstanding tension. Tendons are similar to ligaments and fascia as they are all made of collagen except that ligaments join one bone to another bone, and fascia connect muscles to other muscles. Tendons and muscles work together and can only exert a pulling force.

Structure

• Normal healthy tendons are mostly composed of parallel arrays of collagen fibres closely packed together.

The dry mass of normal tendons, which makes up about 30% of the total mass in water, is composed of about 86% collagen, 2% elastin, 1–5% proteoglycans, and 0.2% inorganic components such as copper, manganese, and calcium.The collagen portion is made up of 97-98% type I collagen, with small amounts of other types of collagen.

These include type II collagen in the cartilaginous zones, type III collagen in the reticulin fibres of the vascular walls, type IX collagen, type IV collagen in the basement membranes of the capillaries, type V collagen in the vascular walls, and type X collagen in the mineralized fibrocartilage near the interface with the bone.

Collagen fibres coalesce into macroaggregates. After secretion from the cell, the terminal peptides are cleaved by procollagen N- and C-proteinases, and the tropocollagen molecules spontaneously assemble into insoluble fibrils. A collagen molecule is about 300 nm long and 1-2 nm wide, and the diameter of the fibrils that are formed can range from 50-500 nm. In tendons, the fibrils then assemble further to form fascicles, which are about 10 mm in length with a diameter of 50-300 μm, and finally into a tendon fibre with a diameter of 100-500 μm. Groups of fascicles are bounded by the epitendon and peritendon to form the tendon organ.

The collagen in tendons are held together with proteoglycan components, including decorin and, in compressed regions of tendon, aggrecan, which are capable of binding to the collagen fibrils at specific locations.

The proteoglycans are interwoven with the collagen fibrils and that their glycosaminoglycan (GAG) side chains have multiple interactions with the surface of the fibrils, showing that the proteoglycans are important structurally in the interconnection of the fibrils. The major glycosaminoglycan (GAG) components of the tendon are dermatan sulfate and chondroitin sulfate, which associate with collagen and are involved in the fibril assembly process during tendon development.

Dermatan sulfate is thought to be responsible for forming associations between fibrils, while chondroitin sulfate is thought to be more involved with occupying volume between the fibrils to keep them separated and help withstand deformation.

The dermatan sulfate side chains of decorin aggregate in solution, and this behavior can assist with the assembly of the collagen fibrils. When decorin molecules are bound to a collagen fibril, their dermatan sulfate chains may extend and associate with other dermatan sulfate chains on decorin that is bound to separate fibrils, therefore creating interfibrillar bridges and eventually causing parallel alignment of the fibrils.

The tenocytes produce the collagen molecules which aggregate end-to-end and side-to-side to produce collagen fibrils. Fibril bundles are organized to form fibres with the elongated tenocytes closely packed between them. There is a three-dimensional network of cell processes associated with collagen in the tendon. The cells communicate with eachother through gap junctions, and this signalling gives them the ability to detect and respond to mechanical loading.

Blood vessels may be visualized within the endotendon running parallel to collagen fibres, with occasional branching transverse anastomoses.

The internal tendon bulk is thought to contain no nerve fibres, but the epi- and peritendon contain nerve endings, while Golgi tendon organs are present at the junction between tendon and muscle.

Tendon length varies in all major groups and from person to person. Tendon length is practically the discerning factor where muscle size and potential muscle size is concerned. For example, should all other relevant biological factors be equal, a man with a shorter tendons and a longer biceps muscle will have greater potential for muscle mass than a man with a longer tendon and a shorter muscle.

• Successful bodybuilders will generally have shorter tendons. Conversely, in sports requiring athletes to excel in actions such as running or jumping, it is beneficial to have longer than average Achilles tendon and a shorter calf muscle.

Tendon length is determined by genetic predisposition, and has not been shown to either increase or decrease in response to environment, unlike muscles which can be shortened by trauma, use imbalances and a lack of recovery and stretching.

Function

Tendons have been traditionally considered to simply be a mechanism by which muscles connect to bone, functioning simply to transmit forces. However, over the past two decades, much research focused on the elastic properties of tendons and their ability to function as springs. This allows tendons to passively modulate forces during locomotion, providing additional stability with no active work.

• It also allows tendons to store and recover energy at high efficiency. For example, during a human stride, the Achilles tendon stretches as the ankle joint dorsiflexes. During the last portion of the stride, as the foot plantar-flexes (pointing the toes down), the stored elastic energy is released. Furthermore, because the tendon stretches, the muscle is able to function with less or even no change in length, allowing the muscle to generate greater force.

• The mechanical properties of the tendon are dependent on the collagen fiber diameter and orientation. The collagen fibrils are parallel to each other and closely packed, but show a wave-like appearance due to planar undulations, or crimps, on a scale of several micrometers.

In tendons, the collagen I fibers have some flexibility due to the absence of hydroxyproline and proline residues at specific locations in the amino acid sequence, which allows the formation of other conformations such as bends or internal loops in the triple helix and results in the development of crimps. The crimps in the collagen fibrils allow the tendons to have some flexibility as well as a low compressive stiffness.

In addition, because the tendon is a multi-stranded structure made up of many partially independent fibrils and fascicles, it does not behave as a single rod, and this property also contributes to its flexibility.

The proteoglycan components of tendons also are important to the mechanical properties. While the collagen fibrils allow tendons to resist tensile stress, the proteoglycans allow them to resist compressive stress. The elongation and the strain of the collagen fibrils alone have been shown to be much lower than the total elongation and strain of the entire tendon under the same amount of stress, demonstrating that the proteoglycan-rich matrix must also undergo deformation, and stiffening of the matrix occurs at high strain rates.

These molecules are very hydrophilic, meaning that they can absorb a large amount of water and therefore have a high swelling ratio. Since they are noncovalently bound to the fibrils, they may reversibly associate and disassociate so that the bridges between fibrils can be broken and reformed. This process may be involved in allowing the fibril to elongate and decrease in diameter under tension.

Pathology

Tendons are subject to many types of injuries. There are various forms of tendinopathies or tendon injuries due to overuse. These types of injuries generally result in inflammation and degeneration or weakening of the tendons, which may eventually lead to tendon rupture. Tendinopathies can be caused by a number of factors relating to the tendon extracellular matrix, and their classification has been difficult because their symptoms and histopathology often are similar.

The first category of tendinopathy is paratenonitis, which refers to inflammation of the paratenon, or paratendinous sheet located between the tendon and its sheath. Tendinosis refers to non-inflammatory injury to the tendon at the cellular level.

The degradation is caused by damage to collagen, cells, and the vascular components of the tendon, and is known to lead to rupture. Observations of tendons that have undergone spontaneous rupture have shown the presence of collagen fibrils that are not in the correct parallel orientation or are not uniform in length or diameter, along with rounded tenocytes, other cell abnormalities, and the ingrowth of blood vessels.

Other forms of tendinosis that have not led to rupture have also shown the degeneration, disorientation, and thinning of the collagen fibrils, along with an increase in the amount of glycosaminoglycans between the fibrils. The third is paratenonitis with tendinosis, in which combinations of paratenon inflammation and tendon degeneration are both present. The last is tendinitis which refers to degeneration with inflammation of the tendon as well as vascular disruption.

Tendinopathies may be caused by several intrinsic factors including age, body weight, and nutrition. The extrinsic factors are often related to sports and include excessive forces or loading, poor training techniques, and environmental conditions.

Healing

The tendons in the foot are highly complex and intricate. If any tendons break it is a long, painful healing process, not to mention the intricacy of the repairing (if fully severed) process. Most people that do not receive medical attention within the first 48 hours of the injury will suffer from severe swelling, pain, and an on-fire feeling where the injury occurred. They are very painful when they are inflamed or not in use.

It was believed previously that tendons could not undergo matrix turnover and that tenocytes were not capable of repair. However, it has been shown more recently that throughout the lifetime of a person, tenocytes in the tendon actively synthesize ECM components as well as enzymes such as matrix metalloproteinases (MMPs) can degrade the matrix. Tendons are capable of healing and recovering from injuries in a process that is controlled by the tenocytes and their surrounding extracellular matrix. However, the healed tendons never regain the same mechanical properties as before the injury.

The three main stages of tendon healing are inflammation, repair or proliferation, and remodeling, which can be further divided into consolidation and maturation. These stages can overlap with each other. In the first stage, inflammatory cells such as neutrophils are recruited to the injury site, along with erythrocytes. Monocytes and macrophages are recruited within the first 24 hours, and phagocytosis of necrotic materials at the injury site occurs. After the release of vasoactive and chemotactic factors, angiogenesis and the proliferation of tenocytes are initiated. Tenocytes then move into the site and start to synthesize collagen III.

The inflammation stage usually lasts for a few days, and the repair or proliferation stage then begins. In this stage, which lasts for about six weeks, the tenocytes are involved in the synthesis of large amounts of collagen and proteoglycans at the site of injury, and the levels of GAG and water are high. After about six weeks, the remodeling stage begins.

The first part of the remodeling stage is consolidation, which lasts from about six to ten weeks after the injury. During this time, the synthesis of collagen and GAGs is decreased, and the cellularity is also decreased as the tissue becomes more fibrous as a result of increased production of collagen I and the fibrils become aligned in the direction of mechanical stress. The final maturation stage occurs after ten weeks, and during this time there is an increase in crosslinking of the collagen fibrils, which causes the tissue to become stiffer. Gradually, over a time period of about one year, the tissue will turn from fibrous to scar-like.

Matrix metalloproteinases or MMPs have a very important role in the degradation and remodeling of the ECM during the healing process after a tendon injury. Certain MMPs including MMP-1, MMP-2, MMP-8, MMP-13, and MMP-14 have collagenase activity, meaning that unlike many other enzymes, they are capable of degrading collagen I fibrils.

The degradation of the collagen fibrils by MMP-1 along with the presence of denatured collagen are factors that are believed to cause weakening of the tendon ECM and an increase in the potential for another rupture to occur. In response to repeated mechanical loading or injury, cytokines may be released by tenocytes and can induce the release of MMPs, causing degradation of the ECM and leading to recurring injury and chronic tendinopathies.

A variety of other molecules are involved in tendon repair and regeneration. There are five growth factors that have been shown to be significantly upregulated and active during tendon healing: insulin-like growth factor 1 (IGF-I), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor beta (TGF-β).

These growth factors all have different roles during the healing process. IGF-1 increases collagen and proteoglycan production during the first stage of inflammation, and PDGF is also present during the early stages after injury and promotes the synthesis of other growth factors along with the synthesis of DNA and the proliferation of tendon cells.

The three isoforms of TGF-β (TGF-β1, TGF-β2, TGF-β3) are known to play a role in wound healing and scar formation. VEGF is well known to promote angiogenesis and to induce endothelial cell proliferation and migration, and VEGF mRNA has been shown to be expressed at the site of tendon injuries along with collagen I mRNA.

Bone morphogenetic proteins (BMPs) are a subgroup of TGF-β superfamily that can induce bone and cartilage formation as well as tissue differentiation, and BMP-12 specifically has been shown to influence formation and differentiation of tendon tissue and to promote fibrogenesis.

Effects of activity on healing

In animal models, extensive studies have been conducted to investigate the effects of mechanical strain in the form of activity level on tendon injury and healing. While stretching can disrupt healing during the initial inflammatory phase,

• it has been shown that controlled movement of the tendons after about one week following an acute injury can help to promote the synthesis of collagen by the tenocytes, leading to increased tensile strength and diameter of the healed tendons and fewer adhesions than tendons that are immobilized.

In chronic tendon injuries, mechanical loading has also been shown to stimulate fibroblast proliferation and collagen synthesis along with collagen realignment, all of which promote repair and remodeling. To further support the theory that movement and activity assist in tendon healing, it has been shown that immobilization of the tendons after injury often has a negative effect on healing. In rabbits, collagen fascicles that are immobilized have shown decreased tensile strength, and immobilization also results in lower amounts of water, proteoglycans, and collagen crosslinks in the tendons.

Several mechanotransduction mechanisms have been proposed as reasons for the response of tenocytes to mechanical force that enable them to alter their gene expression, protein synthesis, and cell phenotype and eventually cause changes in tendon structure. A major factor is mechanical deformation of the extracellular matrix, which can affect the actin cytoskeleton and therefore affect cell shape, motility, and function. Mechanical forces can be transmitted by focal adhesion sites, integrins, and cell-cell junctions. Changes in the actin cytoskeleton can activate integrins, which mediate “outside-in” and “inside-out” signaling between the cell and the matrix. G-proteins, which induce intracellular signaling cascades, may also be important, and ion channels are activated by stretching to allow ions such as calcium, sodium, or potassium to enter the cell.

Uses of sinew

Sinew was widely used throughout pre-industrial eras as a tough, durable fiber. Some specific uses include using sinew as thread for sewing, attaching feathers to arrows (see fletch), lashing tool blades to shafts, etc. It is also recommended in survival guides as a material from which strong cordage can be made for items like traps or living structures. Tendon must be treated in specific ways to function usefully for these purposes. Inuit and other circumpolar people utilized sinew as the only cordage for all domestic purposes due to the lack of other suitable fiber sources in their ecological habitats.

The elastic properties of particular sinews were also used in composite recurved bows favoured by the steppe nomads of Eurasia. The first stone throwing artillery also used the elastic properties of sinew.

Sinew makes for an excellent cordage material for three reasons: It is incredibly strong, it contains natural glues, and it shrinks as it dries, doing away with the need for knots.

Tendon (particularly beef tendon) is used as a food in some Asian cuisines (often served at Yum Cha or Dim Sum restaurants). One popular dish is Suan Bao Niu Jin, where the tendon is marinated in garlic. It is also sometimes found in the Vietnamese noodle dish phở.

[Editor's note:  af   ]

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