Lose Weight By Controlling The Fat Storage Hormone

Trouble Spot Nutrition

Created by Janet Hradil, Trouble Spot Nutrition is a 3 Phase Hormonal Solution That Melts Away Trouble Spot Fat In Less Than 15 Minutes A Day. Leptin, cortisol, and testosterone all have an influence on our weight issues, but not many of us know it. Janet Hradil has created Trouble Spot Nutrition with the intent of teaching people how their hormones affect their weight loss efforts, and how nutrition can easily correct hormone issues and help fight fat faster than ever before. In each of your fat cells, there is an enzyme, 11 beta-hydroxysteroid dehydrogenase-1 (Hsd), that takes inactive cortisone (a hormone) and turns it into cortisol, a fat storing compound. If you have high amounts of Hsd, you will have high amounts of fat storage. While Hsd is genetically determined, you can use nutrition to reduce levels and stop the unwanted fat storage, even on your trouble spots. Continue reading...

Trouble Spot Nutrition Overview

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My Trouble Spot Nutrition Review

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All of the information that the author discovered has been compiled into a downloadable pdf so that purchasers of Trouble Spot Nutrition can begin putting the methods it teaches to use as soon as possible.

This ebook does what it says, and you can read all the claims at his official website. I highly recommend getting this book.

High blood sugar and insulin can increase fat storage

To lose body fat more efficiently, your goal is to maintain steady blood sugar levels. Here's why The over-secretion of insulin activates fat storage enzymes and promotes the movement of triglycerides (fat) in the bloodstream into fat cells for storage. High insulin levels also inhibit enzymes that promote the breakdown of existing stored body fat. You can manage your blood sugar and insulin levels by choosing fewer simple carbohydrates, more complex carbohydrates, eating fiber and having your carbohydrates with lean proteins approximately every three hours.

Regulators of Lipolysis and Fat Storage

The processes of lipolysis and fat storage are regulated by hormonal factors, which either enhance or suppress the activities of HSL and LPL. Through the action of glucocorticoid receptors, glucocorticoids enhance LPL activity and promote abdominal deposition of fat. The density of glucocorticoid receptors is greater in the visceral abdominal depot than in the subcutaneous abdominal depot. Therefore, an increase in glucocorticoid secretion is associated with increases in abdominal fat deposition compared to other fat depots. Insulin favors fat storage by increasing LPL and decreasing HSL activity. Insulin has stronger antily-polytic effects in adipose located in the abdominal region compared to the femoral regions in both men and women. Paradoxically, insulin binding is stronger in the gluteal-femoral region than the abdominal region. Therefore, it has been hypothesized that insulin regulates lipolysis at the postreceptor level. Sex hormones, such as estrogen, testosterone, and...

Leptin ob Protein

For 40 years, scientists searched for a mechanism by which the brain could monitor body fat deposition in order to keep an animal's body weight constant. In 1994, a gene that controlled the expression of a protein produced by adipose tissue was identified. Circulating levels of this protein (the ob protein) could be measured in normal weight mice. However, in obese ob ob mice, which display marked overeating, this protein was absent due to a mutation of the ob gene. A series of studies demonstrated that the absence of this protein was responsible for over-consumption and obesity in the obese ob ob. As the ob protein reduces food intake and also increases metabolic energy expenditure, both of which would result in weight loss, it was named leptin from the Greek 'leptos' meaning thin. In general, circulating levels of leptin appear to reflect the current status of body fat deposition and increase with the level of adiposity demonstrating the responsiveness of endogenous leptin to weight...

Number of fat cells

You were born with a predetermined number of fat cells. Some people are born with more than others. The person born with more fat cells is at a disadvantage compared to someone with fewer fat cells. Fat cell number can increase throughout life but it cannot decrease (except through liposuction, which has many potential hazards). Fortunately, what can change is the size of the fat cells. Even someone with a large number of fat cells can shrink all of them, thereby becoming dramatically thinner and leaner.

Neuroendocrine Effects of Alcohol

Alcohol activates the sympathetic nervous system, increasing circulating catecholamines from the adrenal medulla. Hypothalamic-pituitary stimulation results in increased circulating cortisol from the adrenal cortex and can, rarely, cause a pseudo-Cushing's syndrome with typical moon-shaped face, truncal obesity, and muscle weakness. Alcoholics with pseudo-Cushing's show many of the biochemical features of Cushing's syndrome, including failure to suppress cortisol with a 48-h low-dose dexamethasone suppression test. However, they may be distinguished by an insulin stress test. In pseudo-Cushing's, the cortisol rises in response to insulin-induced hypoglycemia, but in true Cushing's there is no response to hypoglycemia.

Body Weight and Energy Balance

Substitution of nonalcohol calories by alcohol calories, which are 'wasted' during metabolism Alcohol metabolism decreases lipid metabolism, promotes fat storage multicenter studies, alcoholic hepatitis patients demonstrate universal evidence for protein calorie malnutrition, according to the physical findings of muscle wasting and edema, low levels of serum albumin and other visceral proteins, and decreased cell-mediated immunity, whereas their 6-month mortality is related in part to the severity of malnutrition. Anorexia is a major cause of weight loss in alcoholic liver disease, and may be caused by increased circulating levels of leptin. Furthermore, active alcoholic hepatitis contributes to increased resting energy expenditure as another cause of weight loss. On the other hand, resting energy expenditure is normal in stable alcoholic cirrhotics who are also typically underweight or malnourished in part due to preferential metabolism of endogenous fat stores. At the same time, the...

What Is Unique about This Book

The many kinds of hormones that affect fat storage and utilization. This book is one of the first to offer questionnaires to help you realize when your own hormones are working against you. It also discusses how the hormonal changes that occur with menopause and andropause can cause you to become overfat and tells you how exercise and nutrition can help rebalance these hormones.

Delia M Vzquez1 and Seymour Levine2

There is an important caveat in making the assumption that the reduced level of CORT following stress indicates a reduction in biological activity. CORT exists in the circulation in two forms, bound and unbound. The large majority of CORT in the adult is bound to cortisol-binding protein (CBG) and other plasma binding proteins. Only a small fraction exists in the free form, which is considered to be the biologically active form. Following stress, CBG is somewhat decreased, making more of the circulating CORT available as free CORT (Fleshner et al., 1995 Tannenbaum et al., 1997). Another aspect of the SHRP in rodents is the relative absence of CBG during the SHRP (Henning, 1978). Thus, although the absolute values of CORT, which normally include both bound and unbound hormone, are very low in the absence of CBG the actual fraction of CORT that is available in the free form for binding to corticosteroid receptors may actually be higher than is observed in the adult. There are few data...

Caregiver Differences

While the aforementioned studies examined parents and children together, it is important to also examine the effects of parents' behaviors on children's capacities to regulate emotion on their own. Here, the level of parents' autonomy supportiveness versus controllingness in their interactions with their children becomes especially relevant. While not proposing such a model, several studies have examined parent behaviors that can be related to an autonomy support to control continuum. Silverman and Ragusa (1990) found that mothers who were more active in a parent-child compliance task had children who performed more poorly on an independent delay task, even controlling for performance on the compliance tasks. Nachmias, Gunnar, Manglesdorf, Parritz, and Buss (1996) examined the strategies that mothers used to help their wary children deal with a mildly fear-inducing stimulus. Mothers who forced their children to focus on a novel event had children with higher postsession cortisol...

Learn the Difference between Male and Female Fat Patterns

For a variety of reasons, including hormones and metabolic processes that affect fat storage in particular areas of the body, when men and women first begin to gain weight, they do not store it in the same place. A typical overweight man looks like an apple. He carries his weight above the waist, resulting in the classic bulging abdomen, also known as the beer belly. A typical overweight woman carries her fat below the waist in the hips and the buttocks, resulting in a pear-shaped silhouette.

Stress In Sports And Exercise

Physical training involves repeating a set of exercises with increasing intensity over an extended period. Selye2 noticed that exposure to a particular stressor can increase the body's ability to cope with that stressor in the future through a process of physiologic adaptation. The increase in ability and performance with training shows how the body adapts to the required effort. Selye also recognized that severe and extended exposure to any stressor could ultimately exceed the ability of the system to cope. Runners who habitually train more than 45 miles a week at moderate to high intensity are known to have chronically elevated cortisol levels and negative mood states.3 Full recovery from overtraining stress may take months of abstinence from the particular exercise.

Neural Structures Critical to the Expression of Appetite

Substances crossing the blood-brain barrier entering the brain factors such as neurotransmit-ter precursors, leptin or insulin cross the blood-brain barrier and directly alter CNS neurochem-ical activity, particularly in key hypothalamic nuclei and associated limbic areas.

Initiation and Stimulation of Eating Mechanisms Underpinning Hunger

Neuropeptide Y (NPY) is probably the most studied appetite stimulatory peptide. NPY is found throughout the CNS and in particular abundance in the PVN of the hypothalamus. Hypothalamic NPY neurons that are implicated in appetite regulation project from the ARC to the PVN. Infusing NPY directly into the CNS or increasing release of NPY within the PVN promotes meal initiation and produces an immediate and marked increase in food intake, delaying the onset of satiety. The hyperpha-gic effects of NPY appear to be mediated by both NPY Y1 and Y5 receptors. Endogenous NPY is sensitive to a variety of peripherally generated signals. It is stimulated by the gut factor ghrelin, but inhibited by the pancreatic hormone amylin, the adiposity signal leptin, and the satiety neurotrans-mitter serotonin (5-HT). Like NPY, galanin-induced hyperphagia has been well documented. Early studies demonstrated that direct infusion of galanin into the hypothalamus of rodents stimulated feeding behavior....

Integration of Episodic and Tonic Signals within the CNS

Within these sites numerous neurochemicals (first neurotransmitters and then neuropeptides) have been identified as potent inhibitors and stimulators of feeding behavior. 5-HT has been implicated as a critical CNS satiety factor in the short-term regulation of food intake. Specifically, the 5-HT system appears to be sensitive to meal-generated satiety factors such as CCK, enterostatin, and ingested macronutrients. Moreover, 5-HT drugs appear to enhance satiety, suppress CNS NPY release, and inhibit hunger. 5-HT appears to mediate the effects of episodic meal-generated satiety on appetite. The second CNS system to be involved is that of the melanocortins, which appear integral in the action of circulating leptin on intake and (like 5-HT) its agonists also inhibit NPY functioning. Thus, the melanocortins may mediate the effects of tonic energy status on appetite. The melanocortins are one of the inhibitory systems through which the tonic adiposity...

Summary Episodic and Tonic Factors in the Regulation of Appetite

Endogenous 5-HT and leptin represent two aspects of negative feedback integral to the appetite control system (see Figure 3). Both systems appear to inhibit NPY functioning, the effect of leptin being partly mediated by melanocortins and other excitatory and inhibitory neuropeptides. 5-HT mediates the effect of meal-derived satiety factors derived from pre- and postingestive processes (such as CCK and enterostatin relsease) and promotes meal termination, prolonging the intermeal interval. By such a mechanism the body deals with the daily physiological fluxes that result from meal intake ensuring an approximately appropriate daily energy intake. Circulating leptin accurately reflects the current status of the body's energy store. Leptin levels continually modify total daily and meal food intake to maintain a sufficient but not excessive level of energy deposition. Thus, 5-HT and leptin represent two classes of signals short-term episodic and long-term tonic feedback, respectively. The...

Absorption and Metabolism of Retinol and Retinoic Acid

A microsomal retinol dehydrogenase catalyzes the oxidation of CRBP-bound all-frans-retinol to retinaldehyde it also acts as a 3a-hydroxysteroid dehydrogenase. A similar enzyme catalyzes the oxidation of 9-cis- and 11-cis-retinol, but not all-frans-retinol again, it has 3a-hydroxysteroid dehydrogenase activity. In the eye, the major product of this enzyme is 11-cis-retinaldehyde, whereas in other tissues it is 9-cis-retinaldehyde, which is then oxidized to 9-cis-retinoic acid (Section 2.3.2.1 Chen et al., 2000 Duester, 2000, 2001 Gamble et al., 2000 Napoli, 2001). Although there is known to be an isomerase in the eye for the formation of 11-cis-retinaldehyde as a

Susceptibility to Mood Enhancement by Diet

Nevertheless, recent research provides some further support for beneficial effects of carbohydrate-rich protein-poor meals on mood and emotion in some people. When participants were divided into high and low stress-prone groups, as defined by a questionnaire, carbohydrate-rich protein-poor meals prior to a stressful task were found to block task-induced depressive feelings and the release of the glucocorticoid stress hormone cortisol, but only in the high stress-prone group. This finding was replicated using high- and low-tryptophan-containing proteins (a-lactalbumin and casein, respectively). It was argued that, because stress increases 5-HT activity, the poor response to stress of the sensitive group might indicate a deficit in 5-HT synthesis that is improved by this dietary intervention. There is another link between macronutrient intake, stress, and mood. Chronic dysfunction of the stress-sensitive hormone cortisol and its controlling hypothalamic pituitary adrenal (HPA) axis is...

Exercise Can Be a Positive or Negative Stressor

With negative emotion, the musculoskeletal system is less balanced. If an event is interpreted as a negative stressor, more of the stress hormone cortisol is produced as a response. Higher levels and longer secretion of cortisol can change brain wiring, hamper physical performance, and harm health.

Hormonal Responses To Overtraining

A physiologic imbalance of endocrine function has been recognized in athletes suffering from overtraining. Overtrained athletes often have higher-than-normal concentrations of urea in the blood, which is produced by increased protein catabolism. This is thought to be the mechanism responsible for loss of body weight in overtrained athletes. However, there are no conclusive data to confirm that higher levels of cortisol or epinephrine are related to long periods of overtraining. Serotonin is a major neu-rotransmitter that is believed to play an important role in overtraining syndrome. However, the concentration of serotonin in plasma does not match its concentration in the brain. Cytokines also play a significant role, inasmuch as the presence of circulating cytokines have been associated with trauma related to overtrained muscles, joints, and bones, as well as with infection.

Genomic Actions of Retinoic Acid

At pharmacological levels, retinoic acid enhances the expression of uncoupling protein 1 (thermogenin) in brown adipose tissue and decreases the expression of leptin in white adipose tissue, suggesting that it may have an effect on energy homeostasis, but it is not known whether or not the effects are relevant at physiological levels (Kumaretal., 1999 Villarroyaetal., 1999). Retinoic acid also induces synthesis of glucokinase in pancreatic f -islet cells. Increased metabolism of glucose as a result of glucokinase activity is responsible for initiating insulin secretion in response to a rise in blood glucose concentration, and retinoic acid increases the secretion of insulin by pancreatic islets in culture (Cabrera-Valladares et al., 1999).

Physiological factors influencing food intake

Long-term food intake regulation is essential in food-weight management. The hormone leptin appears to be involved in long-term food intake regulation. Leptin is synthesized mainly by adipose tissue it acts through receptors present in afferent visceral nerves and the hypothalamic arcuate Plasma leptin concentrations correlate positively with total body fat stores (Sinha et al., 1996). An energy deficit of more than 24 h leads to decreases of plasma leptin concentration (Boden et al., 1996), whereas an energy surplus of more than 24 h results in increased leptin concentrations (Kolaczynski et al., 1996). Plasma leptin is negatively correlated with appetite and food intake when the energy balance is severely disturbed (Keim et al., 1998 Chin-Chance et al., 2000). When subjects are in energy balance, the relation between leptin concentrations and food intake and appetite is less clear (Karhunen et al., 1997 Joannic et al., 1998 Romon et al., 1999). Therefore, leptin seems to have a role...

The subcutaneous layer

The subcutaneous layer contains the same collagen and elastin fibres as the dermis and contains the major arteries and veins which supply the skin and form a network throughout the dermis. The fat cells contained within this layer help to insulate the body by reducing heat loss.

How low should you go

It's impossible for body fat levels to drop to zero since some fat is located internally and is necessary for normal body functioning. This is called essential fat. Essential fat is necessary for energy storage, protection of internal organs, and insulation against heat loss. Essential fat is found in the nerves, brain, bone marrow, liver, heart, and in nearly all the other glands and organs of the body. In women, this fat also includes sex-related fat deposits including the breast tissue and uterus. Essential body fat is 2-3 for men and 7-8 for women.

Plasma Vitamin D Binding Protein GcGlobulin

The plasma binding protein has a higher affinity for calcidiol and 24-hydroxycalcidiol than for calcitriol or cholecalciferol. The plasma concentration of Gc-globulin is about 6 mmol per L - considerably higher than the concentrations of other hormone binding proteins, such as thyroxine binding globulin (300 mol per L), cortisol binding globulin (800 mol per L), or sex hormone binding globulin (40 mol per L in males and 80 mol per L in females) and far in excess of circulating vitamin D. As a result of this, whereas the other hormone binding globulins are about 50 saturated under normal conditions, the vitamin D binding protein is only about 2 saturated. This means that changes in the circulating concentration of the protein are unlikely to have any significant effect on the small proportion of vitamin D metabolites that is free, rather than protein-bound. Again, unlike other hormone binding globulins, the plasma concentration of Gc-globulin is not affected by vitamin D status or...

Lipidlowering Activity

Depression is often associated with insulin resistance, owing to Cortisol overproduction (McCarty 1994). The reputed antidepressant effects of chromium may be explained by improvements in insulin sensitivity (Davidson et al 2003) and related increases in tryptophan availability and or noradrenaline release (McLeod & Golden 2000). Chromium has also been shown to lower the Cortisol response to challenge with 5-hydroxy-L-tryptophan (5-HTP) and decrease the sensitivity of 5-HT2A receptors (Attenburrow et al 2002).

Skinfold measurements The Pinch an inch test

Skinfold testing is based on the fact that you store most of your body fat directly beneath your skin. These types of fat deposits are called subcutaneous fat. The remainder of your body's fat is located around organs (internal fat) and inside muscle tissue (intramuscular fat).

Glycyrrhizic Acid Glycyrrhizin

The triterpenoid glycyrrhizin is anti-inflammatory and is metabolised to the aglycone glycyrrhizic acid, which inhibits 11-h-hydroxysteroid dehydrogenase, involved in corticosteroid metabolism. The aglycone inhibited N-acetyltransferase activity in human colon tumor cell lines, and inhibited the formation of DNA adducts (118). Although glycyrrhizin did not directly induce apoptosis, it enhanced Fas-mediated apoptotic body formation and DNA fragmentation in T-cell lines (119). The action of licorice root, the main source of glycyrrhizin, on cancer has been reviewed (71).

Carbohydrate type glycaemic response and weight control

Short- and long-term studies in humans and animals indicate that high-GI diets affect appetite and nutrient partitioning to promote fat storage. However, human studies showing reduced bodyweight after consumption of low-GI diets need to be interpreted with caution. The outcome can rarely be attributed solely to the GI, because interventions designed to modify the GI of a diet usually also modify other variables that influence bodyweight (e.g. fibre content, palatability, energy density). Pawlak et al. (2004) assigned rats and mice either to a low- or a high-GI diet. The carbohydrate portion of the low-GI diet consisted of 60 amylose 40 amylopectin starch, whereas the carbohydrate in the high-GI diet was 100 amylopectin starch. Other than this, the two diets were similar in nutrient and energy content. In both mice and rats, animals consuming the high-GI diet had more body fat and less lean body mass than those on the low-GI diet. The rats on the high-GI diet required less food to gain...

Essentiality and Metabolic Functions of Chromium

Stresses that have been shown to alter Cr metabolism in humans are glucose loading, high simple sugar diets, lactation, infection, acute exercise, chronic exercise, and physical trauma. Urinary losses can be used as a measure of the response to stress since once Cr is mobilized in response to stress it is not reabsorbed by the kidney but is lost in the urine. The degree of stress as measured by the stress hormone, cortisol, is correlated with the amount of Cr lost in the urine.

Lack of Restorative Sleep and the Possible Roles of Substance P and HPA Axis

In the 1990s, researchers proposed that exposure to stressful conditions could alter the function of the hypothalamic-pituitary-adrenal (HPA) axis, a major part of the neuroendocrine system that controls reactions to stress and regulates many body processes. Variations in HPA function are characterized by high levels of cortisol, which in turn is associated with the development of widespread pain. When cortisol excretion levels were measured in one research study, with a sample of forty-seven women diagnosed with FM compared to a control sample of fifty-eight healthy women of similar age, it was confirmed the women with FM excreted significantly lower cortisol levels than the healthy women. Other data in FM have demonstrated a blunted cortisol response to the stress of high-intensity exercise. Most recently, a lack of normal daily cortisol variation has been identified in FM. Another hypothesis suggests that reduced sleep leads to reduced production of human growth hormone (HGH)...

Use of Immunotherapy in Conventional Cancer Medicine

Interferons (IFNs) have been the most extensively studied cytokines in cancer treatment. As a group, interferons affect a wide array of immunological functions. They mediate antiviral and antimicrobial activity, stimulate or inhibit leukocyte proliferation, suppress onco-genes, enhance tumor antigen expression, suppress angiogenesis, and augment the activity of NK cells, T lymphocytes, and macrophages. Interferons and tumor necrosis factor (TNF) also increase the burning of body fat stores, possibly to release energy reserves from fat cells for the immune system to use. In this capacity, they play a role in the development of cachexia (tissue wasting disease). Although this is a drawback to their use, interferons still produce an anticancer effect at tolerable doses.

Considering How Fibromyalgia Relates to Womens Ages

By abdominal obesity (a body shape like an apple instead of a pear), high triglycerides, high blood pressure, low levels of high-density lipoprotein (HDL, the good cholesterol), and high fasting glucose (blood sugar) levels. The researchers also found that higher urinary levels of norepinephrine and cortisol were associated with a risk for metabolic syndrome.

Tea Weight Control and Thermogenesis

Black, green, and oolong teas, perhaps because of their limited caffeine content, have been found to increase thermogenesis, to inhibit lipases, and to control body weight and body fat (Table 12 see also Table 9) (87,145-151). The relevant mechanism may be an effect on fat cell synthesis and the endocrine system, modulated by leptin. Green tea and caffeine increased physical activity and lowered body fat in mice. Also, tea, especially epigallo-

Central and nutritional control of adaptive thermogenesis

Signals involved in the long-term regulation of energy balance that convey information to the brain about the size of body fat stores (the so-called 'adiposity signals'), besides affecting food intake, modulate energy expenditure through effects on the activity of the SNS and the pituitary-thyroid axis, and also through direct effects on the oxidative and thermo-genic capacity activity of peripheral tissues. This is the case for leptin, the paradigm of the adiposity signal, which suppresses appetite, and enhances energy expenditure and fat oxidation in peripheral tissues (reviewed in reference 45). In human obesity, leptin deficiency is rare, but leptin resistance is common.

Conclusion Let your results dictate your approach

Some people are born with the propensity to become fatter than others. There are naturally skinny ectomorphs and naturally fatter endormorphs. Some individuals are given more fat cells by heredity, some fewer. But the set point is affected by environment and behavior as well as heredity. You can vary your set point considerably depending on what and how you eat, as well as what kind and how much exercise you do.

Evidence Considered For Estimating The Average Requirement For Carbohydrate

Overall, the key to the metabolic adaptation to extended starvation is the rise in circulating nonesterified fatty acid concentrations and the large increase in ketoacid production. The glycerol released from the hydrolysis of triacylglycerols stored in fat cells becomes a significant source of substrate for gluconeogenesis, but the conversion of amino acids derived from protein catabolism into glucose is also an important source. Interestingly, in people who consumed a protein-free diet, total nitrogen excretion was reported to be in the range of 2.5 to 3.5 g d (35 to 50 mg kg), or the equivalent of 16 to 22 g of catabolized protein in a 70-kg man (Raguso et al., 1999). Thus, it is similar to that in starving individuals (3.7 g d) (Owen et al., 1998). Overall, this represents the minimal amount of protein oxidized through gluconeogenic pathways (Du Bois, 1928). This amount of protein is considerably less than the Recommended Dietary Allowance (RDA) of 0.8 g kg d for adults with a...

Stress Can Make You

Stress has become a condition in which we accept a short-term level of heightened performance at the expense of long-term health. Whether physical or emotional, stress has many negative effects on the body. One of them is the accumulation of a hormone called cortisol. When faced with a stressful situation, the body produces an adrenaline rush that releases fat and glucose as an energy source to help deal with the stressor. Once the crisis subsides, cortisol becomes active and stimulates the appetite so that we can replenish our fat stores. Since most of us don't reach for an apple or a chicken breast when we feel hungry, the release of cortisol usually leads to grabbing a quick carbohydrate snack such as a slice of pizza, a donut, a candy bar, or some type of high-carbohydrate fast food. Unfortunately, living with a high level of daily stress causes the body to produce a consistently high level of cortisol, leading to a vicious cycle of stress, frequent overeating, and fat gain.

Insulin response and sensitivity to carbohydrates

High concentrations of insulin in the bloodstream are lipogenic and anti-lipolytic. This means that when excessive insulin is present, you stop releasing fat from the adipose cells and you go into fat storage mode. This explains why one person can eat a diet high in bread, pasta, potatoes and other carbohydrates and lose body fat easily, while another person will gain body fat and feel terrible on the same diet.

Underlying Factors Glucocorticoids

Maternal glucocorticoids can also influence birth weight of the offspring. Under normal conditions, fetal exposure to glucocorticoids is relatively low due to the presence of placental 11 3-hydroxysteroid dehydrogenase 2 (11 HSD2), an enzyme that acts as a placental barrier by inactivating maternal glu-cocorticoids before they cross into the fetal environment. Maternal glucocorticoid treatment during pregnancy or inhibition of the placental 11 3HSD2 can therefore increase the amount of active gluco-corticoid crossing the placenta. Excess glucocorti-coid exposure has also been implicated in disturbing the normal growth and development of the fetus with consequential effects on the overall health of the adult offspring. There does, however, appear to be a critical window of sensitivity where the developing fetus is particularly sensitive to glu-cocorticoids. Glucocorticoid overexposure in the 3rd trimester is known to cause reductions in birth weight. Studies in rats have established...

Maternal Total Food Intake

Despite the observed significant reduction in birth weight, adult rats exposed to maternal undernutri-tion (30 of ad libitum intake) whilst in utero have been shown to develop obesity. Compared to the control offspring, the feed-restricted offspring appear to have been inappropriately programed and display hyperphagia and elevated food consumption as a consequence of in utero exposure to an adverse maternal diet. The underlying mechanisms leading to the hyperphagia in these offspring remains to be determined. However, the involvement of leptin resistance has been implied as these offspring also display hyperleptinemia and have significantly elevated fat pad mass as adults.

Maternal Protein Consumption

Recently, evidence has been provided suggesting that taurine supplementation to the maternal low-protein diet may benefit the health outcomes of the rat offspring. Maternal taurine supplementation was found to restore and normalize the vascularization of the offspring's endocrine pancreas. Despite these findings, there is little evidence to suggest that a maternal high-protein intake has overall beneficial effects on the metabolic health of the offspring. Some human epidemiological studies and human trials involving high-protein dietary supplementation have in fact demonstrated that the consumption of a high-animal-protein, low-carbohydrate diet throughout late pregnancy can lead to metabolic disturbances in the offspring when they reach adulthood. It has been suggested that these high-protein diets stimulate the hypothalamic-pituitary-adrenal axis and cause maternal cortisol levels to increase. As a result, the developing fetus is presented with the metabolic stress of being exposed...

Postnatal Growth and Later Risk of Disease

Postnatal growth is clearly related to prenatal growth. Some metabolic changes associated with prenatal nutritional sufficiency may affect postnatal physiology and behavior that, in turn, affect growth. In addition, there is intriguing evidence from animal studies that prenatal nutritional restriction alters appetite and induces hyperphagia, and also reduces physical activity in adult animals (see Figure 2). If true in humans, this would be an important pathway by which disease risk is affected. Suggestive evidence comes from human infants whose cord blood leptin levels at birth were inversely related to weight gain in the first 4 months of life, independent of birth weight. Leptin may relate to subsequent growth by affecting appetite and energy intake.

Adipose Tissue Hormones

The adipose tissue secretes different hormones called adipocytokines. Their secretion seems to vary in relation to the amount of adipose tissue accumulated, although the exact mechanism is not known. During profound weight loss, as in anorexia nervosa, there is a marked decrease in the adipose tissue mass with the typical changes in adipocytokines secretion that occur in these circumstances. One of the most studied adipocytokine changes is decreased leptin secretion. Increased fat mass stores are accompanied by an increased leptin secretion decreased fat mass stores decrease leptin secretion. Low serum levels of leptin reaching the hypothalamus increase the activity of the 'hunger center,' in part by increasing the local activity of neuropeptide Y. Individuals with anorexia nervosa have very low levels of leptin in blood and cerebrospinal fluid, in relation to their decreased adipose tissue. This should cause an increase in hypothalamic neuropep-tide Y content and hunger, but this...

Hypothalamic Control of Hunger in Anorexia Nervosa

In normal individuals fasting and weight loss increase hunger by multiple mechanisms (decreased serum levels of leptin, insulin, and blood glucose and increased levels of ghrelin). At the level of the hypothalamus there is an increase in the potent orexigenic neuropeptide Y and other changes in neurotransmitters secondary to the fasting state. Some of these neurotransmitter changes may be the cause or a mechanism of anorexia nervosa, and for this reason they have received considerable attention in the past several years. It is important to understand that appetite control is a very complex hypothalamic function that involves many local and systemic neuropeptides, amines, and hormones.

Plant ingredients interfering with the sympathoadrenal system

An increase in the thermic effect of food in women by adrenergic amines extracted from Citrus aurantium has been described, but this acute response may not translate into a chronic effect or a clinically significant weight loss over time.167 Synephrine has lipolytic effects in human fat cells only at high doses, and octopamine does not have lipolytic effects in human adipocytes.168 The only randomized placebo-controlled clinical trial of Citrus aurantium for weight loss conducted so far tested a combination product with high levels of caffeine (in addition to energy restriction and physical exercise over 6 weeks) and did not find an effect superior to placebo on body weight loss reduction of body fat mass was higher in the treated group, but this effect cannot be attributed to Citrus aurantium alone (see references 169 and 170). In addition, concerns have been raised about the safety of products containing synephrine, since this compound increases blood pressure in humans and other...

Ovarian Cancer Chemoprevention in the General Population

Several investigations have evaluated lower doses of oral contraceptive formulations and its association with ovarian cancer risk. One of the investigations in the meta-analysis of Hankinson and associates5 included subjects who used lower doses of oral contraceptives. From 1980 to 1982, the Cancer and Steroid Hormone Study7 enrolled 546 women with ovarian cancer and 4228 controls. Use of oral contraceptives was associated with risk of ovarian cancer of 0.6 (95 CI, 0.5-0.7). A benefit was seen in women with as little as 3 to 6 months of contraceptive use and was independent of oral contraceptive formulation. Ness and colleagues8 reported findings from the Steroid Hormones and Reproductions (SHARE) Study Group. From 1994 to 1999, the investigation enrolled 767 women with ovarian cancer and 1367 community controls. Oral contraceptive use was associated with a 40 reduction in ovarian cancer risk. Both high-estrogen high-progestin pills and low-estrogen low progestin pills conferred an...

Emotion and the Animal Brain

CS information coming from either the auditory THALAMUS or the cortex arrives in the lateral nucleus of the amygdala and is then distributed to the central nucleus by way of internal amygdala connections that have been elucidated in some detail (Pitkanen et al. 1997). The central nucleus, in turn, is involved in the control of the expression of conditioned responses through its projections to a variety of areas in the brainstem. These behavioral (e.g., freezing, escape, fighting back), autonomic (e.g. blood pressure, heart rate, sweating), and hormonal (adrenaline and cortisol released from the adrenal gland) responses mediated by the central nucleus are involuntary and occur more or less automatically in the presence of danger (though they are modulated somewhat by the situation).

The hypothalamicpituitary adrenal axis

Glucocorticoids hormones are the last step of the activation of the HPA axis. Afferent inputs to the hypothalamus induce the release of corticotropin-releasing factor (CRF) CRF reaches the pituitary via the hyphophyseal portal system and activates the release of ACTH in the bloodstream, which, in turn, triggers the secretion of glucocorticoids (Cortisol in humans and corticosterone in rodents) by the cortical part of the adrenal gland (for review, see McEwen et al., 1986). In humans, as in animals, the secretion

Activation of the hypothalamuspituitaryadrenal axis

Depression is often accompanied by hypercortisolemia. Associated findings include attenuation of the corticotropin response to the administration of corticotrophin-releasing factor and nonsuppression of cortisol secretion after dexamethasone administration. Hypercortisolemia in association with blunted growth and sex hormones promotes central obesity and contributes to increased insulin resistance and diabetes among depressed subjects 31 . The presence of hypercortisolemia in insulin resistance has been documented in some, but not all, studies. A small case-control study has shown some evidence for increased cortisol production in the metabolic syndrome as well 32 . Notably, a contributory role for cortisol metabolism in the pathogenesis of the metabolic syndrome has been postulated. Deregulation of 11 betahydroxysteroiddehydrogenase, an enzyme that converts cortisol into cortison (which cannot activate the glucocorticoid receptor), may result in excess cortisol exposure at the tissue...

Fatty Acid Unsaturation and the Essential Fatty Acids

As noted earlier, the most abundant fatty acids in humans include a saturated fatty acid (16 0) and a monounsaturated fatty acid (18 1n-9). Humans can readily insert a ds-double bond nine carbons from the carboxyl carbon atom of a fatty acid (A9) in a reaction catalyzed by stearoyl-CoA desaturase (SCD1 so-named because the preferred substrate is the CoA derivative of 18 0, stearic acid). Because SCD1 is involved in the synthesis of such an abundant fatty acid, 18 1, the importance of this enzyme in metabolism was initially overlooked. However, 18 1 produced by SCD1 appears to be directed specifically towards triacylglycerol synthesis. Mice in which the SCD1 gene is disrupted have decreased adiposity. Furthermore, genetically obese leptin-deficient (ob- ob-) mice in which the SCD1 gene is also disrupted have significantly reduced body weight compared with ob- ob- mice, leading to the hypothesis that leptin regulates the synthesis of SCD1. Interestingly, dietary 18 1 seems to be more...

Regulation of food intake role of neuropeptides

Leptin is a protein encoded by the gene LEP, and is a member of cytokine receptor family (Aleman et al. 2002). It is produced by adipocytes and acts on specific receptors in the hypothalamus (Brown et al. 2001). Leptin levels regulate a network of orexigenic and anorexigenic neuropeptides and are correlated with body fat mass (Brown et al. 2001). Neuropeptide Y (NPY) and ghrelin (an orexigenic signal from the gut to the brain, mostly expressed in neuroendocrine cells of the gastric fundus) (Pinkney and Williams 2002), are the most potent feeding stimuli. They are released with falling levels of leptin, in conjunction with other orexigenic peptides (orexin, endorphin dynorphine, and melanin-concentrating hormone (MCH)) (Inui 1999). Corticosteroids and medroxyprogesterone acetate (MPA) stimulate the release of NPY (Tisdale 2002). Conversely an increase in leptin generates the release of potent anorexigenic substances, such as neurotensin, melanocortin, colecistokinine,...

Digestion Absorption and Metabolism

Trans fatty acids occur mainly in positions 1 and 3 of triacylglycerols, the predominant lipids in adipose tissue. The concentration of trans fatty acids in adipose tissue is approximately proportional to long-term dietary intake, and determination of the concentrations in storage fat is one method used to estimate trans fatty acid intake. However, this is not entirely straightforward as variation has been reported in the composition of adipose tissue obtained from different sites and depths, and factors that influence adipose tissue turnover rates such as dieting and exercise are also complicating factors. Trans-18 1 isomers account for approximately 70 of the trans fatty acids found in adipose tissue, and trans-18 2 isomers (trans,trans, trans,cis, and cis,trans) account for about 20 .

Adaptogenic And Tonic Effects

Ginseng is used by many athletes to improve stamina and to facilitate rapid recovery from injuries. To examine the effects of ginseng supplements on hormonal status following acute resistance exercise, eight male college students were randomly given water (control group) or 20 g ginseng root extract treatment immediately after a standardised training exercise. Human growth hormone, testosterone, Cortisol, and insulin-like growth factor 1 levels were determined by radioimmunoassay. The responses of plasma hormones following ginseng consumption were not significant between the control and the ginseng groups during the 2-hour recovery period (YouI et al 2002).

The significance of psychosocial stress

Other studies have linked sympathetic hyperresponsivity to the induction of myocardial ischemia during exercise and mental stress and to predictions of the future development of hypertension and progression of atherosclerosis 66-72 . Increased systemic vascular resistance during mental stress testing is the most significant hemodynamic factor associated with mental stress-induced myocardial ischemia and most likely is the result of peripheral endothelial dysfunction 73 . Inhibition of cortisol production has been shown to prevent mental stress-induced endothelial dysfunction and baroreflex impairment, again pointing to a significant role of the HPA axis 74 . Interestingly, endothelial dysfunction after mental stress has been shown in hypertensive subjects but not in patients who have hypercholesterolemia 75 . This finding is noteworthy because both hypertension and hypercholesterolemia are risk factors for atherosclerosis and cardiovascular disease, and endothelial dysfunction is a...

Progesterone derivatives

The exact mechanism of action of these agents remains to be elucidated. It has been postulated that central appetite stimulation effect (probably mediated by NPY) (Engelson et al. 1999 McCarthy et al. 1994), reduction of serotonin and cytokine release (Mantovani et al. 1997, 1998), and a corticosteroid-like effect (Beller et al. 1997), suppressing baseline cortisol levels, suggest an impact on the HPA axis (Oster et al. 1994). MA inhibits secretion of LH and follicle-stimulating hormone (FSH) in males and females (Engelson et al. 1999) and reduces testosterone levels (Engelson et al. 1999 Venner et al. 1988). In vitro studies have identified that MA enhances the differentiation of pre-adipocyte mouse fibroblasts to adipocytes (Engelson et al. 1999) which suggests that MA increases not only cell size, but also cell number (Neuenschwander and Bruera 1998). Data are contradictory on the possible down-regulation of IL-6 levels by MA (Mantovani 2002 Jatoi et al. 2002). The effect of these...

Food stress and reward

The hypothalamus, especially the arcuate nucleus, is relatively accessible to circulating factors and receives inputs from other areas of the brain, including the tractus solitarius and the area postrema 79 . The hypothalamus receives signals that relate to total energy stores in fat and to immediate changes in energy availability, including insulin, leptin, and nutrients within the gut. Afferent signals from the gut to the brain are carried in vagal and splanchnic nerve pathways. The gut also releases several hormones that have incretin- (GLP-1, GIP), hunger- (Ghrelin), and satiety-stimulating (PYY, GLP-1, OXM) actions 79 . In addition, major afferent input originates from the adipose tissue. The adipocyte is now recognized as a bona fide endocrine cell. Adipocyte hormones such as adiponectin, resistin, and visfatin influence appetite, glucose homeostasis and insulin sensitivity, and vascular function, among other functions 80 . 59 Rosmond R, Bjorntorp P. Occupational status,...

Feed Your Humpty Dumpty Body Right

Refined food depletes cortisol, a hormone from the adrenals, which is required to shut off insulin when protein in the diet is low. When insulin stays elevated, your extra carbs are converted to fat around the belly in males and buttocks in females. Over time, with a breakdown of adrenal and pancreas function, exhaustion occurs. Once exhausted, the body no longer burns carbs effectively and therefore cannot provide fuel for the body. At that point, your body begins to rob muscle of nutrients. Arms begin to breakdown first resulting in skinny arms and legs. You end up with a Humpty Dumpty physique. It is best to then minimize refined carbs and sweet fruits and focus on more protein. Build up your natural body to maintain an A-1 spiritual body.

Fructose Consumption Body Weight and Obesity

Data comparing the effects of ingesting fructose-and glucose-sweetened beverages with meals indicate that fructose ingestion results in smaller increases in blood glucose and insulin concentrations following the meals. In addition, circulating leptin concentrations are lower, and the normal suppressive effect of meal consumption on ghrelin concentrations is attenuated with fructose beverages. Glucose, insulin, leptin, and ghrelin are all involved in the long-term control of food intake and body weight regulation through the central nervous system. Since these key signals are absent or weakened with fructose consumption, chronic consumption of a diet high in fructose could contribute, along with dietary fat and inactivity, to increased energy intake, weight gain, and obesity.

Very low carbohydrate high fat high protein

The basic assumption of the very low carbohydrate approach is that carbohydrates cause fat storage because they increase insulin production. Insulin is portrayed as an evil fat-storing monster that makes everything you eat turn into fat. The objective of these programs is to control insulin by cutting out carbohydrates and this will supposedly cause rapid body fat loss.

Pathophysiology of Stone Formation

Other conditions predisposing to gall bladder disease Insulin-resistant diabetes predisposes to cholelithiasis. A Swedish study showed that the prevalence of gall stones in Crohn's disease was twice that seen in the general population. Cirrhosis is another major risk factor for gall stones. The incidence of gall stone formation in cirrhosis is 10 times that seen in the general population. The incidence increases with the severity of cirrhosis, being worse in Child's class B and C disease and in patients with higher body mass index. High estrogen level and reduced hepatic synthesis and transport of bile salts are reasons for the increased risk in cirrhosis. The Physicians' Health Study showed that 30 minutes of endurance-type exercise five times per week prevents approximately one-third of cases of symptomatic gall stones in men. The Nurses' Health Study confirmed the same trend in women.

Friedman Jeffrey 1954 MD PhD

F riedman led the team that discovered the obesity hormone, Leptin, by studying genetic mechanisms of weight regulation in mice. The fat mouse had been discovered at the Jackson Laboratory in Bar Harbor, Maine in the early 1950s. This mutant mouse was so huge that researchers assumed that it was pregnant, until it was discovered that it was a male mouse. Friedman was inspired by the work of Ethan Allen Sims, a physician at the University of Vermont College of Medicine who had been exploring the link between obesity and diabetes using male inmates at the Vermont state prison. Allen found that only very few inmates could easily put on weight, and these found it the most difficult to lose it. were already known to Friedman and his colleagues. The next step was to continue to narrow down where on the chromosome ob is by comparing it to other genes close to it (by making a genetic map, which gets increasingly specific). After this, they had a very small (comparatively) region of DNA which...

Eating more sugar while dropping the fat creates a whole new problem

When people began dropping the fat out of their diets, they created a whole new problem - their blood sugar and insulin levels went through the roof Without fat, there's nothing to slow the absorption of carbohydrates into the bloodstream. The result is a huge blood sugar and insulin spike. One of the secrets of fat loss is insulin management. A seesaw cycle of blood sugar and insulin ups and downs contributes to fat storage and a variety of diseases. Eating fat-free, high sugar food makes this up and down cycle worse and can eventually create a diabetes-like condition in the body.

Hunger Physiological Determinants

Stomach distension and the detection of macro-nutrients such as fat or protein within the gut are all powerful satiety cues. They bring a meal to an end and for a time inhibit further consumption. Eventually, hunger again prevails and food intake follows. The flux between hunger and satiety is episodic and underpins the expression of our eating behavior throughout the day. However, it is not just the absence of episodic satiety cues (e.g., stomach distension and intestinal or absorbed nutrients) that influence the expression of hunger. Reduction in blood glucose levels or in levels of the circulating adipose tissue hormone leptin indicates a deficit in available energy and in energy reserves. Fluctuation of these factors indicates the metabolism and storage of the body's energy reserves. These are a tonic class of physiological signals that also influence the expression of appetite. Like episodic satiety signals, these tonic signals normally act on inhibitory mechanisms with the...

Mineralocorticoid Effect

The GA constituent in licorice (and its metabolite 3-monoglucuronyl-glycyrrhetinic acid) inhibits the enzyme 11 HSD (Kato et al 1995), which catalyses the conversion of Cortisol into its inactive metabolite, cortisone. This results in delayed excretion and prolonged activity of Cortisol. Additionally, GL and GA bind to mineralocorticoid and glucocorticoid receptors and may displace Cortisol from its carrier molecule, transcortin (Nissen 2003). Pseudohyperaldosteronism As Cortisol levels rise, they stimulate mineralocorticoid receptors in the distal renal tubule (Walker et al 1992). This creates pseudohyperaldosteronism, which has the same clinical features as primary aldosteronism, including sodium retention, fluid retention and oedema, hypertension, hypokalemia and metabolic alkalosis (Armanini et al 1996, Heldal & Midtvedt 2002, Kato et al 1995, vanUum et al 1998, Walker & Edwards 1994). A case report suggests that the symptoms occur despite low plasma levels of aldosterone...

Hepatic Glucose Metabolism

Gluconeogenesis is elevated in head and neck cancer patients and also in lung cancer patients. Gluconeogen-esis accounts for approximately 50 of the overall glucose production after an overnight fast. It was demonstrated that glucose carbon recycling was elevated in five of seven published studies. Glucose carbon recycling is an indicator of increased gluconeogenesis. The ability to measure gluconeogenesis was not possible in humans until recently, when a method using U-13C glucose and isotopomer analysis was developed. The Cori cycle is increased in cancer patients and has been estimated to account for 300 kcal of energy loss per day. In 70 of published studies, cancer patients have a significant elevation in the rate of gluconeogenesis compared to normal weight-matched controls. Gluconeo-genesis was directly related to the morning blood cortisol concentration in both the normal volunteers (r 0.913, p < 0.01) and the cancer patients (r 0.595, p < 0.05). In the septic host, the...

Hormonal Response to Injury Infection and Cancer

Infection, cancer, or any injury to the body result in an increase in counterregulatory hormones as well as insulin concentration. As a result of cancer, sepsis, or injury, many patients develop the syndrome of insulin resistance even though they had no history of diabetes prior to cancer. In cancer patients, when the overall injury is smaller, many studies have failed to demonstrate an elevation in counterregula-tory hormones. Mild elevations in cortisol concentrations may contribute to the protein catabolism and increased gluconeogenesis. When serum insulin is measured with a sensitive assay, cancer patients demonstrate a small but significant elevation in serum insulin concentration. This is consistent with the observation that these patients have insulin resistance. Cancer patients, like diabetics, have a reduced glucose utilization and loss of the first-phase insulin The rise in serum cortisol as the host's response to the tumor is one of many factors that are responsible for the...

Fat across the Species Barrier

I n 1997, researchers presented a claim at the Experimental Biology meeting in New Orleans (a city known for food) that obesity could be caused in part by an infectious agent, adenovirus-36 (Ad-36). Nikhil Dhurandhar (then at Wayne State University, Detroit, Mich. and now at the Pennington Biomedical Research Center at Louisiana State University in Baton Rouge) and Richard Atkinson (Obetech, Richmond, Virg.) undertook to show that this increase in obesity is the type of pattern that might occur with a new infectious disease, as has been seen with the AIDS virus (Anon. Virus May Be Linked to Obesity 1997). Both were engaged in obesity research. Indeed, Atkinson was a founder of the American Obesity Association and an editor of the association's flagship journal. They speculated that Ad-36 makes animals fat by stimulating the growth and reproduction of adi-pocytes (fat cells), as well as by causing immature adi-pocytes to mature more quickly. Thus, they claimed that animals infected...

Memory Storage Modulation of

Emotionally exciting experiences induce the release of adrenal hormones, including the adrenal medullary hormone epinephrine (Adrenaline) and the adrenal cortex hormone corticosterone (in humans, cortisol). Experiments with animal and human subjects indicate that these hormones, as well as other hormones released by learning experiences, play an important role in regulating memory storage (Izquierdo and Diaz 1983 McGaugh and Gold 1989). Administration of epinephrine to rats or mice shortly after training enhances their long-term memory of the training (Gold, McCarty, and Sternberg 1982). b-adrenergic antagonists such as propranolol block the memory enhancement induced by epinephrine. Comparable findings have been obtained in studies with human subjects. The finding that b-adrenergic antagonists block the enhancing effects of emotional arousal on long-term memory formation in humans supports the hypothesis that b-adrenergic agonists,

Correlates Of Adjustment

There are relatively few investigations of the relations between personality attributes and adjustment in patients with AC, but preliminary evidence suggests that the dispositional traits of emotional expressiveness, low chronic anxiety, and optimism may predict psychological well-being. Emotional regulation styles typified by conscious suppression or lack of awareness of affect appear problematic for patients with AC. For example, high dispositional emotional control (i.e., suppression) was associated with greater mood disturbance in a study of 101 metastatic or recurrent breast cancer patients.55 Similarly, a study by Weihs and colleagues56 demonstrated that AC patients who are habitually unaware of their emotions report more negative mood states than those that are less repressive. In addition, the individuals in this sample who reported the most mood disturbance were those that were both emotionally constrained and dispositionally anxious, suggesting that...

Hormonal Control of Secretory Activation

The decrease in progesterone around parturition is generally agreed to be required for the onset of milk secretion. In humans, it is known that removal of the placenta, the source of progesterone, is necessary for the initiation of milk secretion. In swine, timing of the increase in milk lactose correlates closely with timing of the decrease in plasma progesterone at parturition. Exogenous progesterone prevents lactose and lipid synthesis in mammary glands of pregnant rats and sheep after removal of their ovaries, the source of progesterone in these species. Progesterone also suppresses -casein expression in the rat mammary gland during pregnancy and the decrease in progesterone levels is linked to increased -casein synthesis at parturition. Receptors for progesterone are not detected in lactating mammary tissues, which explains why progesterone does not inhibit established lactation. It is likely that the decline in progesterone is insufficient to activate secretion and that the...

Protein intake and gaining lean body weight

You need more calories to gain weight, but if you added all the extra calories in the form of fat or carbohydrate, you would probably find yourself quickly gaining body fat As bodybuilders know all too well, excess carbohydrates, especially in the presence of a calorie surplus, can easily cause fat storage. The same goes for dietary fats. A high calorie diet with 70 of the calories from carbohydrates might be okay for a long distance runner, but chances are, most people would get as smooth as a baby's butt

Protein intake and low carbohydrate dieting

Some people are very sensitive to carbohydrates. When they eat a lot of carbohydrates, their bodies overreact. There's an unusually large surge in their blood sugar and insulin levels, which may increase fat storage and inhibit enzymes that promote the breakdown of stored body fat. One solution to this problem is less carbohydrate and -you guessed it - more protein.

Detoxified for Health

There are many thoughts and hypothesis by Western medical thinkers as to the cause of breast lesions. Studying natural therapeutics for over 30 years, I must tell you from my experience that the three leading causes of unchecked elevated estrogen levels arise from 1) synthetic HRT (sourced from horse urine), 2) congested livers not capable of clearing estrogen, and 3) obesity. Eating high-fiber food and whole food B vitamins are absolutely necessary to combat high estrogen levels. An optimally functioning thyroid is needed to have proper bowel movements. Flax oil, rich in Omega 3 fat, promotes overall optimal hormonal function. A congested liver from consuming too much caffeine from coffee, tea, and chocolate can also lead to breast cysts.

The many types of carbohydrates

There are simple and complex carbohydrates, starchy and fibrous carbohydrates, refined and natural carbohydrates, high-glycemic and low-glycemic carbohydrates. Some of these carbohydrates are good and some are bad. The good carbohydrates are your friends they will supply you with energy and nutrients and help you get leaner and more muscular. The bad carbohydrates are your foes they have a greater potential for fat storage, they are nutritionally void and rob you of energy.

Nutrition Alcohol And Drugs

Cally leptin, a hormone secreted by fat tissue that affects the brain's appetite control centers. In some studies, mice given injections of leptin lost their appetites and, consequently, lost weight. The human response to leptin varies dramatically, and the relationship between plasma leptin levels and obesity in humans is not yet clear or confirmed. According to one study, mutations in the leptin gene are indeed responsible for obesity in both mice and humans, but these mutations are quite rare outside of the laboratory setting. Another study shows that leptin is a signal to the hypothalamus of peripheral fat deposits, but further studies are being conducted to determine if obese individuals have trouble with leptin access into the brain. Other researchers have found that lean, physically active men have lower levels of leptin than heavier, sedentary men (ages 47 to 83). Leptin research continues since solid findings could help in the treatment and prevention of obesity and diseases...

Virginia Uhley and KL Catherine

Hormone-binding globulin production is elevated levels of free estrogen in blood circulation. As a result, the risk for breast cancer is increased. Patients with metabolic syndrome or elevated levels of insulin and IGF-1 also have an increased risk for colon cancer.12,13 Other metabolic abnormalities observed in obesity as part of the metabolic syndrome include high levels of total cholesterol, low-density-lipoprotein cholesterol (LDL-C) and triglyceride, low levels of high-density-lipoprotein cholesterol (HDL-C), and hypertension.7 A low HDL-C has been shown to be associated with high levels of blood estrogen, leptin, and insulin, and thus may serve as a marker for breast cancer risks in postmenopausal women.14-16 (3) Other metabolic alterations. Obesity is characterized with elevated blood leptin levels.17,18 Leptin, the protein product of the ob gene, is secreted by adipose tissue and is directly correlated to total adipose tissue mass in the body.18 Leptin has been reported to be...

Psychological Stress the Stress Response and the Impact on Immunity

Stress is an intrinsic part of life, and successfully adapting to stimuli that induce stress is necessary for the survival of an organism in its environment that is constantly changing. Although there is not a commonly used definition of stress, the concept of stress is often broken down into the challenge (called the stressor) and the behavioral and physiological responses to this challenge (called the stress response). A stressor is any stimulus that disrupts internal homeostasis, and can involve psychological, physical, or physiological stimuli. Initiation of the response to physiological and physical stressors is often subconscious and completely biological in nature. But, psychological stressors evoke an additional cognitive processing where the stressors must first be encoded as exceeding the organism's ability to cope with the demand. This cognitive processing sets into motion a coordinated behavioral and physiological response that is similar to the response to physiological...

Calorie density of carbohydrates

In addition to choosing carbohydrates on the basis of whether they are refined or natural, another criteria you should use for carbohydrate selection is calorie density. Eating more calories than your body can handle at once is the primary cause of fat storage. Therefore, it makes sense that you should choose foods with a low calorie density if you want to lose fat.

Regulation of Meal Size by Satiety Peptides and Adiposity Signals

Adiposity signals such as leptin act in conjunction with satiety signals in the brain during digestion and their concentration is determined in relation to the degree of adiposity. Like CCK, the effect on meal consumption and body weight of their exogenous administration is dose dependent. Leptin is a peptide hormone produced predominantly by adipocytes, and it is also secreted by the epithelial cells of the stomach. The definitive role of leptin in digestive physiology is still being determined, but it is thought to play a part in limiting food intake in conjunction with CCK. It is when the adiposity signals interact with, and influence, the satiety signals originating from the gut that an attempt at controlling energy intake and meal size is made.

Mineral Tissue Analysis

I commonly see a deficiency of zinc in individuals who have low energy. Zinc is needed to make insulin, a factor needed for carbohydrate metabolism. Copper is often elevated in individuals with a low zinc level. When copper is elevated in females, I also see high estrogen levels with associated symptoms of PMS heavy menstrual flow and tender breast tissue.

Israel Liberzon1 Samir Khan2 and Elizabeth A Young3

The most extensively characterized neuroendocrine change associated with PTSD involves abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis. A wide variety of psychological and physiological stressors are known to produce acute activation of this axis (Herman and Cullinan, 1997) and termination of HPA activation is accomplished through a negative feedback system involving stimulation of glucocortiocoid receptors by Cortisol at the level of the hippocampus, hypothalamus, and or pituitary. PTSD patients are shown to have lower 24-h circulating levels of Cortisol in some studies (Mason et al., 1986 Yehuda et al., 1995b) although others have found no sustained baseline differences (Mason et al., 2002). Their HPA axis is also characterized by an enhanced negative feedback system. A number of studies have demonstrated increased suppression of plasma Cortisol in PTSD patients following administration of low doses of the glucocorticoid agonist dexamethasone (Yehuda et al., 1993...

Prenatal Stressor Induced Alterations to Microflora Development

To determine the impact of a prenatal stressor on microflora development, an acoustical startle stressor (i.e., 3 random 110 dB beeps over a 10 min period occurring 5 days per week) was used to evoke a stress response from pregnant rhesus monkeys either early (days 50-92) or late (days 105-147) in the 169 day gesta-tional period. These periods represent crucial time periods in nervous system and GI system development, thus making it likely that disruption of physiological homeostasis at these time points affects fetal development. This stressor resulted in a significant increase in cortisol in the pregnant mothers, but did not appear to significantly affect the number of miscarriages, gestational length, or birth weight (Bailey et al. 2004b). The stressor did, however, significantly affect the development of the intestinal microflora.

Toward a Mechanism of Stressor Induced Alterations in Microflora

It is tempting to speculate on the mechanisms through which the intestinal microflora could have been altered by stressful pregnancy conditions. For example, it is known that cortisol can affect many aspects of infant development, and many of the effects of prenatal stress on the immune system can be mimicked by administration of ACTH or the synthetic glucocorticoid, dexamethasone (Coe et al. 1996). And, others have found that giving corticosterone to pregnant rats significantly reduced the concentrations of total and Gram-negative aerobes and facultative anaerobes (Schiffrin et al. 1993). The mechanisms through which glucocorticoids might affect the microflora are not known, but fetal development of the gi tract is thought to be influenced by glucocorticoids. For example, maturation of the intestines occurs concomitantly with the prepartum surge in cortisol in pre-cocial species, such as pigs, sheep, and humans (Trahair and Sangild 1997). Moreover, very high levels of glucocorticoids...

Hazard Identification

No signs of neurological damage have been reported in humans. For example, in adult males given a chemically defined diet in which glutamate was the only source of dispensable nitrogen for periods of 14 to 42 days, no changes in neurologic or hepatic function were detected (Bazzano et al., 1970). However, concern was raised by a report that a large dose of glutamate taken orally stimulated the secretion of prolactin and cortisol (Carlson et al., 1989). Earlier findings that rats injected with 1 g kg of glutamate showed stimulation in the secretion of luteinizing hormone and testosterone (Olney et al., 1976) were interpreted as indicating that the high concentration of glutamate had penetrated the neuroendocrine parts of the hypothalamus. Similarly, it was shown that the same dose of glutamate stimulated release of prolactin and inhibited the release of growth hormone (Terry et al., 1981). The data of Carlson and coworkers (1989) might therefore be interpreted to imply that the...

Potential Explanations for the Decreasing Age of Pubertal Onset

Other hypotheses regarding the earlier onset of puberty focus on more intrinsic factors. For example, perinatal factors, such as birth weight, have been found to play a role in subsequent pubertal development. In one study, girls who were smaller at birth but had a rapid catch-up period of growth between birth and age 6 were earlier maturers (Persson et al., 1999). Mechanisms for this association are not clear, but it is likely that the prenatal environment may influence subsequent timing of onset of development, given that sex hormones are active prenatally in organizing the brain for subsequent pubertal development and reproductive functioning (Fechner, 2002). A more widely discussed hypothesis is that higher body fat is associated with earlier maturation. In general, overweight girls tend to mature earlier than girls of normal weight, and thin girls tend to mature later. Numerous studies have indicated that in the past thirty years, there is an increasing prevalence of obesity in...

Potential Reasons for Ethnic Differences in Age of Pubertal Onset

A finding across three large-scale studies conducted in the 1980s and 1990s, the PROS study (Her-man-Giddens et al., 1997), NHANES III (Wu et al., 2002), and the National Heart, Lung, and Blood Institute Growth and Health Study (Morrison et al., 1994), is that African American girls begin breast and pubic hair development about a year earlier than White girls and begin menses about half a year earlier. The reasons for the earlier age of secondary sexual characteristic onset for African American girls are not clear. Possible factors to consider include differences in diet and weight, environmental hazards or environmental estrogens, or differences in contextual stress and cultural attitudes between ethnic groups (Graber, 2003). Physiological differences that have been hypothesized to play a role in timing of pubertal onset include lower insulin sensitivity (Arslanian, Suprasongsin, & Janosky, 1997) and higher serum leptin levels (Wong et al., 1998) in African American children...

Uses of Anthropometric Measurements

In adults and children, anthropometric measurements can be used to estimate body fat and lean body mass and assess their distribution and change over time. Body fat includes storage fat, found inter-and intra-muscularly, around the organs and gastrointestinal tract and subcutaneously, as well as lipids in bone marrow, central nervous tissue, mammary glands, and other organs. Normal-weight men and women have about 10 and 20 body fat, respectively. Lean body or fat-free mass is mostly water and protein with relatively small amounts of glyco-gen and minerals. Inadequate diets are associated with low body fat stores and reduced lean body mass in adults and growth failure of children. Consumption of food greater than requirements results

Examining Pathways Between Pubertal Effects and Adjustment in Girls

A series of regression models were run to examine the potential mediated pathways from either hormonal levels or pubertal timing to depressive affect or aggression, controlling for age. Despite the hypothesis that estradiol would lead to emotional arousal which would lead to depression, there was no support for this pathway in the analyses. However, as seen in Figure 16.6, the effect of pubertal timing on depressive affect was mediated by emotional arousal. The fact that emotional arousal did not explain the estradiol effect on depressive affect as expected warranted further exploration. Because links between adrenal response (e.g., cortisol response) and psychosocial stress have been extensively noted, DHEAS levels (another indicator of adrenal response) were examined in association with early maturation. The interaction between hormonal arousal (the upper third of the distribution of DHEAS considered high hormonal arousal) and timing (early versus other) was predictive of depressive...

Learn How to Exercise at the Right Level of Intensity

Our goal in this exercise program is not maximum effort but doing each type of exercise at a level of intensity, based on your gender, which will guarantee the greatest amount of fat loss and increased metabolic efficiency in the shortest amount of time. Because somewhat different hormonal responses occur during fat storage and fat metabolism in each gender, men and women tend to respond best to different exercise intensities. According to a study published by the IDEA Health and Fitness Source, women lose more fat by exercising at low to moderate levels of intensity while men seem to lose more fat by exercising at moderate to high levels of intensity. The reason is that women sustain a lower respiratory exchange rate (RER) than men during exercise at lower intensities. RER is the numeric index that indicates the amount of carbohydrates and fat used during exercise based on the ratio between the amount of carbon dioxide you produce in relationship to the amount of oxygen you consume....

Sequelae of Altered Metabolism in Visceral

Leptin is a hormone that is produced in the adipose cells and can act on the hunger center in the hypothalamus to reduce hunger and appetite and thereby lower food intake. Plasma leptin levels are correlated with body fat. Researchers have discovered a leptin receptor gene that is responsible for obesity due to the mutation or absence of the gene. This condition is extremely rare in humans. In general, in obese humans the leptin levels are elevated (hyperleptinemia). There is a progressive increase in plasma levels during puberty in girls due to the increase in body fat during this period and in response to the effect of estrogens. Circulating leptin levels tend to decrease in response to testosterone in boys, thus resulting in higher plasma leptin levels in women compared to men. Leptin levels are also affected by insulin and glucocorticoids.

R 0CHrCh R Nch Cn ihjn

Recent views are that breast tissue is capable of synthesising oestrogens mainly from the action of a sulphatase on oestrone sulphate. The oestrone produced provides oestradiol by the action of a 17p-hydroxysteroid dehydrogenase. Inhibitors of steroid sulphatase are being developed as potential adjuvants to aromatase inhibitors to further deplete oestrogen levels. One of these compounds emate (8.113) is an irreversible inhibitor of the sulphatase.

Obesity Associated with Recognized Medical Condition

Single gene defect affecting leptin metabolism Congenital leptin deficiency Leptin receptor defect Prohormone convertase-1 defect Melanocortin-4 receptor defect Peroxisome proliferators activated receptor POMC deficiency Biemond's syndrome Alstrom's syndrome Bardet-Biedl syndrome Biemond's syndrome (some) Carpenter's syndrome Cohen's syndrome proportion of obese children. With the exception of very rare single gene defects in leptin metabolism, obesity is a secondary feature in these conditions and presentation is usually for some other aspect of the condition. Single gene defects affecting leptin are associated with progressive gross obesity from early life and may respond with dramatic fat loss with leptin treatment. Where obesity is only a part of a spectrum of abnormalities, common associated features are short stature, developmental delay, and craniofacial and other bony abnormalities.

Drugs For Dyskinesia Sarizotan

64 dyskinetic PD subjects, sarizotan, at doses ranging from 2 mg BID to 10 mg BID, prolonged the amount of on time without dyskinesia (55). PD symptoms were not worsened, as assessed by amount of off time or UPDRS scores, although some patients did report worsening of parkinsonism as an adverse event. Additional adverse events reported included sedation and nausea. Higher doses have been associated with suppression of the cortisol response to ACTH challenge, but this was not seen in PD. A large multicenter Phase III trial did not demonstrate a difference between sarizotan and placebo and consequently the development of this compound for PD has been abandoned (56).

Abnormalities of Hormones and Other Circulating Factors

Syndrome, including abdominal obesity, insulin resistance, impaired glucose homeostasis, hypertension, and lipid abnormalities. These similarities led to the hypothesis that a dysregulation of the HPA axis in the form of functional hypercortisolism could potentially be a cause for abdominal obesity and its different metabolic consequences. High levels of emotional or physical stress are thought to increase cortisol secretion or turnover and thereby increase visceral obesity. Another potential mechanism involves the peripheral metabolism of cortisol. The enzyme 11- -hydroxysteroid dehydrogenase, which converts steroid precursors to cortisol, is expressed in adipose tissue. With increasing obesity, more cortisol is derived from cortisone in adipose tissue due to the increased activity of this hormone. Urine studies in obesity also show an increase in the ratio of tetra-hydrocortisol to tetrahydrocortisone, indicating a relative increase in the pathways leading to cortisol formation....

Avoid fatproducing food combinations

Dallas Clouatre, author of Anti-Fat Nutrients, explains, When fat is eaten at the same time as simple carbohydrates, both the fat and the carbohydrates are pushed into fat storage. The 'bad' coupling of fats with carbohydrates slows down your metabolism and causes you to gain weight.

What are the causal relationships between fatigue and depression

There is considerable evidence to suggest that the correspondence between fatigue and depression in cancer patients may be due to their causal relationship to a third factor. Along these lines, attention has focused on certain cancers that are believed to cause depressive symptoms. Pancreatic cancer is one neoplasm that appears to display these characteristics. The prevalence of depression-related disorders among patients with pancreatic cancer is estimated to be as high as 71 (Green and Austin 1993). Moreover, numerous reports have documented the presence of depressive symptoms in patients before their pancreatic cancer was diagnosed (Joffe et al. 1986 Holland et al. 1986 Kelsen et al. 1995). Recent physiological findings provide further evidence of a causal link between pancreatic cancer and depression. Pancreatic tumours have been shown to secrete various neuropeptides and neurohormones, such as adrenocor-ticotropic hormone (ACTH) and cortisol (Raddatz et al. 1998 Drake et al....

Biological Consequences

Cancer survivors, by virtue of persistent high levels of both physical and psychological stress, may also be susceptible to the adverse biological effects of elevated stress-related hormones, such as excessive cortisol secretion (e.g., ref. 52) and production of catecholamines such as adrenaline.53,54 Sustained increases in stress hormones can in turn have inhibitory effects on functional immunity.55 For example, elevated cortisol secretion can decrease antibody production, and inhibit natural killer (NK) cell activation,56-58 important aspects of immune functioning that may protect cancer survivors from disease recurrence and other infections. Not surprisingly, compromised immune and neuroendocrine function have been noted in cancer patients (e.g., refs. 59-63), features inimical to recovery from disease. In addition, elevated basal cortisol levels and blunted cortisol responses to acute stress tasks have been observed among some individuals with cancer,64-66 and have been associated...

How are MS attacks treated Why are there different drugs to treat attacks of MS

ACTH (or corticotrophin) is a hormone that is made in the brain and is stored in the pituitary gland, which is situated at the base of the brain. This hormone is normally released in miniscule amounts during the early hours of the morning to stimulate the adrenal glands' production of steroid hormones. Cortisol, the active form of cortisone, is one product of ACTH stimulation. Dr. Leo Alexander began using ACTH a half-century ago at Harvard Medical School. He showed in a series of studies that it speeded recovery from MS attacks. Later, a national study, published in 1970, proved that it did indeed significantly speed the recovery for patients with acute exacerbations of MS. glands secrete steroid hormones that are important in the body's response to stress. Cortisol the stored form of cortisol produced by the adrenal cortex.

Placental Buffering of Maternal Dietary Intake

Some of the maternal nutritional adaptations in pregnancy. For example, placentally derived leptin is a potent stimulator of lipolysis and there is evidence that the rate of export into the maternal circulation is controlled to allow the placenta to modulate its own substrate supply in response to the fetal demand for fats. The various homeostatic mechanisms within the placenta and their interaction with maternal physiological adaptations during pregnancy act to ensure a constant supply of substrate to the fetus, free of large diurnal fluctuations corresponding to the timing of maternal meals, and to protect the fetus against a transiently poor intake during critical periods of fetal growth. These adaptations help the mother to meet the full fetal requirement for nutrients such as LCPUFA and iron whilst consuming apparently poor diets.

Liposuction No Heart Saver

Liposuction can remove fat cells, but unlike diet and exercise may not cut your risk of heart disease and diabetes. Researchers removed roughly 20 pounds of mostly abdominal fat from l5 obese women (each had at least a 40-inch waist). But after 10 to 12 weeks, there was no change in their insulin resistance, blood sugar, blood pressure, cholesterol, C-reactive protein, or other risk factors for heart disease.53 Natural Prescription for Health If you're overweight, eat less and exercise more. Liposuction may shed pounds but not risk. It doesn't make you take in fewer calories than you burn. Another possibility Although it removes fat cells that are subcutaneous (just under the skin), liposuction doesn't shrink fat cells or remove the fat that's deeper in the abdomen, liver, and muscles.

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