Lose Weight By Controlling The Fat Storage Hormone
Cortisol is often regarded as the stress hormone. It is important to realize that fasting, especially prolonged fasting, is a form of stress and stress results in the release of cortisol from the adrenal glands along with epinephrine mentioned in the previous question. Cortisol also supports the breakdown of glycogen and the conversion of amino acids, lactate, Table 4.5 Actions Of Insulin, Glucagon, Cortisol, and Epinephrine in Carbohydrate Metabolism Cortisol Increases muscle protein breakdown to amino acids which can and glycerol to glucose in our liver. Because cortisol also promotes the breakdown of our body protein, especially skeletal muscle protein, it ensures a supply of amino acids for conversion to glucose in our liver (Figure 4.5). Adrenal glands Cortisol Figure 4.5 During fasting and endurance exercise (at least moderate intensity) cortisol causes the breakdown of muscle protein and some amino acids can be used to make glucose in our liver. Quite simply, the greater the...
A person's body weight is determined by the factors hunger satiation and energy intake energy use. Ever since hereditary forms of obesity were discovered in mice in the 1950s, researchers have investigated the regulation of these factors. About 20 years ago, it was found that the so-called ob mouse (for obese) is missing a satiety factor that would normally circulate in its blood. Finally, in 1994, the ob gene was cloned. The expression product, leptin, consists of 167 amino acids. Administering lep-tin to ob mice normalized their body weight by reducing energy intake and increasing energy use, mainly by increasing body temperature. Leptin and its effects have since been confirmed in humans. Leptin controls energy uptake and use by regulating various satiety factors (A) in the hypothalamus, such as neuropep-tide Y (NPY) or glucagon-like peptide 1 (GLP-1). Since leptin is synthesized in white adipocytes, fat mass functions as a sort of central control sensor. The expression of the ob...
Research studies have supported the notion that all calories are not equal when it comes to leading to body fat accumulation. For instance, all foods increase our metabolism to some degree, which scientists refer to as the thermal effect of food. However, when people eat different meals containing the same number of calories but with different nutrient compositions, in some cases they burn more calories in the couple of hours that follow. In particular, foods with more calories from protein and unsaturated fat tend to increase calorie burning more than if those same calories came from carbohydrate and saturated fat. So less of the food calories would be available for fat storage.
Scientific investigations have shown that physical activity, including aerobic and muscular strengthening exercises, not only prevent bone mineral loss, they also help alleviate many menopausal symptoms, including the increased percentage of body fat, abdominal-fat storage, hot flashes, fatigue, and sleep disturbances.
As a female gains weight during pregnancy, usually about 7 to 8 pounds is attributable to the weight of the infant at birth. The rest of the weight is distributed throughout the mother in various tissues developed during pregnancy. These tissue include the placenta, amniotic fluid, increased breast tissue, expanded blood volume, and fat storage and muscle. These all help support the mother and fetus during pregnancy and after birth. Even the mother's bones will become a little denser during pregnancy.
The need for dietary fat is not necessarily for energy purposes. Fat is needed in our diet as a means of providing two essential fatty acids, linoleic acid, an ra-6 PUFA, and a-linolenic acid, an ra-3 PUFA. Since the amount of these fatty acids in fat storage (adipose tissue) is limited, this suggests that their role in our body isn't really to provide calories, although they will be used for energy. Linoleic and a-linolenic acid are used to make longer, more complex fatty acids that have special functions.
Fat tissue provides some protection to various tissues in the body. For instance, fat tissue around our internal organs provides some cushioning. This helps protect the organs against external trauma. Furthermore, the subcutaneous layer of fat storage also provides some cushioning, which protects muscle. Subcutaneous fat is not well vasculated, meaning that there aren't a lot of blood vessels in that tissue relative to other tissue. Meanwhile, skeletal muscle is heavily endowed with blood vessels which provide oxygen and energy nutrients during activity and exercise. In the absence of subcutaneous fat it would be easier to rupture smaller blood vessels in skeletal muscle, which then would be evident in bruises. As an example, prior to competition, bodybuilders will be very cautious not to bang into things or play contact sports (rugby, football, roller hockey, etc.). As they attempt to lean out for the competition, they reduce their subcutaneous fat to nadir levels, which would allow...
Women store essential fat in their hips, thighs, and breasts. This fat is readily available to nourish a healthy baby if a woman becomes pregnant. If you are a woman fighting the battle of the bulging thighs, you may be fighting a losing battle. The activity of the enzymes that store fat in women's thighs and hips is very high compared with the enzyme activity in other fat storage areas in women and compared with fat storage in the hips and thighs of men. Moreover, the activity of the enzymes that release the fat is low, making it difficult to lose fat in these areas. The easiest time for women to lose fat in this area is during the last trimester of pregnancy and while breastfeeding. At those times, the activity of the fat-storing enzymes drops, and the activity of the fat-releasing enzymes increases. Nature, again, is protective of a woman's ability to care for her offspring.
In a second study in resistance training elderly subjects, strength gains during the study were similar between the HMB-supple-mented group and the placebo-supplemented group.47 However, HMB supplementation significantly improved functional ability as measured by a get up and go (GUG) test,47 which measures the time to get up out of a chair, walk a set distance, turn around, and return to the chair and sit down again. Decreasing body fat and improving muscle function are both important findings in the elderly. Body fat, and in particular visceral fat storage, is linked to the development of insulin resistance (type II diabetes)48 and cardiovascular disease.49 Additionally, improving functional ability in the elderly should improve the quality of life and may result in decreasing falls, a common cause of injury in the elderly population.
For a number of years, particularly since the 1980s, when rates of overweight and obesity in the United States began to climb rapidly, experts have been concerned by the effects of different foods on appetite and blood sugar regulation. Scientists became interested in how different foods affect blood sugar, insulin release, and, in turn, energy usage and fat storage. In exploring the impact of foods on blood sugar, scientists constructed the glycemic index (GI), a scale for measuring and classifying foods based on how quickly they raise blood sugar. The best foods, according to these scientists, are foods that rank low on the index foods that are digested slowly, cause a gradual rise in blood sugar, and lead to a moderate insulin response. The least favorable foods in terms of glucose response are those that elevate blood sugar levels quickly and lead to a rapid insulin response that results in a burst of energy that drops off rapidly.
Yo-yo dieting may result in a higher risk of heart disease and diabetes. When fat is regained after dieting, it may be stored around the abdomen. Abdominal fat storage, in contrast to fat stored in the leg or hip region, appears to be a risk factor in the development of certain diseases. Yo-yo dieting also may increase your percent of body fat. When you lose weight through dieting, you lose both fat and muscle tissue. However, when you stop dieting, excess calories are stored in the form of fat. Therefore, even if you regain only as many pounds as you lost through dieting, your body is likely to be fattier than it was previously.
The presence of certain types of fatty acids in either a plant or an animal largely depends upon the nature of the plant or animal and the purpose of the fat for that life-form. For instance, fish that live in deeper water tend to be better sources of ra-3 PUFA because these fatty acids are found in the cell membranes of these fish and play a protective role against the increased pressure and decreased temperatures at greater depths as well as help regulate their buoyancy. Land animals create storage fat that is largely composed of saturated fatty acid. Since these fat molecules can pack tightly in fat cells it minimizes the necessary space.
For a long time fat tissue and their cells were viewed as somewhat inert containers of energy storage. However, today we know that adipose tissue functions as a gland with the capability to release a variety of factors relative to its size and endowed energy. As mentioned previously, some of these factors may promote the formation of more fat cells. Perhaps some of the most interesting released factors are those that circulate to the brain and provide insight to our energy storage status. One of the most important factors seems to be the hormone leptin. Fat cells release more and more leptin into our circulation when fat cells accumulate more fat. Leptin then signals the brain to reduce appetite. In addition, as fat cells swell due to excessive calorie consumption, some of the chemicals they release can promote the development and worsening of diabetes, high blood pressure and other medical conditions.
During pregnancy, the fetus receives nutrients from across the placenta, including glucose, amino acids, and fatty acids via either active transport or facilitated diffusion. In the first trimester, maternal glycogen storage and endogenous glucose production increase. Pregnancy hormones (human placental lactogen and cortisol), estrogen, progesterone, and the constant fetal demand of glucose lower fasting maternal blood glucose levels 15, 16 . The maternal appetite is stimulated resulting in consumption of additional calories. Fasting and postprandial glucose levels rise in response to the extra glucose required for fetal growth. Elevated hormonal levels increase insulin resistance and the beta-cells produce and secrete additional insulin as glucose is transported across the placenta. Insulin resistance peaks by the latter part of the third trimester, which is characterized by a three-fold increase in insulin production and secretion. After delivery, insulin production returns to...
Can We Discern Hopeful Signs In The Middle Of The Current Difficulties Created By These Disease Stat
Several discoveries over the past 10 years have created opportunities for prevention and or treatment, including discoveries of new genes, molecules, and regulatory pathways. Central, in my opinion, may prove to be developments in the field encompassed by the question How does negative energy balance lead to neuroendocrine abnormalities Recent work, mainly from our laboratory, has demonstrated that levels of an adi-pocyte-secreted hormone, circulating levels of which reflect the amount of energy stored in fat, i.e. leptin, fall in response to negative energy balance and this fall can lead to the neuroendocrine dysfunction that has traditionally been associated with energy, and thus leptin, deficiency states, such as anorexia nervosa and exercise-induced or hypothalamic amenorrhea. Importantly, exogenous administration of leptin, in replacement doses, can correct these neuroendocrine abnormalities in these leptin deficiency states. These novel advances, discussed in the relevant...
In energy deficiency states we clearly need to advance further our understanding of the role of leptin (and other hormones) to improve and or correct the neuroendocrine abnormalities of women with hypothalamic amenorrhea and anorexia nervosa as well as those of obese subjects dieting to lose weight and or having had surgery for obesity. We also need conclusive evidence from randomized trials on whether leptin and or other treatment options could also improve the osteoporosis of subjects with anorexia nervosa or hypothalamic amenorrhea. Importantly, we need to learn whether the effect of leptin in improving neuroendocrine function could facilitate weight maintenance of obese subjects who strive to lose weight. Much needed investigations are underway in this area.
In addition to the immediate control of feeding by hunger and satiety, there is also long-term control of food intake and energy expenditure, in response to the state of body fat reserves. In 1994 it was shown that the normal product of the gene that is defective in the homozygous recessive mutant (ob ob) obese mouse is a small peptide that is secreted by adipose tissue. Administration of the synthetic peptide to genetically obese mice caused them to lose weight, and administration of excessive amounts of the peptide to normal mice also caused weight loss. It was called leptin, from the Greek A, TCTOO - lean or thin. Further studies showed that the administration of leptin to the genetically obese diabetic ( fa fa) rat had no effect on body weight, and indeed these rats secreted a normal or greater than normal amount of leptin. The defect in these animals is a mutation in the membrane receptor for leptin. Initially, the leptin receptor was found in the hypothalamus, and because the...
In overweight women conceiving after in vitro fertilization (IVF) or intracytoplasmic sperm injection, miscarriage rate is also reportedly higher in obese compared with lean or average weight women. A systematic review of the literature by Maheshwari et al. 11 found that when compared with women with a BMI 25 kg m2, women with a BMI 25 kg m2 had a 29 lower likelihood of pregnancy and a 33 higher risk of miscarriage following IVF. In this same study, obese women were found to have a reduced number of oocytes retrieved despite requiring higher doses of gonadotropins. Mechanisms for the relationship between obesity and infertility are unknown. Suggested roles of hyper-androgenism, insulin resistance, high leptin levels, and polycystic ovarian syndrome are currently under investigation 12 . Regardless of mechanism, these data suggest that obesity may delay or prevent conception in women who want to become pregnant. Of some consolation, weight loss before infertility therapy may improve a...
Physiological studies have indicated that ghrelin serves as a peripheral signal for hunger and meal initiation Blood levels increase during fasting, peak sharply just before feeding, and fall rapidly following food intake (95). Prolonged administration of ghrelin in rodents leads to chronic hyperphagia and weight gain, and obese persons typically have high plasma leptin and low ghrelin levels (96). There is a diurnal rhythm in ghrelin secretion, with peak levels in the morning and the nadir at night (95). PYY3-36 appears to exert its anorectic effect through coordinate inhibition of orexigenic NPY neurons and stimulation of POMC neurons in the arcuate nucleus. These molecular changes are observed following peripheral administration of PYY3-36 (99). High-affinity hypothalamic Y receptors are the target of PYY3-36 action. Activation of the Y2 receptor subtype on NPY neurons triggers inhibitory presynaptic signals. Consonant with this mechanism, Y2 receptor knock-out mice lose their...
Hormones involved in fetal growth are nutritionally regulated in the fetus and also regulate substrate uptake and metabolism. The major fetal growth factors are the insulinlike growth factors (IGF)-I and II, with insulin having a passive role in fetal growth. The roles of other hormones such as growth hormone (GH), placental lactogen, leptin and ghrelin are as yet less clear. The role of other hormones that are involved in postnatal nutrition and growth, such as leptin and ghrelin, are beginning to receive more attention in the fetus.215 Both leptin and ghrelin are expressed in the placenta216-218 and both can be nutritionally regulated.218-221 The precise role of these hormones, and other nutritionally regulated hormones such as placental lactogen, remains to be elucidated, but a recurring theme for hormones that are also expressed in the placenta is the possibility that they may play a role in nutrient partitioning between mother and fetus.
In addition to reducing adipose tissue mass, the t10c12 CLA isomer has been linked to increased insulin resistance in men who have symptoms of the metabolic syndrome.2627 A CLA mixture also appeared to cause hyperinsulinemia in C57BL 6J mice24 that was accompanied by severe adipose tissue ablation and decreased leptin levels. The effects of the CLA mixture on adipose tissue depletion were reversed by continuous leptin infusion. In a follow-up study, decreasing the amount of a CLA mixture from 1 to 0.1 g 100 g diet, while increasing the amount of total fat in the diet from 4 to 34 g 100 g diet, did not lead to lipodystrophy, while fat mass was modestly reduced.25 Insulin resistance was present in the group fed the 1 g CLA 100 g diet, but not present in the 0.1 g CLA 100 g diet group.
The fat stored in fat cells is available to us when food energy is not being absorbed (fasting) and when we exercise. Just as the hormone insulin promoted the storage of fat when energy was coming into our body, the process of mobilizing fat from fat cells is promoted by the hormones released into our blood when we are fasting and or exercising (Figure 5.8). These hormones are glucagon, epinephrine, and cortisol, and all promote the release of fat from fat stores.
Driven by primarily by cortisol as well as epinephrine, both of which are elevated in circulation during exercise. Cortisol promotes muscle protein breakdown during the exercise while epinephrine promotes the conversion of amino acids to glucose in the liver. Since cortisol is a stress-related hormone, the degree to which this happen depends on how hard you exercising and for how long. Thus for shorter, less intense exercise sessions (for example, walking and casual bicycling) this isn't a consideration however for recreational and competitive endurance athletes and heavyweight trainers it is. We will explore this further in Chapter 11.
Eto et al. tested the effects of ARG-glutamate salt (AGs) ingestion on exercise-induced hormonal changes in highly trained cyclists, aged 18 to 22 years. There was no effect on resting plasma GH, insulin, or cortisol levels. However, ingestion of AGs dramatically diminished the elevation of cortisol and hGH during and after exercise. The results, related to the AGs and exercise-induced hormonal changes, led the authors to state the possibility that AGs supplementation may alter energy metabolism during exercise.19 Additional studies related to hormones and ARG supplementation are reviewed with AA blends and GH release in Section 220.127.116.11.
Depending on the duration of exercise, amino acids may be counted on to generate as much as 6 to 10 percent of the fuel with the remainder split between fat and carbohydrate. The use of amino acids for energy is mostly a consideration for higher-level endurance athletes. This would include people who train seriously several times a week for extended periods such as a couple of hours. This is one reason why marathoners often look very lean but not as muscular as sprinters or milers, for example. One of the most significant reasons that more and more amino acids are used for energy is because cortisol levels in the blood are increased as the higher intensity activity is endured. Cortisol can cause the breakdown of muscle protein and the freed amino acids can be used for energy. Some amino acids will be used directly by muscle to make ATP, while others will circulate to the liver and be converted to glucose.
Hormones may be grouped into one of two general categories amino acid-based hormones and steroid hormones. The amino acid-based hormones include hormones that are proteins and those hormones that are derived from the amino acid tyrosine. Examples of protein hormones include insulin, growth hormone (GH), glucagon, and antidiuretic hormone (ADH). Examples of hormones made from the amino acid tyrosine are epinephrine (adrenaline) and thyroid hormone (T3 and T4). Steroid hormones are made from cholesterol and include testosterone, estrogens, cortisol, progesterone, and aldosterone.
Two hormones, adrenaline and Cortisol, appear to be responsible for most of the destructive effects. When we experience stress, both hormones are released in large concentrations and as we age, Cortisol release is more prolonged. The physiological events that occur with stress are called allostasis unrelieved stress is known as an allostatic load. Dr. Bruce McEwen, director of the Laboratory of Neuroendocrinology at Rockefeller University, has demonstrated through a series of experiments conducted on animals the importance of the brain's response to the allostatic load. He found that unrelieved stress could destroy stem cells in a portion of the hippocampus of the brain, which is vital to memory storage and which contains more Cortisol receptors than any other part of the brain.466 In addition, stress destroyed synaptic connections and dendrites as well.
This is the key time to take advantage of the one thing high GI carbs do well raise blood sugar and insulin quickly. Post workout, the catabolic (muscle wasting) hormone cortisol rises. Drinking a post workout drink consisting of high GI carbs and fast acting proteins is perhaps the best way to prevent the post workout effects of cortisol due to the sharp rise in insulin which is known to counter act the effects of cortisol (Kraemer, W.J., et al, 1998). High GI foods can help refill liver and muscle glycogen stores immediately following exercise and may reduce the catabolic effects of cortisol post workout.
More and more research concludes that strength training helps reduce anxiety. Your body's response to stress is to release chemicals to prepare your body for it, like adrenaline, norepinephrine, and cortisol. Also called the fight or flight response. Being anxious about the holidays, your job, getting fit, or money also produces the stress response. But you still have those chemicals floating around in your bloodstream. Being sedentary and anxious is where stress wreaks havoc on your health - heart disease, high cholesterol, hypertension, and aging. Lifting against a resistance is a great way to burn up those lingering stress hormones and help you feel better.
The complete digestion and absorption of a meal can take several hours, depending upon its size and composition. Therefore, carbohydrate or more specifically glucose from that meal may be available for several hours as well. However, once this ends, a new blood glucose scenario begins to take shape. Cells throughout the body will continue to help themselves to glucose in the blood to help meet their energy needs. The net effect is that our blood glucose concentration will begin to decrease. When this happens the pancreas responds again. However, this time it responds by releasing the hormone glucagon into our blood (see Figure 4.3). In addition, epinephrine (adrenaline) and cortisol will promote efforts in different tissue that will help maintain blood glucose levels in-between meals.
Situations can occur that increase the use of body protein for energy. Eating too few calories or fasting increases the reliance on body protein as an energy source. In these situations the level of circulating glucagon and cortisol increase. Cortisol, the stress hormone, will promote the breakdown of our body proteins to amino acids. Meanwhile, both of these hormones promote the conversion of amino acids to glucose in our liver which is released to serve as fuel. The amount of amino acids used to make glucose is related to the length and degree of caloric restriction and the intensity and duration of exercise. Simply stated, as glycogen stores in the liver and muscle become depleted, as in prolonged fasting and aerobic exercise, the reliance upon amino acids to make glucose increases.
I could instantly read the anxiety in his eyes indicating a nine-fold increase of cortisol from the perceived screw-up. In my usual diplomatic style, I continued You are pregnant or you are not. There is no in-between. Next time, record just 5 reps please. The poor guy was probably producing more cortisol wondering if he had done 5.2 or 5.3 reps.
When you're stressed and anxious, your body produces chemicals in the fight or flight response, like adrenaline and cortisol. But stress hormones can also break down your body and burn you out when the fight or flight response is chronic. These chemicals have nowhere to dissipate, so they keep building up in your body, causing long-term damage. Exercise is another form of stress, which helps to burn up those chemicals.
Research is confirming that postpartum depression negatively affects mother-infant interactions during the first year of life. Field's program of research has repeatedly reported that postpartum depression negatively affects maternal-infant interaction. Field 31 , for example, reported a dysregulation profile for infants of mothers suffering from postpar-tum depression. Infants of postpartum depressed mothers have lower responsivity on the Brazelton scale, higher levels of indeterminate sleep, and elevated levels of norepinephrine and cortisol, activation of right frontal electroencephalogram, decreased responsivity to facial expressions, lower vagal tone, neurological delays, decreased play, decreased Bay-ley mental and motor scale scores, and lower weight percentiles 32 . Field 31 reported that postpartum depressed mothers displayed two predominant styles of interaction, withdrawn or intrusive. Mother-infant dyads matched negative behavior states more often and positive states less...
Disordered eating, present with low BMD in the absence of menstrual dysfunction 74,78 . Studies aimed at correcting the hypoestrogenic state, using estra-diol replacement (without an increase in energy intake), generally have not succeeded in the normalization of BMD after years of treatment 81-84 , indicating that factors other than estrogen also are important for bone. The most convincing evidence that low energy availability may have a direct effect on bone was published in an article by Ihle and Loucks 85 , who showed that markers of bone formation and resorption changed unfavorably within 5 days in sedentary women who were exposed to low energy availability through dietary restriction or increased exercise energy expenditure 85 . Whether this is also the case in athletic women has yet to be determined. Nevertheless, it seems highly plausible that an energy and nutrient deficit affects metabolic substrates and hormones, including insulin, growth hormone, insulin-like growth...
Cholesterol can be made in many cells, and under normal situations we seem to make all that we need. In fact, we will make about 1 gram of cholesterol each day depending on how much cholesterol is in the diet. The liver is by far the most productive organ when it comes to making cholesterol and one of its jobs is to share with the rest of the body. Cholesterol is a necessary component of cell membranes and many vital substances in the body are made from cholesterol (Figure 5.2). These substances include bile components, vitamin D, testosterone, estrogens, aldosterone, progesterone, and cortisol.
On the other hand, more significant changes in body weight and composition over time are more attributable to regular over-consumption or under-consumption of calories as well as the type of diet we eat and the exercise we perform. In general, the effects of these factors are relegated to specific hormones and other signals. The handling of energy nutrients being absorbed from the digestive tract is primarily influenced by insulin. In contrast, glucagon, cortisol, and epinephrine largely control the handling of stored body nutrients during fasting or exercise. In addition, serious exercise leads to additional signals in muscle to adapt and possibly get bigger (thus influencing body composition).
Prolonged strenuous exercise is associated with a temporary immunodepression that affects macrophages, neutrophils, and lymphocytes.36-38 The mechanisms involved are not fully established and appear to be multifactorial, including the actions of stress hormones (e.g., catecholamines and cortisol), inhibition of macrophage and T-cell cytokine production, altered heat shock protein expression, increased oxidative stress, and a fall in the plasma concentration of glutamine.38,39 BCAAs are nitrogen
RA and its isomer, 9-ds-retinoic acid (9cRA), serve as ligands that activate ligand-activated transcription factors that belong to a superfamily of nuclear receptors.10 This superfamily of related genes expresses nuclear receptors for steroids (the female sex hormones estrogen and progesterone, the mineralocorticoid aldoster-one, the glucocorticoid cortisol, the male sex hormones testosterone and dihy-drotestosterone), prostanoids, the thyroid hormone, the hormonal form of vitamin D, calcitriol, and peroxisome proliferators. Additionally, more than 50 orphan receptors belong to this family. Two classes of retinoid receptors occur retinoic acid receptors (RAR) and retinoid X receptors (RXR). Each has three different versions (a, p, and y) encoded by distinct genes. Each version also has multiple isoforms resulting from differential promoter use and alternative RNA splicing. Thus, multiple forms of each occur (e.g., RARa1, RARa2, etc.). Moreover, RAR functions as a heterodimer with RXR....
Cholesterol may be released directly into the gall bladder by hepatocytes or enzymatically modified into bile acids. Integrated in lipoproteins, it can be transported to hormone-synthesizing gland cells and used to synthesize steroid hormones such as cortisol, progesterone, estradiol, testosterone, and aldosterone.
Transform a sound meal plan into a disaster In addition even the most sensible diets ignore the cruc
Incledon, T. and Bocics, M. (1997). Testosterone and Cortisol in relationship to dietary nutrients and resistance exercise. J Appl Physiol. 82(l) 49-54. Anderson, K., et al. (1987). Diet-hormone interactions protein carbohydrate ratio alters reciprocally the plasma levels of testosterone and Cortisol and their respective binding globulins in man. Life See. 40 1761-1768.
As you've probably heard before, your post-workout meal may very well be your most important meal of the day. The reason is that when you're finished with an intense workout, you're entering a catabolic state where your muscle glycogen is depleted and increased cortisol levels are beginning to excessively break down muscle tissue. These conditions (if left to go too long) are not good and the only way to reverse this catabolic state (and promote an anabolic state) is to consume a quickly digestible post-workout meal as soon as you can after training. The goal is to choose a meal with quickly digestible carbs to replenish muscle glycogen as well as quickly digestible protein to provide the amino acids needed to jump start muscular repair. The surge of carbohydrates and amino acids from this quickly digested meal promotes an insulin spike from the pancreas, which shuttles nutrients into the muscle cells. The post-workout meal should generally contain between 300-500 calories to get the...
Chronic stress results in chronic elevations in cortisol and eventually abdominal fat and insulin resistance.38,44 The resulting visceral obesity increases the production of inflammatory mediators such as TNF-a and IL-6. Patients caught in this cycle of inflammation and adiposity may need a clinician's help to reverse the unfavorable environment. Nutritional interventions such as improved-quality carbohydrates, vitamin D, magnesium, and chromium, each discussed in later chapters, can improve insulin sensitivity and, eventually, phenotypic expression.
Simple tools have been used to identify the hypermetabolic state indirect calorimetry to measure energy expenditure, and N balance to follow protein loss. These measurements have shown that blunting the N loss in such patients is not as simple as supplying more calories, more amino acids, or different formulations of amino acids. What becomes clear is that although a nutritional problem exists, nutritional replacement will not correct the problem instead, the metabolic factors that cause the condition must be identified and corrected. Wilmore has categorized the factors that produce the hypermetabolic state into three groups stress hormones (cortisol, catecholamines, glucagon), cytokines (tumor necrosis factor, interleukins, etc.), and lipid mediators (prostaglandins, thromboxanes, etc.) ( 182). Strategies have been developed to address these various components. For example, insulin and growth hormone have been administered to provide anabolic hormonal stimuli to improve N balance....
The human body is made up of several distinct components, which differ in their chemical and structural characteristics. The extracellular compartment consists of support structures like bone lamellae, tendons and ligaments, and the extracellular fluid systems, blood plasma, and lymph. The totality of cells can be viewed as distinct from fatty tissue, which serves either as energy reserve (fat deposits), or as structural support or building material, as in cheeks or in the soles of the feet. The latter will be broken down only in extreme cases of nutritional deficiency or during illnesses accompanied by consumption. The fat deposits, however, may be subject to rather extreme fluctuations.
When you're fully hydrated, the bloodstream has all the fluid it needs to transport fatty acids from place to place. Drinking water also enhances your body's ability to release fatty acids from within cells into the bloodstream to go to the muscles for burning.
An argument can easily be made that nearly all aspects of our being have a genetic basis. Thus genetic disposition must be involved in determining body weight and composition. But how Although faulty genes can certainly play a role in establishing a sluggish metabolism in some people, scientists estimate that this may account for only a small percentage of obese individuals. Here the problem may lie in hormonal imbalances, such as lowered thyroid hormone. Scientists also believe that some people are genetically inclined to store body fat and hold on to it once it is stored. In this situation the cause is not hormonal as much as altered activity of the enzymes and other factors involved in storing fat.
Q You ve done a lot of research on insulin. Is it a bodybuilder's friend or foe Should hardgain -ers try to get insulin surges throughout the day via high-glycemic-index carb intake to kick-start anabolism and blunt Cortisol release, or will that have negative effects A Insulin is a storage hormone that has the capacity to increase fat deposition, foster carb storage as glycogen and help increase muscle protein synthesis by promoting amino acid uptake in muscle while blunting Cortisol's catabolic effects. One study attributes 30 percent of muscle protein synthesis to insulin activity. I think it's beneficial to have an insulin spike as soon as possible after training, since many studies show that increased insulin at that time promotes increased muscle glycogen synthesis, greater amino acid uptake into muscle and decreased Cortisol. The best way to do that is to consume half a gram of simple carbs per pound of body weight along with enough protein to equal 40 percent of the carb dose....
Established risk factors, 35-41 possible risk factors, 41 -43 Corticotropin-releasing hormone (CRH), 234 Cortisol, elevated levels of, 126 Coumarins, herbal source of, 353 Cowherd, William, 528 Creatine supplementation, 288, 290 Creutzfeldt-Jakob disease (CjD), 145 Creutzfeldt-Jakob variant, 139 CRH, see Corticotropin-releasing hormone Crop(s)
With other lipoproteins, it can be considered a key substance in the complex lipid transport system. During the early absorption phase, levels of enzymes involved in fat storage rise. These are mainly acetyl-CoA car-boxylase, fatty acid synthase, the malate enzymes, and a series of pentose phosphate cycle enzymes. Extracellular lipoprotein lipase activity in fatty tissues increases as well, which is necessary for fatty acid uptake from VLDL coming from the liver. At the same time, the activity of hormone-sensitive lipase, catalyzing the release of fatty acids from adipocytes, is reduced. All these events are subject to hormonal control (insulin and thyroid hormones), regulating necessary enzyme levels by up- or down-regulating transcription and translation.
Behavioral and Metabolic Effects of Leptin evidence strongly disputes that claim. Insulin fulfills the role (shared by leptin) of serving as a marker of adipose tissue mass and is secreted in direct proportion to fat mass. Insulin secretion also serves as an acute response to caloric influx Increased secretion begins within minutes of initiation of feeding, is maintained for the duration of food intake, and returns to basal secretory rate in the postabsorptive period. If insulin were an appetite stimulant (like ghrelin), its secretion would have preceded, not followed, ingestion of food. The timing and pattern of postprandial insulin secretion suggest a role in the regulation of satiety and meal termination. Indeed, direct administration of insulin to the central nervous system suppresses food intake in rodents (88). Since circulating insulin reaches the central nervous system via receptor-mediated transport across the blood-brain barrier, it is possible that peak insulin levels...
The peripheral hormones that regulate food intake include several gastrointestinal, pancreatic, and adipocyte-derived peptides (Table 1.2). Based on extensive studies in rodents and limited human data, these peptides can be classified as having orexigenic (e.g., ghrelin) or anorexigenic (e.g., insulin, peptide YY, glucagon-like polypeptide, cholecystokinin, leptin) effects. Leptin Peptide YY There is a mature and growing literature on the roles of several adipocyte products (including nonesterified fatty acids, adipocytokines, and leptin) in the regulation of metabolic fuel economy, energy balance, glucoregulation, food intake, and body weight. Products such as nonesterified fatty acids have long been proposed as mediators of obesity-associated insulin resistance and glucose dysregulation (33-35), as discussed elsewhere in this book. The adipocytokine TNF-alpha (also known as cachectin, for its association with cachexia or wasting) is a mediator of insulin resistance and is secreted...
While you may not be aware of it, a struggle for biochemical domination is occurring within you. The victor of this war ultimately determines whether you make muscular gains or lose muscle and even get fat. The two combating armies are collectively called anabolic and catabolic hormones. The most familiar of them from a bodybuilding perspective are testosterone (anabolic), growth hormone (anabolic), insulin (anabolic) and Cortisol (catabolic). Anabolic refers to the metabolic building processes. The actions of anabolic hormones involve either an increase in muscle protein synthesis or a decreased breakdown of muscle protein. Increased breakdown of muscle is the chief characteristic of catabolic reactions. You would think that since Cortisol, the body's primary catabolic hormone, is so outnumbered by the anabolic forces, it would be more or less an ineffectual player in the hormonal battle between anabolic and catabolic reactions, but that isn't the case. Since Cortisol, a product of...
The structure and outward appearance of each person's body is, in part, a reflection of the food and drink he or she consumes. All the organs of the body, as well as the skin, bones, muscles, and nerves, need nutrition to survive, regenerate, maintain function, and develop structural foundations. The vital organs, such as the liver, heart, brain, and kidneys, depend upon essential nutrients from food and drink to sustain life, increase strength, and improve health. Throughout life, the body constantly breaks down the food products that are ingested, using some components to rebuild the tissues that contribute to good health. Similarly, the body also disposes of the waste products of food through excretory processes or in storage centers (fat deposits, for instance) in the body.
Fructose, in the form of high-fructose corn syrup (HFCS), has come under scrutiny as a possible culprit contributing to the obesity epidemic (Wylie-Rosett, Segal-Isaacson, and Segal-Isaacson 2004). HFCS is made using chemical processes that first convert cornstarch to corn syrup and then convert 42 to 55 percent of the glucose in the corn syrup to fructose as a way to make it taste sweeter. Animal research suggests that fructose can lead to weight gain because of changes in insulin and leptin, two hormones that influence appetite. Whether or not HFCS promotes obesity in humans requires more study. Some research hints that fructose is digested, absorbed, and metabolized differently than glucose in ways that favor fat production (Bray, Nielsen, and Popkin 2004 Vertanian, Schwartz, and Brownell 2007).
There are indications that vitamin E supplementation elevates the testosterone cortisol ratio suggesting that vitamin E has a stress reducing effect on the body. It is able to reduce lipid peroxidation in both animals and humans as measured by an enhanced appearance of penthane in exhaled air. Studies at high altitude indicate that vitamin E can influence metabolic performance parameters and reduce penthane (an indirect marker of free radical induced cell damage) exhalation, suggesting that vitamin E may have a protective effect. However, it is not known which tissues undergo lipid peroxidation most during exercise. It may be that the most important site is tissue that is prone to some ischaemia during exercise, such as the gastrointestinal system, but not muscle.
Sleep deprivation itself is also associated with weight gain. Adults who sleep less than seven hours per night tend to be heavier than their well-rested counterparts. When you are sleep deprived, your appetite grows. The hormone that curbs your appetite (leptin) is reduced, and the hormone that increases your appetite (grehlin) become more active (Taheri et al. 2004). Hence, you can have a hard time differentiating between being hungry or tired. In either case, cookies and chocolate can be very tempting.
A fairly recent series of studies found that infant animals treated with MSG have higher cortisone levels than normal mice, and following stress it takes longer for the high levels to normalize.255 This same process occurs in the elderly, and is known to endanger the brain. High levels of cortisone, especially over a long period of time, can destroy neurons in the hippocampus, a part of the brain damaged in Alzheimer's disease. Some have proposed that the elevated levels of Cortisol and slow clearance following stress eventually lead to Alzheimer's dementia. That our children may be constantly exposed to high cortisone levels from early childhood is a frightening prospect.
Scientists have long recognized that some forms of obesity are hereditary, but the links between fat and genes remained a mystery until December 1994. That is when the obesity gene was discovered in mice. From that, a human obese gene was cloned. Found in fat cells, the obese gene makes a protein message that travels via the bloodstream to the brain and says I've had enough food, stop eating. In the strain of obese mice that were studied, the protein message is mutated and the message never gets to the brain. Since the principle action of this protein is to make the animal thin, researchers have named this obese gene leptin from the Greek root Leptos which means thin. Grossly obese mice were given daily injections of leptin, and after one month, food intake and body weight dropped by 50 percent. Because of this, researchers had to find mice (with obesity traits) that more closely resemble obesity in humans. They found a strain of mice that grow plump when their diet contains too much...
The melanocortins are derived from site-specific, posttranslational cleavage of the precursor parent molecule proopiomelanocortin (POMC). Cleavage of POMC within the anterior pituitary gives rise to Adrenocorticotrophic hormone (ACTH), which acts through the MC2 receptor to stimulate adrenal steroidogenesis. Elsewhere in the brain, POMC is cleaved to another melanocortin, alpha-MSH, which is an agonist for the MC3 and MC4 receptors. Administration of alpha-MSH (i.c.v.) in rodents results in weight loss through inhibition of food intake and stimulation of energy expenditure (22). These actions are mediated through activation of two neuronal melanocortin receptor subtypes (MC3r and MC4r) and antagonized by an adjacent subset of hypothalamic neurons that express AgRP and NPY. The NPY AgRP neurons that inhibit MC3r and MC4r are themselves inhibited by leptin and insulin. The integrated physiology of the interactions of these opposing neuropeptides is evident from their weight-related...
The healing process for most wounds requires an increase in caloric intake over basal levels. This is especially true in severely injured, burned, or critical patients in whom the stress response has placed them in a hypermetabolic state.82,83 Induction of the stress response via the hypothalamus is initiated by proinflammatory cytokines and results in increased levels of the stress hormones (e.g., glucagon, cortisol, and catecholamines). These hormones then result in a protein-catabolic state as well as The previously mentioned endocrine function of WAT may also play a role in wound metabolism during the early stages of wound healing. Leptin production increases during inflammation.47 Interestingly, leptin activity has been detected in the fluids of experimental wounds in pigs during the first few days following injury,105 and it was suggested by the authors that this hormone may function in an autocrine and paracrine manner during wound healing. The significance and role of leptin...
Interestingly, NPY expression in the arcuate nucleus is potently antagonized by the anorexigenic hormone leptin. Furthermore, activation of the Y2 receptor subtype on NPY neurons triggers inhibitory presynaptic signals. Central administration of PYY3-36 (a Y2 receptor agonist secreted by intestinal endocrine L cells) into the AgRP is expressed exclusively in the arcuate nucleus of the hypothalamus and colocalizes to the same neurons that secrete NPY (10). Several reports have confirmed the status of AgRP as a potent orexigenic factor A single i.c.v. injection of AgRP increases food intake for several days in rodents (11). In contrast to the shortlived effect of NPY, chronic treatment with AgRP leads to sustained hyperphagia and obesity (12). The orexigenic effect of AgRP is mediated through antagonism of MC3 and MC4 receptors. Such antagonism effectively reverses the inhibition of food intake induced by alpha-MSH. The arcuate neurones that cosecrete NPY AgRP are potently inhibited by...
Fatty acids introduced to the tissues are either utilized for energy or stored for later use, depending on the energy state of the body. In a fed state, fatty acids are primarily used for the synthesis of triglycerides in subcutaneous and deep visceral adipose tissue. While only approximately 450 g of glycogen can be stored in the body at one time, a nearly unlimited capacity for fat storage exists. Fat storage depends on the individual. For nonobese males, average triglyceride storage ranges between 9 and 15 kg, translating into a total energy storage of 80,000 to 140,000 kcal.9 While trained athletes have less fat reserves, ample amounts remain to provide energy in times of prolonged periods of insufficient energy intake. Not only in caloric deprivation, but in states of high energy expenditure, carbohydrate availability may be limited and utilization of fat stores may be warranted. In addition to the fat storage in adipose tissue, a small amount of fat is present as lipid droplets...
The influence of hormones on amino acid partition to the skin and wool growth appears to be indirect. This could be attributed to passive changes in the skin that result from hormone-induced alteration of amino acid metabolism in the body. Adams et al. (2000) reviewed the effects of hormones, including IGF-1, insulin, growth hormone, androgens, p-adrenergic agonist, thyroxine and Cortisol on wool growth and follicle activities, and pointed out 'there are no hormones with a homeorrhoetic function to direct nutrients to the skin. However, hormones do affect wool growth through their effects on whole body protein synthesis, or by affecting protein metabolism in other organs'.
Since this value is very strongly correlated to strength gains (r 0.86), one may infer that training under depressed androgen levels is counter-productive, since the catabolic effects of the glucocorticoids would negate the anabolic effects of the androgens. Apparently an hour pause is sufficient to allow the testosterone levels to normal. This is why modern strength training has evolved to multiple daily sessions from the traditional two-hour workouts.
Rapid rise in glucose may contribute to the development of diabetes, but it also causes more of the glucose to be converted to fats for storage. This fat storage contributes to obesity, if the energy is not used in exercise. The original pyramid did not differentiate between these types of carbohydrates.
Because of the limitations in the NBAL method, Young and Bier have been instrumental in devising a conceptual framework from which to determine optimal protein intakes using stable isotopic tracers. They have coined the terms nutrient deficiency, accommodation, adaptation, and nutrient excess.147 148 In a state of protein deficiency, there would be a maximal reduction in amino acid oxidation and a reduction in protein synthesis to all but the essential organs (e.g., brain) that ultimately would result in muscle wasting (negative NBAL). The state of accommodation would be the state where NBAL is achieved with a decrease in a physiologically relevant process. The state of adaptation would be the dietary intake that provided for optimal rates of protein synthesis for growth, interorgan amino acid exchange, and immune function. Finally, the state of protein excess would be defined as that intake where amino acids are oxidized for energy or used in fat storage, and protein synthesis is not...
However, as mentioned throughout this chapter, the effects fats have on bodyfat is a complicated issue as certain fats are helpful for reducing bodyfat, blocking fat storage, increasing beta oxidation, etc. Though the effect of fat on TEM is important to know, it's even more important in my view to remember not all fats are created equal in this regard or their effects on metabolism.
Their weight is more or less constant. As discussed in section 1.3.2, leptin is central to the control of both food intake and energy expenditure, and there are a number of mechanisms involved in short-term control of food intake, with regulation of both hunger and satiety.
Estimates of the likely genetic component to obesity are in the order of 2040 depending on the type of study (13). Polymorphisms in the leptin gene may be one of the important genetic variables which regulate appetite. Leptin protein levels have been clearly related to the obese state in animals but less clearly so in humans (14). Despite genetic factors, the important principles are that increasing weight (adiposity) results in movement towards the obese state, and that gain in adiposity (fat mass) results from a long-term imbalance between energy intake (energy from food and drink) and energy expenditure (basal metabolic rate + thermic effect of eating + involuntary muscle activity (shivering) + voluntary activity (day-to-day living and specific 'exercise')). A review of the intricacies of food intake, energy balance and body weight control is provided by Doucet and Tremblay (15) (Fig. 11.1).
An elaborate network of central and peripheral neurohormonal signals has evolved to regulate feeding, one of the primal activities necessary for survival and self-preservation. Despite decades of animal and human research, the full extent of the processes and humors involved in the regulation of food intake remains to be elucidated. Current understanding indicates that energy homeostasis in health is predicated upon a balance between orexigenic and anorexigenic factors, both centrally and peripherally. Virtually all of the peripheral signals (e.g., insulin, PYY, leptin, CCK) are triggered by food ingestion and attenuated by fasting or starvation, indicating a response system that is tailored at satiety and meal termination. Ghrelin, the only peripheral signal activated preprandially, may be unique in its role as a rare peripheral signal for hunger and meal initiation.
Lean people can increase their energy expenditure to match their food intake leptin (section 1.3.2) increases the activity of mitochondrial uncoupling proteins (section 18.104.22.168). The result of this is an increased rate of metabolism of metabolic fuels and increased heat output from the body, especially after meals and while asleep.
Several new drugs show promise for future treatment of obesity. Axokine, a genetically engineered recombinant human variant ciliary neurotrophic factor that signals through leptinlike pathways in the hypothalamus, has been shown to bypass leptin resistance.43 Topiramate is a broad-spectrum anticonvulsant that stimulates gamma -aminobutyric acid activity. In a 14-week, double-blind trial comparing
In humans, studies of polygenic obesity are based on the analysis of single nucle-otide polymorphisms (SNPs) or repetition of bases (polyCAs or microsatellites) located within or near a candidate gene. These studies are carried out in family members (family study) or unrelated individuals (case-control study), and their objective is to determine a potential association between a gene's allelic variant and obesity-related traits (70). However, unlike monogenic obesity, many genes and chromosomal regions contribute to the common obese phenotype (7,71). For this purpose, large DNA banks have been established from different populations throughout the world and are used for the extensive investigation of large number of genes and chromosomal regions. The findings of these genetic studies are reported every year by the Human Obesity Gene Map consortium. According to their latest report, 253 QTL have been identified, in 61 genome-wide scans (7). All chromosomes, except the Y chromosome, have...
What does PS offer the athlete One affect of PS may be its ability to reduce levels of the catabolic (muscle wasting) hormone cortisol after exercise. Two early studies done in Italy appeared to show that chronic intakes of PS reduced the release of cortisol after intense exercise. When the body senses stress, whether physical and or emotional, it releases cortisol as part of the fight or flight cascade that prepares us for short term survival. Prolonged stress from malnutrition, surgery, over training and sleep deprivation, as well as psychological stress, causes a systemic effect that includes increased cortisol secretion resulting in a decline in certain aspects of immune system and other problems. As the reader can see, over long periods of time, high cortisol levels are detrimental to our over all health and muscle mass. PS does suffer from one key draw back, which is its shear cost. The most recent study that found PS reduced post exercise cortisol levels, used 800mg per day...
Eto et al. investigated highly trained cyclists ages 18 to 22 ingesting 20 g of glutamate-ARG (AG) salt per day and found that although AG had no effect on resting plasma levels of hGH, the AG subjects had marked reduction in cortisol and hGH compared to the placebo group during and after exercise. Those results suggest that AG may modify energy metabolism during endurance exercise.
Using seven young male and seven elderly subjects, the effects of 40 hr sleep deprivation on sleep EEG and the secretion of growth hormone, cortisol, and prolactin were studied.41 The results indicated that SWS was less in the elderly than in the young . Total sleep deprivation (TSD) decreased sleep onset latency, REM density, and, by trend, REM latency in the elderly. The use of GABA-benzodiaz-epine can improve sleeplessness and nighttime hormone secretion for TSD patients The GABA receptor is one of the calcium receptors induced from tranquilizers, and it inhibits nerve activity by GABA Therefore, GABA may improve sleeplessness, including discontinuing sleep, cycling sleep, and HPA system activity.42-44
GDM is similar to type 2 diabetes, as it is associated with insulin resistance and insen-sitivity. The exact mechanism responsible for the development of GDM is not fully understood however, pancreatic beta-cell dysfunction may be responsible. As hormonal levels continue to rise in the second and third trimesters, beta-cells are unable to produce or secrete sufficient insulin for glucose regulation. Fasting blood glucose levels are elevated as insulin deficiency and resistance increase. Delayed insulin response, insulin resistance, and placental hormonal antagonism are responsible for postprandial glucose excursions. Human placental lactogen and cortisol block insulin receptors, which creates a deficiency in circulating insulin production, and results in increased glucose intolerance. In normal pregnancy, the beta-cells compensate by increasing insulin secretion in GDM the decreased insulin response will result in elevated glycemic levels 57 .
Although there are many hormones that directly and indirectly affect protein turnover (e.g., insulin, cortisol, testosterone, growth hormone, and insulin-like growth factor), only testosterone and insulin will be discussed here. Testosterone is of interest because of the significant controversy surrounding its unethical use in sporting events and its potent effects on protein metabolism. For many years testosterone was assumed to possess stimulatory effects on net protein synthesis, based on observations of male female differences in lean mass as well as the increases noted for those who supplemented with pharmacological doses. Consequently, proper investigations into the metabolism and efficacy of testosterone administration followed.57 124-127 Even without resistance exercise, testosterone administration can increase lean body mass,124 126 127 and a resistance exercise training program can magnify these effects.127 At the muscle level, testosterone acts by increasing protein...
Different types of stress, including exercise, infection and physical trauma, are known to exacerbate the signs of marginal chromium deficiency. In the case of exercise this occurs most probably because exercise enhances chromium losses with urine. Additionally, CHO rich diets, especially high glycaemic CHO sources, such as sugars, are known to increase chromium losses with urine. This is most likely an effect of these CHOs on quantitative insulin secretion and subsequent degradation (5). On the other hand it has been shown that CHO loading reduces the rate of trace elements loss, notably chromium and zinc (405). The explanation for this observation is that the level of actual exercise stress influences urinary excretion of these trace elements. In this study, the CHO loading regimen reduced the level of exercise stress as measured by changes in serum cortisol. Losses of potassium, magnesium and calcium were not influenced. These opposite findings on the effects of CHO on chromium...
And those animals which didn't have a lot of fat were only hunted at certain times of the year. Such as late Summer when their fat deposits were at a high. Stone age Australian Aboriginals would not bother to carry back to camp any kangaroo that was too lean. North American cavemen would not hunt female bison in Spring because pregnant animals burn off all their stored fat in Winter.
Heart disease, or coronary artery disease, is a result of improper function of the heart and blood vessels. There are many forms of heart disease. Atherosclerosis (hardening of the arteries) and hypertension (high blood pressure) are two of the most common. Fat deposits disrupt the flow of blood to the heart muscle, increasing the risk of myocardial infarction (heart attack).
In contrast, raw plant fats do not cause the body to gain excessive weight unnecessarily. In fact, as one transitions away from cooked food, s he can actually lose weight eating a significant portion of raw plant fats. Eating raw plant fats can help a person lose weight as they contain their lipase enzymes which allow body fat to be burned. Lipase enzymes are typically missing in the excessive fat tissues of the body. Lipase enzymes, from raw plant fats and their oils, help metabolize cooked fat deposits which have stagnated and accumulated throughout the body. Each raw essential fatty acid replaces each cooked trans-fatty acid incorporated into the cell walls. Raw plant fats are easily recognized by the liver and distributed properly throughout the body.
The BMI is the current standard for evaluating body weight since it correlates fairly well with total body fat and is rather independent of height. However, a man with a BMI of 27 kg m2 may have a body fat content ranging from 10 to 31 of body weight. Not only fat, but muscle mass, extracellular water, and or bone mass may contribute to high body weight. For instance, athletes frequently have a rather high BMI without large fat deposits. To address this inaccuracy, subcutaneous fat is measured. Theoretically, this could be done with
Initial knowledge on the genetic involvement in monogenic obesity was derived from large-scale linkage analysis in obese mice carrying naturally occurring mutations. These analyses have pointed to disease-related loci and have identified the majority of gene mutations leading to monogenic obesity in mice (3). In particular, the genetic characterization of naturally occurring obese animal models, such as ob ob, db db, fat and tubby mice, led to the discovery of recessive mutations in the genes encoding leptin (Lep or ob), leptin receptor (Lepr or db), carboxypeptidase E (Cpe, or fat), and tubby (Tub) (5,6). Furthermore, the latest murine obesity gene map identified 248 genes that, when mutated or expressed as transgenes in the mouse, result in phenotypes affecting body weight and adiposity (7). Transfer of this knowledge to clinical cases has confirmed the role of the above genes in human monogenic obesity and uncovered the critical role of the leptin melanocortin pathway in the...
Interest in the behavioral and autonomic effects of caffeine led to investigations of the hormonal effects of caffeine. Increases in brain levels of serotonin and 5-hydroxyindoleacetic acid were observed after both acute and chronic administration of caffeine (33). Plasma epinephrine and norepinephrine were increased after 220250 mg caffeine consumption (34, 35). Higher doses on the order of 500 mg can cause endocrine stress symptoms characterized by increased serum adrenocorticotropic hormone (ACTH) and cortisol (36). After 7 days of caffeine consumption, no increases in hormone levels were observed, suggesting that habitual consumers are the least sensitive to caffeine's effects on the endocrine system. Based on the high doses of caffeine required to produce these effects, it is unlikely that normal consumption of cocoa and chocolate-containing foods would produce any observable endocrine effects.
By consuming the prescribed 500 to 1,000 additional calories per day, you should see some weight gain. Be sure to include muscle-building resistance exercise (weight workouts, push-ups) to promote muscular growth rather than just fat deposits. Consult with the trainer at your school, health club, or gym for a specific exercise program that suits your needs. You may also want to have your body fat routinely measured to make sure your weight gain is indeed mostly muscle, not fat. Untrained men might gain about 3 pounds (1.5 kg) of muscle per month initially. The rate of gain in well-trained athletes is slower.
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