Fax mentis incedium gloriae

"The passion of glory is a torch for the mind."

Greetings, the following questions are reviewed in this issue:

#1 What causes elevated cholesterol and what can be done to reduce it?

#2 What increases serum triglyceride levels?

#3 How does training effect carbohydrate metabolism?

#4 What causes loss of muscle mass (sarcopenia) with aging?

#5 What causes fat-weight gain and what can be done to reduce it?

ADDENDUM: What short-term protocol is recommended for losing body fat weight?

#1 What causes elevated cholesterol and what can be done to reduce it?

Elevated serum cholesterol is called Cholesterolemia. The first set of suggestions indicates diet is the best method to reduce cholesterol. Vegetarians typically have the lowest cholesterol levels from their nutritional effect. Supplements also may be employed to reduce cholesterol if dietary interventions are not fully employed. Approximately 30% of the body's cholesterol content is derived from dietary sources while another 50% of cholesterol is reabsorbed through the gut, and the remainder passes through the body unused and is excreted (via the bile).

Regulating Cholesterol Synthesis[1]

Normal healthy adults synthesize cholesterol at a rate of approximately 1g/day and consume approximately 0.3g/day. A relatively constant level of cholesterol in the body (150-200 mg/dL) is maintained primarily by controlling the level of de novo synthesis. The level of cholesterol synthesis is regulated in part by the dietary intake of cholesterol. Cholesterol from both diet and synthesis is utilized in the formation of membranes and in the synthesis of the steroid hormones and bile acids (see below). The greatest proportion of cholesterol is used in bile acid synthesis.

The cellular supply of cholesterol is maintained at a steady level by three distinct mechanisms:

1. Regulation of HMGR activity and levels
2. Regulation of excess intracellular free cholesterol through the activity of acyl-CoA:cholesterol acyltransferase, ACAT
3. Regulation of plasma cholesterol levels via LDL receptor-mediated uptake and HDL-mediated reverse transport.

Regulation of HMGR activity is the primary means for controlling the level of cholesterol biosynthesis. The enzyme is controlled by four distinct mechanisms: feedback inhibition, control of gene expression, rate of enzyme degradation and phosphorylation-dephosphorylation.

The first three control mechanisms are exerted by cholesterol itself. Cholesterol acts as a feedback inhibitor of pre-existing HMGR as well as inducing rapid degradation of the enzyme. The latter is the result of cholesterol-induced polyubiquitination of HMGR and its degradation in the proteosome (see proteolytic degradation). This ability of cholesterol is a consequence of the sterol-sensing domain, SSD of HMGR. In addition, when cholesterol is in excess the amount of mRNA for HMGR is reduced as a result of decreased expression of the gene. The mechanism by which cholesterol (and other sterols) affect the transcription of the HMGR gene is described below under regulation of sterol content. Regulation of HMGR through covalent modification occurs as a result of phosphorylation and dephosphorylation. The enzyme is most active in its unmodified form. Phosphorylation of the enzyme decreases its activity. HMGR is phosphorylated by AMP-activated protein kinase, AMPK (this is not the same as cAMP-dependent protein kinase, PKA). AMPK itself is activated via phosphorylation. The phosphorylation of AMPK is catalyzed by one or more AMPK kinases (AMPKKs). Visit AMPK: The Master Metabolic Regulator for more detailed information on the role of AMPK in regulating metabolism.

Regulation of HMGR by covalent modification. HMGR is most active in the dephosphorylated state. Phosphorylation is catalyzed by AMP-activated protein kinase, AMPK, (used to be termed HMGR kinase), an enzyme whose activity is also regulated by phosphorylation. Phosphorylation of AMPK is catalyzed by AMPK kinase (AMPKK). Hormones such as glucagon and epinephrine negatively affect cholesterol biosynthesis by increasing the activity of the inhibitor of phosphoprotein phosphatase inhibitor-1, PPI-1. Conversely, insulin stimulates the removal of phosphates and, thereby, activates HMGR activity. Additional regulation of HMGR occurs through an inhibition of its' activity as well as of its' synthesis by elevation in intracellular cholesterol levels.

The activity of HMGR is additionally controlled by the cAMP-signaling pathway. Increases in cAMP lead to activation of cAMP-dependent protein kinase, PKA. In the context of HMGR regulation, PKA phosphorylates phosphoprotein phosphatase inhibitor-1 (PPI-1) leading to an increase in its' activity. PPI-1 can inhibit the activity of numerous phosphatases including protein phosphatase 2C and HMG-CoA reductase phosphatase, which remove phosphates from AMPK and HMGR, respectively. This maintains AMPK in the phosphorylated and active state, and HMGR in the phosphorylated and inactive state. As the stimulus leading to increased cAMP production is removed, the level of phosphorylations decreases and that of dephosphorylations increases. The net result is a return to a higher level of HMGR activity.

Since the intracellular level of cAMP is regulated by hormonal stimuli, regulation of cholesterol biosynthesis is hormonally controlled. Insulin leads to a decrease in cAMP, which in turn activates cholesterol synthesis. Alternatively, glucagon and epinephrine, which increase the level of cAMP, inhibit cholesterol synthesis. The ability of insulin to stimulate, and glucagon to inhibit, HMGR activity is consistent with the effects of these hormones on other metabolic pathways. The basic function of these two hormones is to control the availability and delivery of energy to all cells of the body.

Long-term control of HMGR activity is exerted primarily through control over the synthesis and degradation of the enzyme. When levels of cholesterol are high, the level of expression of the HMGR gene is reduced. Conversely, reduced levels of cholesterol activate expression of the gene. Insulin also brings about long-term regulation of cholesterol metabolism by increasing the level of HMGR synthesis.

The Utilization of Cholesterol

Cholesterol is transported in the plasma predominantly as cholesteryl esters associated with lipoproteins. Dietary cholesterol is transported from the small intestine to the liver within chylomicrons. Cholesterol synthesized by the liver, as well as any dietary cholesterol in the liver that exceeds hepatic needs, is transported in the serum within LDLs. The liver synthesizes VLDLs and these are converted to LDLs through the action of endothelial cell-associated lipoprotein lipase. Cholesterol found in plasma membranes can be extracted by HDLs and esterified by the HDL-associated enzyme LCAT. The cholesterol acquired from peripheral tissues by HDLs can then be transferred to VLDLs and LDLs via the action of cholesteryl ester transfer protein (apo-D) which is associated with HDLs. Reverse cholesterol transport allows peripheral cholesterol to be returned to the liver in LDLs. Ultimately, cholesterol is excreted in the bile as free cholesterol or as bile salts following conversion to bile acids in the liver.

How do some endurance athletes get high cholesterol?

Diet effects between 20-30% of your blood level cholesterols:

DIETARY SOURCES OF CHOLESTEROL (mg of Cholesterol per 100 grams)

DAIRY

Butter240

Cream109

Cream Cheese 103

Ice Cream 45

Cottage Cheese 15

Milk12.3

Yogurt 12.2

Parmesan Cheese 68

EGGS

Eggs - Chicken 550

Egg Yolk - 1,500

FATAnimal Lard - 95

MEATS

Brain - Sheep 2,200 - Beef 65

Kidneys - Sheep 375

Liver - Sheep300

Lamb - 70

Chicken - 60

Pork - 65

Heart - 150

Mutton - 65

Veal - 90

Chicken (breast) - 60

Turkey (leg) - 75

SEAFOOD

Caviar - 300

Lobster - 200

Shrimp - 125

Crab - 125

Cod- 50

Oysters - 50

Salmon- 35

WHAT CAN I TAKE TO LOWER TOTAL SERUM CHOLESTEROL?

Eat less meat, beef, poultry, substitute fish, which contain very low cholesterol and high omega-3 healthy fats.

Spirulina lowers total serum cholesterol levels.

Royal Jelly (50-100 mg per day) lowers total serum cholesterol levels (by approximately 14%).

Yogurt can lower total serum cholesterol by up to 30% by facilitating the conversion of cholesterol to coprostanol in the colon (due to the hydroxymethyl glutarate content of yogurt).

Apples lower total serum cholesterol levels (due to the apple pectin content of apples) pectins lower total serum cholesterol levels by binding to cholesterol, causing its excretion:

-Apple Pectin (2,000-3,000 mg per day) lowers total cholesterol.

-Grapefruit Pectin lowers total cholesterol.

Bananas (especially green, unripened bananas) cause serum cholesterol levels to fall by up to 33%.

Grapefruit lowers total serum cholesterol levels (due to the grapefruit pectin content of grapefruit).

Oranges lower total serum cholesterol levels (primarily due to the pectin content of oranges).

Pears lower total serum cholesterol levels (due to the pectin content of pears).

Strawberries lower total serum cholesterol levels (due to the pectin content of strawberries).

Shiitake mushrooms lower total serum cholesterol levels (due to the eritadenin content of shiitake mushrooms).

Barley lowers total serum cholesterol levels (by 6% to 12%).

Oats lower total serum cholesterol by washing away bile acids in the gastrointestinal tract that would otherwise be converted to cholesterol (due to the beta glucans content of oats and oat bran).

Oat bran lowers total serum cholesterol by washing away bile acids in the gastrointestinal tract that would otherwise be converted to cholesterol (due to the beta glucans content of oats and oat bran).

Barley grass lowers total serum cholesterol levels.

American ginseng lowers total serum cholesterol levels.

Arjun lowers total serum cholesterol levels.

Artichoke leaf lowers total serum cholesterol levels.

Black cohosh lowers serum cholesterol levels.

Carob lowers total serum cholesterol levels by up to 15%.

Chillis lower total serum cholesterol levels (due to the capsaicin and dihydrocapsaicin content of chillis).

Ginger lowers total serum cholesterol levels.

Ginseng lowers total serum cholesterol levels.

Green tea lowers total serum cholesterol levels.

Guggulipid (extract) lowers elevated serum cholesterol levels (by stimulating the function of the thyroid, inhibiting the endogenous production of cholesterol and facilitating the excretion of cholesterol).

Hawthorn (berries) lower total serum cholesterol levels.

Holy basil lowers total serum cholesterol levels.

Indian gooseberry lowers total serum cholesterol levels.

Jiaogulan lowers total serum cholesterol levels.

Milk thistle lowers elevated total serum cholesterol levels (due to the silymarin content of milk thistle).

Skullcap inhibits increases in serum cholesterol levels.

Turmeric lowers total serum cholesterol levels (due to the curcumin content of turmeric).

Yarrow lowers total serum cholesterol levels.

Soybeans lower total serum cholesterol levels.

One tablespoon (8 grams) of powdered, activated charcoal taken after every meal reduces total serum cholesterol by 20-25%.

Almonds lower total serum cholesterol levels (due to the oleic acid content of almonds).

Pecan nuts lower total serum cholesterol levels (due to the beta-sitosterol content of pecan nuts).

Coconut oil lowers elevated total serum cholesterol levels (it is speculated that this occurs from coconut oil stimulating the conversion of cholesterol to pregnenolone).

Fish oils reduce the absorption of dietary cholesterol and reduce the synthesis of cholesterol within the liver. Specific fish oils lower cholesterol are:

DocosaHexaenoic Acid (dha) lowers total serum cholesterol levels. EicosaPentaenoic Acid (EPA) lowers total serum cholesterol levels.

Flax seed oil lowers total serum cholesterol levels (due to the high content of alpha-linolenic acid in flax seed oil).

Olive oil lowers total serum cholesterol, by preventing it from entering the bloodstream (due to the cycloartenol content of olive oil).

Rice bran oil lowers total serum cholesterol levels.

Salmon oil (4 grams per day) lowers elevated serum cholesterol levels.

Perilla oil lowers elevated serum cholesterol levels (due to the high alpha-linolenic acid content of flax seed oil).

Lecithin (10,500 mg per day) lowers elevated serum cholesterol levels (by approximately 33%).

Clams can lower serum cholesterol by 9%.

Crabs can lower serum cholesterol by 9%.

Oysters can lower total serum cholesterol by 9%.

Fenugreek seeds lower total serum cholesterol levels.

Flax seeds (20 grams per day) lower total serum cholesterol levels by up to 9%.

Psyllium seed husks can reduce total serum cholesterol levels by 15% (due to the psyllium content of psyllium seed husks).

Avocado lowers serum cholesterol levels.

Cabbage helps to lower total serum cholesterol levels.

Consumption of 200 grams of raw carrots lowers total serum cholesterol levels by an average of 11%.

Celery can lower total serum cholesterol by 7%, even at low doses (due to the 3-n-butyl-phthalide content of celery).

Garlic (and garlic oil) lowers total serum cholesterol levels: aged garlic extract lowers total serum cholesterol levels (by approximately 7%).

Globe artichoke lowers total serum cholesterol levels (due to the cynarin content of globe artichokes).

Onions lower total serum cholesterol levels.

Rutabaga lowers total serum cholesterol levels.

Sweet potatoes lower total serum cholesterol levels (by binding to cholesterol).

Turnips lower total serum cholesterol levels.

Red yeast rice lowers elevated total serum cholesterol levels (by inhibiting the HMG-CoA reductase enzyme that catalyzes the endogenous production of cholesterol).

OTHER SUBSTANCES THAT MAY LOWER TOTAL SERUM CHOLESTEROL:

Capsaicin, Pangamic Acid Dihydrocapsaicin, Arginine, Carnitine, Creatine Monohydrate, Ethylene-Diamine-Tetra-Acetate (EDTA is the synthetic amino acid used in chelation therapy - lowers total serum cholesterol levels.) Hydroxy Methylbutyrate (HMB) (3,000 mg per day) lowers total serum Cholesterol levels.Taurine lowers serum cholesterol levels by combining with cholesterol to form bile. Dimethyl Glycine (DMG) lowers total serum cholesterol levels (by inhibiting enzymes involved in the endogenous synthesis of cholesterol. Chitin lowers total serum Cholesterol levels (by inhibiting HMG-CoA Reductase (an enzyme that contributes to the endogenous production of cholesterol). Chitosan lowers total serum cholesterol levels (by inhibiting HMG-CoA Reductase (an Enzyme that contributes to the endogenous production of Cholesterol).

Chondroitin Sulfate (CSA) (3,000 mg per day) lowers total serum cholesterol levels by up to 15%.

Glucomannan (1,000 mg taken approximately one hour prior to each meal = 3,000 mg per day) lowers total serum cholesterol levels.

Dietary Gums lower cholesterol are:

Guar Gum (18,000 mg per day) lowers cholesterol by up to 15%.

Gum Arabic (6,000 mg per day) lowers total cholesterol.

Crocetin can lower total serum cholesterol levels.

Sunlight and ultra-violet radiation lower total serum cholesterol levels (by facilitating the conversion of cholesterol to vitamin D).

Progesterone lowers total serum cholesterol levels.

Alpha-Linolenic Acid (12 grams per day) lowers total serum cholesterol levels by up to 9%.

Capric Acid, Caproic Acid, Caprylic Acid slightly lowers total serum cholesterol levels.

Conjugated Linoleic Acid (CLA) lowers total serum cholesterol levels.

Guggulsterones lowers elevated serum cholesterol levels (by stimulating the function of the Thyroid, inhibiting the endogenous production of cholesterol and facilitating the excretion of cholesterol).

Policosanol lowers elevated total serum cholesterol levels (by inhibiting the synthesis of endogenous cholesterol).

Saponins lower total serum cholesterol levels.

Squalene lowers total serum cholesterol levels.

Stearic acid (paradoxically and contrary to the effect of other long-chain saturated fatty acids) can actually lower total serum cholesterol levels.

Lactobacillus acidophilus lowers total serum cholesterol levels.

1. Lactobacillus acidophilus - dds-1 strain lowers total serum cholesterol levels.
2. Lactobacillus sporogenes significantly lowers total serum cholesterol levels.

Calcium (2,200 mg per day) lowers total serum cholesterol levels (by up to 6%).

Chromium polynicotinate (1-2 mg per day) lowers total serum cholesterol levels by up to 15%.

Elevated total serum cholesterol levels may be a symptom of copper deficiency.

Germanium (100-300 mg per day) lowers total serum cholesterol levels.

Magnesium (especially the magnesium aspartate form) lowers total serum cholesterol levels and elevated serum cholesterol levels can occur as a result of magnesium deficiency.

Preliminary reports indicate that adenosine may lower serum cholesterol levels.

3-N-Butyl-Phthalide lowers total serum cholesterol by up to 7% even in small doses.

Curcumin lowers total serum cholesterol levels.

Cynarin can lower total serum cholesterol levels.

Epigallo-Catechin-Gallate (EGCG) lowers total serum cholesterol levels.

Hesperidin lowers total serum cholesterol levels.

Isoflavonoids lower total serum cholesterol levels.

Naringin lowers elevated serum cholesterol levels.

Quercetin lowers total serum cholesterol levels.

Resveratrol lowers total serum cholesterol levels.

Silymarin lowers elevated total serum cholesterol levels.

Soy Protein lowers total serum cholesterol levels.

Coenzyme Q10 (100 mg per day) lowers total serum cholesterol levels.

Xanthinol Nicotinate (a synthetic variation of the Nicotinic Acid form of Vitamin B3) lowers total serum cholesterol levels (due to its ability to dilate the blood vessels).

Alliin (a derivative of cysteine that is a constituent of garlic) lowers total serum cholesterol levels.

Tocotrienols lower elevated serum cholesterol levels (primarily by inhibiting the action and production of the enzyme HMG-CoA Reductase that is involved in the endogenous production of cholesterol).

Vitamin B5 (900 mg of the pantethine form of vitamin B5 per day) lowers total serum cholesterol levels by up to 19%.

Caterpillar Fungus lowers total serum cholesterol levels by an average of 17.5%.

Vitamin B6 lowers total serum cholesterol levels.

Glucose Tolerance Factor (GTF) can lower total serum cholesterol levels by 25%.

Lignin removes excess cholesterol via the intestine.

Xanthinol Nicotinate (a synthetic variation of the Nicotinic Acid form of Vitamin B3) lowers total serum cholesterol levels (due to its ability to dilate the blood vessels).

#2 What increases serum triglycerides?

Fructose is incorporated into triglycerides more readily than glucose. Fructose has a greater propensity to increase serum triglycerides as compared to glucose, especially in diabetes mellitus patients and those with blood sugar disorders. Insulin stimulates the conversion of glucose (blood sugar) to triglycerides for storage within adipose tissue. Excessive circulating glucose (blood sugar) is converted to glycerol and stored within the body as triglycerides. Excessive consumption of sucrose increases the body's production of triglycerides (due to the body converting excessive sucrose into triglycerides in order to protect itself from the toxic effects of excessive sucrose).

Cafestol, a diterpene lipid found in unfiltered coffee, increases serum triglycerides levels.

Excessive consumption of dietary fats may also increase serum triglyceride levels - 95% of dietary fatty acids are consumed in the form of triglycerides.

Trans-fatty acids increase triglyceride levels by up to 47%.

Alcohol (ethanol) increases the endogenous production of triglycerides. Liver cells eliminate the excess hydrogen formed from the breakdown of alcohol by utilizing it to form alpha-glycero-phosphates and fatty acids, which are immediate precursors for triglycerides.

Synthesis of Triglycerides

Fatty acids are stored for future use as triacylglycerols in all cells, but primarily in adipocytes of adipose tissue. Triacylglycerols constitute molecules of glycerol to which three fatty acids have been esterified. The fatty acids present in triacylglycerols are predominantly saturated. The major building block for the synthesis of triacylglycerols, in tissues other than adipose tissue, is glycerol. Adipocytes lack glycerol kinase, therefore, dihydroxyacetone phosphate (DHAP), produced during glycolysis, is the precursor for triacylglycerol synthesis in adipose tissue. This means that adipoctes must have glucose to oxidize in order to store fatty acids in the form of triacylglycerols. DHAP can also serve as a backbone precursor for triacylglycerol synthesis in tissues other than adipose, but does so to a much lesser extent than glycerol.

The glycerol backbone of triacylglycerols is activated by phosphorylation at the C-3 position by glycerol kinase. The utilization of DHAP for the backbone is carried out through the action of glycerol-3-phosphate dehydrogenase, a reaction that requires NADH (the same reaction as that used in the glycerol-phosphate shuttle). The fatty acids incorporated into triacylglycerols are activated to acyl-CoAs through the action of acyl-CoA synthetases. Two molecules of acyl-CoA are esterified to glycerol-3-phosphate to yield 1,2-diacylglycerol phosphate (commonly identified as phosphatidic acid). The phosphate is then removed, by phosphatidic acid phosphatase, to yield 1,2-diacylglycerol, the substrate for addition of the third fatty acid. Intestinal monoacylglycerols, derived from the hydrolysis of dietary fats, can also serve as substrates for the synthesis of 1,2-diacylglycerols[2].

COMMENT: Processed foods, processed sugars, too much cooked dietary fats, transfats, and alcohol are the culprits that raise triglycerides and have no place nor need in healthy human nutritional pathways.

#4 What specifically causes loss of muscle mass (sarcopenia) with aging?

Aging-related sarcopenia is defined and characterized by a loss of muscle mass and strength and increased fatigability. However, studies of its determinants in elderly men are scarce.

Researchers (1) analyzed 845 men aged 45-85 y who belonged to the MINOS cohort. Lifestyle factors (physical activity, tobacco smoking, alcohol intake, caffeine intake) were evaluated by using a standardized questionnaire. Appendicular skeletal muscle mass (ASM) was estimated by using dual-energy X-ray absorptiometry. The RELATIVE APPENDICULAR SKELETAL MUSCLE MASS INDEX (RASM) was calculated as ASM/body height2.3. Apparent free testosterone concentration (AFTC) and free testosterone index (FTI) were calculated on the basis of concentrations of total testosterone and sex hormone-binding globulin.

RASM decreased with age (r = -0.29, P < 0.0001). Current smokers had lower RASM than did subjects who never smoked (-3.2%; P < 0.003). RASM increased with the intensity of physical activity at work (P for trend < 0.001). Men who participated in regular exercise during leisure time had 2.2% higher RASM than did those who did not (P < 0.03). Men whose values for AFTC, FTI, or 25-hydroxycholecalciferol [25(OH)D] were >2 SDs below the mean for young men had significantly lower RASM than did men with higher values. Men with sarcopenia, defined as the lowest quartile of RASM in the studied cohort (<6.32 kg/m2.3), were significantly older than men with normal RASM, weighed significantly less, smoked more, and spent significantly less time on leisure-time activities. Sarcopenic men also had lower values for testosterone, AFTC, FTI, and 25(OH)D.

In elderly men, low physical activity, tobacco smoking, thinness, low testosterone (AFTC and FTI), and decreased 25(OH)D concentrations are risk factors for sarcopenia.

COMMENT: With increasing age, smoking, low exercise, low testosterone, low 25-hydroxycholecalciferol are factors associated with the result of lean muscle mass loss in male subjects. Calcidiol (25(OH)D3) is metabolized by several forms of Vitamin D. It is the major circulating form of Vitamin D as the first intermediate form of Vitamin D synthesized during the conversion of Vitamin D3 to Calcitriol. Vitamin D3 is transported to the Liver for conversion to Calcidiol by Vitamin D-binding protein. Calcidiol is manufactured in the liver from its precursor, Vitamin D-3. Sarcopenia rate is 20% of all elderly males and 30% of all elderly females, but in some populations, it may be as high as 1 out of every 2 persons. I have a paper currently in peer-reviewed in which I analyzed a 70-120-food item intake consumed by 20 subjects, (10 men and 10 women, 16 were athletes, 4 were sedentary). Of those subjects, 19 of the subjects (10 women, 9 men) were not consuming the Reference Daily Intake RDI-preventative deficiency-disease dose of vitamin D3 through whole foods consumed. Only one subject, an active male athlete was consuming an adequate Reference Daily Intake RDI-preventative deficiency-disease dose of vitamin D3. Unless these factors are addressed in terms of activity, menu, and lifestyle choices, loss of lean muscle mass will result higher than is best for optimal health.

THE SUBSTANCES/FACTORS THAT ENHANCE MUSCLE GROWTH

Alpha-Ketoglutarate (such as the AKG in Race Caps Supreme) is speculated to enhance muscle growth can reverse muscle wasting in hospital patients by increasing glutamine stores within the muscles.

Arginine facilitates Muscle Growth (by inhibiting Muscle Loss - i.e. it is Anti-Catabolic).

Supplemental Branched Chain Amino Acids (BCAAs) (when used in conjunction with isotonic exercise (Weight lifting) facilitate muscle growth. Supplemental BCAAs help to minimize the body's need to catabolize endogenous BCAAs from muscles during isotonic exercise (and other forms of exercise) by providing an alternate source of BCAAs for the body to convert to alanine. By preventing the catabolism of BCAAs from muscles, muscle BCAA levels are preserved and muscle growth is not impaired. BCAAs are found in Hammer Gel, Hammer Whey, Hammer Soy, Sustained Energy, and Perpetuem.

HAMMER WHEY PROTEIN facilitates muscle growth by increasing the body's retention of nitrogen - nitrogen retention from whey protein is believed to be sixteen times that of free amino acids and twice that of whole food (primarily due to the lactalbumin content of whey protein). Glutamine stimulates the synthesis of endogenous proteins within the muscles, thereby facilitating muscle growth (i.e. It is anabolic). Glutamine can also prevent the breakdown of proteins within the muscles (i.e. It can prevent catabolism) during intensive exercise. It also improves muscle growth by increasing muscle cell volumization (increasing the retention of water within muscle fibers). Six grams glutamine is contained in every serving of Hammer Whey.

HAMMER SOY PROTEIN (indirectly) facilitates Muscle Growth (by enhancing nitrogen retention which helps to prevent the catabolism of endogenous Proteins in the Muscles). Preliminary research shows that Daidzein facilitates muscle growth (but only in men - it appears to inhibit muscle growth in women). Methoxyflavone is claimed to facilitate muscle growth.

Sleep is essential to muscle growth (inadequate sleep causes the body's testosterone levels to decline and human growth hormone (hGH) is released during sleep). REM Caps are designed to enhance deep REM sleep state cycle to increase hGH release during sleep.

Superunsaturated fatty acids facilitate muscle growth (when used in conjunction with isotonic exercise) - due to their ability to increase nitrogen retention. Fish oil DHA/EPA and Omega-3 Flaxseed oils meet and exceed this requirement at between 4-6 grams per day.

Calcium (600-1,000 mg per day) facilitates muscle growth in athletes: in one study basketballers who supplemented with 600-1,000 mg of calcium carbonate or calcium citrate per day recorded a 3.2% increase in muscle mass after 12 months compared to a 1.2% increase in muscle mass in control subjects. Calcium is formulated in Premium Insurance Caps and Endurolytes.

Hydroxy Methylbutyrate (HMB), Ketoisocaproate (KIC), Isoleucine, Leucine, Ornithine Alpha-Ketoglutarate (OKG), Colostrum (Bovine Colostrum), Orotic Acid, Valine, Serine, Proline, are protein-like amino acid safe supplements each have been shown to facilitate muscle growth.

THE SUBSTANCES/FACTORS THAT INHIBIT LEAN MUSCLE MASS GROWTH

Excessive corticosterone causes the proteolysis (catabolism) of endogenous proteins in the muscles - this impedes muscle growth.

Animal and dairy byproducts may result in excessive production of Prostaglandin E2 (PGE2) stimulates the degradation (catabolism) of skeletal muscle, which inhibits muscle growth.

Ibuprofen, Paracetamol, Cortisol (stress-induced) interferes with the ability of isotonic exercise (body building) to stimulate muscle growth.

Endurance exercise reduces muscle growth (i.e. It causes muscle loss).

HARMFUL SUBSTANCES TO AVOID ENHANCE MUSCLE GROWTH

AVOID all "Androgen-like substances" that may stimulate the formation of new myofilaments (the contractile filaments in muscle) and cause enlarging myofibrils (muscle cells) to divide. Androgen-class (male steroid hormones) that stimulate muscle growth (in the presence of isotonic exercise (weight-bearing exercise) such are: Luteinizing Hormone Releasing Hormone (LHRH), Human Growth Hormone, Beta-2 Adrenergic Receptor Agonists (e.g. Salbuterol), Insulin, pharmaceutical Chorionic Gonadotrophic Hormone (CGH), Follicle Stimulating Hormone (FSH), Dehydroepiandrosterone (DHEA) Testosterone, Androstenedione, Androstenediol, Norandrostenedione, 7-Keto DHEA, Anabolic-Androgenic Steroids (A-ASs) stimulate muscle growth (but possess numerous toxic side effects when used chronically). I do not recommend these or the temporal periodic use of these substances due to ethics of sport and unpredictable health-safety issues downstream effects on the body.

Reference

#5 What causes fat-weight gain what can be done to prevent or reverse it?

Obesity is a state characterized by excess adipose tissue (body fat). The term obesity is applied to persons who are more than 20% above their recommended body weight as measured by body mass index (BMI). Another means of determining obesity is the waist-to-hip ratio.

A healthy body fat percentage for women is 20% to 30% and for men a healthy body fat percentage is 8% to 20%. One pound of human fat contains 3,500 calories.

What country has the least overweight males?

What country has the most overweight males?

What country has the least overweight females?

What country has the most overweight females?

What country has the most overweight percent of their population?

What country has the least overweight percent of their population?

This table indicates (as of 1992) the percentage of the populations of various countries of the world who are regarded as obese:

At some stage, 78% of women and 40% of men (in western nations) have attempted to lose weight through dieting. Fasting or dieting can actually cause weight gain due to the fact that these practices decrease the body's basal metabolic rate. They fool the body into "thinking" that it is starving which results in the body conserving energy in the form of adipose tissue. Overeating in only 10% of cases causes obesity - in the remaining 90% important nutrients are lacking in the diet. Diet Restriction reduces the risk of Obesity. Monkeys fed a calorie-restricted diet for 15 years exhibited a reduced rate of Obesity. Fasting (especially prolonged Fasting) facilitates weight loss in persons afflicted with Obesity. Weight loss while fasting can reach 1.1 kg per day during the first ten days of fasting and stabilizes at 0.36 to 0.47 per kg at the end of the first month. Fasting is NOT recommended as a viable means of attaining permanent weight reduction for Obesity patients as it also results in loss of Lean Body Mass and negative Nitrogen Balance. During the first month of fasting, nitrogen losses average 4 grams per day and stabilize at 2.4 grams per day. During the first two weeks of fasting, approximately 40% of weight loss is from water losses, protein (muscle) loss accounts for approximately 6-10% of weight loss and body fat (adipose tissue) loss accounts for the remaining 50-54% of weight loss.

CAUSES OF OBESITY

AGE: The risk of obesity increases in tandem with the progression of the aging process.

DIET: A high-Glycemic Index diet increases the risk of obesity (by increasing insulin levels, which in turn suppresses the "burning" of body fat for the production of energy and redirects glucose to be stored as body fat.

Holt, S., et al. Interrelationships among postprandial satiety, glucose and insulin responses and changes in subsequent food intake. Eur J Clin Nutr.50:788-797, 1996.

Sigal, R., et al. Acute postchallenge hyperinsulinemia predicts weight gain: a prospective study. Diabetes. 46:1025-1029, 1997.

Excessive consumption of dietary carbohydrates especially simple sugars such as glucose and sucrose especially exacerbate obesity (by substituting for dietary fats and adipose tissue in the body's production of energy).Dietary carbohydrates that are not used in the production of energy are eventually stored as body fat (adipose tissue).

Excessive consumption of dietary fats increases the risk of obesity (to a greater extent than an equivalent number of calories ingested from proteins or carbohydrates). The ingestion of dietary fats initiates a process that results in the deposition of triglycerides (derived from the fatty acids in dietary fats) in adipose tissues - i.e. The body "prefers" to store dietary fats in adipose tissue in preference to utilizing them for the endogenous production of energy (this process is known as lipogenesis). Dietary fats can be readily incorporated into the triglycerides of adipose tissue due to the fatty acids in dietary fats being a principal component of triglycerides.

Unlike calories derived from other sources, calories derived from dietary fats require very little endogenous energy to be expended in digesting and metabolizing them, therefore ingestion of dietary fats do not increase the body's Basal Metabolic Rate (BMR) to the extent that calories derived from other sources do. Long-chain saturated fatty acids contribute to weight gain in people who are predisposed to obesity (when people who are predisposed to obesity consume long-chain saturated fatty acids, these fatty acids are incorporated into adipose tissue rather than being metabolized for the production of energy).

Excessive fructose-induced triglycerides are implicated in obesity (due their storage as adipose tissue).

Excessive Glucose-6-Phosphate Dehydrogenase (G6PD) activity contributes to or exacerbates Obesity (G6PD facilitates the storage of fats in adipose tissue).

Excessive activity of lipoprotein lipase in adipocytes contributes to obesity (lipoprotein lipase catalyzes the breakdown of triglycerides from lipoprotein into their constituent fatty acids and glycerol for uptake into adipocytes).

People with a low ratio of Brown Adipose Tissue (BAT) to White Adipose Tissue are more prone to Obesity. Lowered Basal Metabolic Rate (BMR) can result in Obesity. The Basal Metabolic Rate (BMR) of people afflicted with Obesity is an average of 8% lower than that of non-obese people.

Excessive levels of Cortisol contribute to the development of Obesity. The in vitro effects of cortisol and GH on basal and stimulated lipolysis in human adipose tissue were studied using a tissue incubation technique. After preincubation for 3 days in control medium containing insulin, adipose tissue pieces were exposed to cortisol for 3 days. GH was added to the cortisol-containing medium during the last 24 h (day 6). Adipocytes were then isolated, and lipolysis was studied in the absence and presence of isoprenaline, noradrenaline, forskolin, and N-6-monobutyryl-cAMP. Cortisol reduced the basal rate of lipolysis (P < 0.01) and the sensitivity to isoprenaline compared to the control values (P < 0.01). Addition of GH to the cortisol-containing medium increased the basal rate of lipolysis (P < 0.01) and the sensitivity to isoprenaline (P < 0.01) to the control level and increased the maximum isoprenaline-induced lipolytic activity (P < 0.01).Similar effects were obtained in the presence of noradrenaline.Maximum forskolin-induced lipolytic activity was reduced after exposure of the tissue to cortisol (P < 0.05), whereas addition of GH antagonized this effect (P < 0.01). Induction of the maximum lipolytic activity with N-6-monobutyryl-cAMP was not influenced by the preceding hormone exposure. Addition of GH alone during the last 24 h of incubation increased the basal rate of lipolysis (P < 0.05) and resulted in a borderline significant increase in the maximum isoprenaline-induced lipolytic activity (P = 0.055), suggesting that GH induces lipolysis also in the absence of glucocorticoids.Cortisol and GH have opposite effects on the basal lipolytic activity in human adipose tissue in vitro as well as on the sensitivity to catecholamines, GH being the lipolytic and cortisol the antilipolytic agent. (Ottosson, M., et al. Effects of cortisol and growth hormone on lipolysis in human adipose tissue. J Clin Endocrinol Metab.85(2):799-803, 2000.)

THYROID ISSUES & OBESITY

Obesity can occur as a result of the lowered basal metabolic rate that occurs as a result of hypothyroidism (underactive thyroid). Persons afflicted with obesity tend to exhibit Triiodothyronine (T3) levels that are an average 30% lower than those of non-obese subjects (which suggest that raising triiodothyronine levels to normal ranges may facilitate weight loss in the obese):

Thyroid hormones are derivatives of the amino acid tyrosine bound covalently to iodine.

The two principal thyroid hormones are:

thyroxine (known affectionately as T4 or L-3,5,3',5'tetraiodothyronine)

triiodotyronine (T3 or L-3,5,3'-triiodothyronine).

As shown in the following diagram, the thyroid hormones are basically two tyrosines linked together with the critical addition of iodine at three or four positions on the aromatic rings. The number and position of iodinated molecules are generated that have little or no biological activity; so called "reverse T3" (3,3',5'-T3) is such an example. The number and position of the iodines is important. Several other iodinated molecules are generated that have little or no biological activity; so called "reverse T3" (3,3',5'-T3) is such an example:

A large majority of the thyroid hormone secreted from the thyroid gland is T4, but T3 is the considerably more active hormone. Although some T3 is also secreted, the bulk of the T3 is derived by deiodination of T4 in peripheral tissues, especially liver and kidney. Deiodination of T4 also yields reverse T3, a molecule with no known metabolic activity.

Thyroid hormones are poorly soluble in water, and more than 99% of the T3 and T4 circulating in blood is bound to carrier proteins. The principle carrier of thyroid hormones is thyroxine-binding globulin, a glycoprotein synthesized in the liver. Two other carriers of import are transthyrein and albumin. Carrier proteins allow maintenance of a stable pool of thyroid hormones from which the active, free hormones are released for uptake by target cells.[3]

Thyroid Hormone Receptors and Mechanism of Action

Receptors for thyroid hormones are intracellular DNA-binding proteins that function as hormone-responsive transcription factors, very similar conceptually to the receptors for steroid hormones.

Despite being derived from an amino acid, thyroid hormones are hydrophobic in character and appear to enter cells and nuclei by diffusion through cell membranes. Once inside the nucleus, the hormone binds its receptor, and the hormone-receptor complex interacts with specific sequences of DNA in the promoters of responsive genes. The effect of receptor binding to DNA is to modulate gene expression, either by stimulating or inhibiting transcription of specific genes.

For the purpose of illustration, consider one mechanism by which thyroid hormones increase the strength of contraction of the heart. Cardiac contractility depends, in part, on the relative ratio of different types of myosin proteins in cardiac muscle. Transcription of some myosin genes is stimulated by thyroid hormones, while transcription of others in inhibited. The net effect is to alter the ratio toward increased contractility. For additional details on mechanism of action and how these receptors interact with other transcription factors, examine the section Thyroid Hormone Receptors.

Physiologic Effects of Thyroid Hormones

It is likely that all cells in the body are targets for thyroid hormones. While not strictly necessary for life, thyroid hormones have profound effects on many "big time" physiologic processes, such as development, growth and metabolism. Many of the effects of thyroid hormone have been delineated by study of deficiency and excess states, as discussed briefly below.

Metabolism: Thyroid hormones stimulate diverse metabolic activities most tissues, leading to an increase in basal metabolic rate. One consequence of this activity is to increase body heat production, which seems to result, at least in part, from increased oxygen consumption and rates of ATP hydrolysis. By way of analogy, the action of thyroid hormones is akin to blowing on a smouldering fire. A few examples of specific metabolic effects of thyroid hormones include:

• Lipid metabolism: Increased thyroid hormone levels stimulate fat mobilization, leading to increased concentrations of fatty acids in plasma. They also enhance oxidation of fatty acids in many tissues. Finally, plasma concentrations of cholesterol and triglycerides are inversely correlated with thyroid hormone levels - one diagnostic indiction of hypothyroidism is increased blood cholesterol concentration.
• Carbohydrate metabolism: Thyroid hormones stimulate almost all aspects of carbohydrate metabolism, including enhancement of insulin-dependent entry of glucose into cells and increased gluconeogenesis and glycogenolysis to generate free glucose.

Growth: Thyroid hormones are clearly necessary for normal growth in children and young animals, as evidenced by the growth-retardation observed in thyroid deficiency. Not surprisingly, the growth-promoting effect of thyroid hormones is intimately intertwined with that of growth hormone, a clear indiction that complex physiologic processes like growth depend upon multiple endocrine controls.

Development: A classical experiment in endocrinology was the demonstration that tadpoles deprived of thyroid hormone failed to undergo metamorphosis into frogs. Of critical importance in mammals is the fact that normal levels of thyroid hormone are essential to the development of the fetal and neonatal brain.

Other Effects: As mentioned above, there do not seem to be organs and tissues that are not affected by thyroid hormones. A few additional, well-documented effects of thyroid hormones include:

1.      Cardiovascular system: Thyroid hormones increases heart rate, cardiac contractility and cardiac output. They also promote vasodilation, which leads to enhanced blood flow to many organs.

2.      Central nervous system: Both decreased and increased concentrations of thyroid hormones lead to alterations in mental state. Too little thyroid hormone, and the individual tends to feel mentally sluggish, while too much induces anxiety and nervousness.

3.      Reproductive system: Normal reproductive behavior and physiology is dependent on having essentially normal levels of thyroid hormone. Hypothyroidism in particular is commonly associated with infertility.

Thyroid Disease States

Disease is associated with both inadequate production and overproduction of thyroid hormones. Both types of disease are relatively common afflictions of man and animals.

Hypothyroidism is the result from any condition that results in thyroid hormone deficiency. Two well-known examples include:

1. Iodine deficiency: Iodide is absolutely necessary for production of thyroid hormones; without adequate iodine intake, thyroid hormones cannot be synthesized. Historically, this problem was seen particularly in areas with iodine-deficient soils, and frank iodine deficiency has been virtually eliminated by iodine supplementation of salt.
2. Primary thyroid disease: Inflammatory diseases of the thyroid that destroy parts of the gland are clearly an important cause of hypothyroidism.

Common symptoms of hypothyroidism arising after early childhood include lethargy, fatigue, cold-intolerance, weakness, hair loss and reproductive failure. If these signs are severe, the clinical condition is called myxedema. In the case of iodide deficiency, the thyroid becomes inordinantly large and is called a goiter. The most severe and devastating form of hypothyroidism is seen in young children with congenital thyroid deficiency. If that condition is not corrected by supplemental therapy soon after birth, the child will suffer from cretinism, a form of irreversible growth and mental retardation. Most cases of hypothyroidism are readily treated by oral administration of synthetic thyroid hormone. In times past, consumption of desiccated animal thyroid gland was used for the same purpose.

Elevated insulin levels increase the risk of obesity. Insulin resistance is a very common underlying cause of obesity (in the presence of insulin resistance excessive serum glucose (blood sugar) is converted to adipose tissue (body fat) rather than being utilized by the body's cells for the endogenous production of energy).

Persons afflicted with Obesity have blood levels of Leptin that are five times higher than those of normal, healthy persons (although Leptin exerts anti-Obesity effects, persons afflicted with Obesity are insensitive to its effects).

Excessive secretion or production of Neuropeptide Y can cause obesity (by stimulating excessive appetite for carbohydrates and by stimulating excessive insulin secretion, leading to insulin resistance).

Excessive production/release of prolactin may contribute to obesity (as it increases the formation of adipose tissue).

Wilson's thyroid syndrome patients are prone to obesity and have extreme difficulty losing weight (due to their low basal metabolic rate).

Trans-Fatty Acids increase the size and quantity of adipose tissue (body fat) and therefore increase the risk of obesity.

Lead has been implicated in obesity. Epidemiological studies have found a direct correlation between the incidence of obesity and the exposure of persons afflicted with obesity to lead, especially during childhood.

Excessive zinc has been associated with obesity.

Slow (decreased) activity of the Adrenergic Nervous System can be an underlying cause of Obesity due to lowered Basal Metabolic Rate and fewer Nerve Impulses that activate Adrenergic Receptors on Brown Adipose Tissue. Alpha-2 Adrenergic Receptors are located on Adipocytes (and are especially prolific on Adipocytes in the lower half of the body. Did you know that the lower half of the female body contains nine times the number of Alpha-2 Adrenergic Receptors compared to Beta-1 Adrenergic Receptors? Stimulation of Alpha-2 Adrenergic Receptors located on adipocytes blocks the mobilization of triglycerides out of the adipocyte (i.e. Alpha-2 adrenergic receptor agonists inhibit lipolysis). In other words stimulation of alpha-2 adrenergic receptors inhibits weight loss in persons afflicted with obesity. Persons with a genetic predisposition to obesity have a diminished number of and/or defective Beta-3 Adrenergic Receptors.

Obesity can occur as a result of Cushing's Syndrome.

Temporary obesity can occur as a result of seasonal affective disorder (SAD).

Alcohol (ethanol) intake even while dieting, significantly reduces the body's ability to burn fat and increases the body's tendency to store fat;when alcohol replaces other foods in calorie equivalent quantities in the diets of healthy young males, the rate at which their bodies burned fat decreased by 33%.

The drugs Clonidine, Histamine H1 Receptor Antagonists, Medroxyprogesterone (a Progestin), Pharmaceutical Corticosteroids, can exacerbate obesity.

Obesity can occur as a symptom of male menopause. Sudden weight gain can occur as a result of the PMS-H (Hyperhydration) form of Pre-Menstrual Syndrome (PMS).

Obesity harmfully increases the risk to health through cardiovascular disease, atherosclerosis, hypertension (high blood pressure), ischemic heart disease, pulmonary hypertension, stroke, thrombosis, varicose veins and aggravates varicose veins, disorders of the gallbladder, greater incidence of gallstones excretory system, kidney disease, cataracts, suppresses the production of human growth hormone, toxicity to the immune system (due to autoxidation), some forms of cancer (breast cancer, cervical cancer, colon cancer (especially in males), endometrial cancer, lung cancer, (non-hodgkin's) lymphomas, ovarian cancer (in women), prostate cancer, uterus cancer, malignant melanoma form of skin cancer), elevated serum cholesterol, diabetes mellitus type 2, peroxidized fats than normal healthy people, backache, gout, osteoarthritis, asthma, excessive bleeding during menstruation, polycystic ovary syndrome (pcos), reduces anabolic testosterone and growth hormone.

Obesity interferes with the body's ability to manufacture vitamin D from the uv-b component of sunlight (this causes an increased prevalence of vitamin D deficiency in persons afflicted with obesity).

Acupuncture is not an effective therapy for achieving weight loss in persons afflicted with obesity (several scientific studies have indicated that Acupuncture is effective against obesity however later studies have revealed flaws in the original studies).

THESE SUBSTANCES FACILITATE WEIGHT LOSS IN OBESITY PATIENTS

Caffeine (percutafeine gel form applied topically) is prescribed in France to stimulate weight loss in specific areas of the body (in persons afflicted with obesity).

Capsaicin facilitates weight loss in persons afflicted with obesity by increasing the body's basal metabolic rate (BMR) and by stimulating lipolysis.

Dihydrocapsaicin facilitates weight loss in persons afflicted with obesity.

Ephedrine facilitates weight loss in people afflicted with obesity (by stimulating thermogenesis, increasing the body's basal metabolic rate (BMR) and by activating beta-3 adrenergic receptors). Aspirin further potentiates the ability of ephedrine to stimulate weight loss and thermogenesis - aspirin suppresses modulators that normally (partially) inhibit ephedrine's thermogenic effects. The dosage of aspirin used in clinical trials that demonstrated its ability to potentiate the weight loss caused by ephedrine was 325 mg of aspirin + 20 mg ephedrine, three times per day (= 975 mg aspirin + 60 mg ephedrine).

Ephedrine is even more effective in the treatment of obesity when it is combined with caffeine - caffeine further suppresses modulators that normally inhibit ephedrine's thermogenic effects. The combination of Ephedrine + Caffeine is regarded as the best anti-Obesity treatment but considerations for safety are inconclusive. Ephedrine + Caffeine is the only weight loss therapy that spares muscle during weight loss. Ephedrine + caffeine causes 100% more fat loss and 72% less muscle loss than the results obtained by dieting alone. The current scientific consensus is that the maximum weight loss effects of ephedrine are achieved when a combination of 20 mg ephedrine + 82 mg aspirin + 200 mg caffeine is used three times per day. Willowbark enhances the ability of ephedrine to facilitate (via thermogenesis) weight loss in people afflicted with obesity (when consumed concurrently with ephedrine or ephedra) (due to the salicin content of willowbark). CAUTION: I do not recommend use of the CAE stack for weight loss.

Nicotine helps to prevent obesity (by increasing the body's basal metabolic rate) - nicorette (chewing gum form of nicotine) is under investigation as a novel means of preventing obesity: CAUTION:NICOTINE presents several toxic side effects.

Synephrine increases the body's Basal Metabolic Rate (BMR), stimulates thermogenesis and thereby facilitates weight loss in persons afflicted with obesity (primarily by stimulating adrenaline and norepinephrine release and by activating various adrenergic receptors).

Yohimbine facilitates weight loss (especially weight loss in areas of the body below the waist, particularly the thighs) in persons afflicted with obesity (by stimulating the process of thermogenesis and the process of lipolysis via antagonism of Alpha-2 Adrenergic Receptors).

5-Hydroxytryptophan 5-HTP (900 mg per day) reduces appetite in people afflicted with Obesity. 5-HTP is formulated in REM Caps & Appestat.

Alanine reduces body weight in persons afflicted with obesity (by approximately 10%).

Arginine facilitates weight loss in persons afflicted with obesity by stimulating the Pituitary to release Human Growth Hormone.

Branched-Chain Amino Acids (BCAAs) supplementation (combined with a low-calorie diet) facilitates weight loss in persons afflicted with obesity.

Carnitine (2,000-3,000 mg per day) alleviates obesity. Carnitine allows the body to use the fats stored in adipose tissue for energy production.

Cysteine facilitates the body's use of adipose tissue as a source of energy.

Glutamine reduces body weight in persons afflicted with obesity (by approximately 10%).

Hydroxy Methylbutyrate (HMB) (3 grams per day combined with isotonic exercise) causes significant weight loss in persons afflicted with obesity.

Lysine enhances arginine's role in facilitating weight loss in persons afflicted with obesity.

Tyrosine reduces adipose tissues.

Beta 1,6 Glucan enhances weight loss in persons afflicted with obesity.

Chitosan facilitates weight loss in persons afflicted with obesity - it inhibits the further digestion of dietary fats from the digestive tract by binding to lipids (including fatty acids) and thereby facilitating their excretion. Within the intestines, chitosan forms a gel that binds to approximately 5 times its own weight of dietary fats - once the dietary fats are bound to chitosan, they become unavailable for further metabolism by the body and are eliminated via the feces. Chitosan decreases the absorption of dietary fats by up to 26% in the small intestine. For Chitosan to be maximally effective in the inhibition of the absorption of dietary fats, it must be present in high concentrations (i.e. Approximately 7.5% of the total diet).

Chondroitin sulfate facilitates weight loss in persons afflicted with obesity (by inhibiting the activity of pancreatic lipases, reducing the absorption of dietary fats in the small intestine and by decreasing the uptake of fats into adipose tissue).

Glucomannans (3,000 mg per day) cause significant weight loss in persons afflicted with obesity.

Guar Gum facilitates weight loss in persons afflicted with obesity.

Hemicelluloses enhance weight loss in persons afflicted with obesity.

Psyllium facilitates weight loss in obesity patients (by delaying the emptying of the stomach psyllium seeds/husks suppress the appetite).

Xylitol enhances the process of thermogenesis and may thereby facilitate weight loss in obesity patients.

Exposure to sunlight facilitates weight loss in persons afflicted with obesity (by stimulating the thyroid gland and increasing the body's basal metabolic rate). Caution: the detrimental effects of excess exposure to sunlight may occur.

Supplemental pancreatic enzymes can cause weight loss in persons afflicted with obesity (by causing decreased food intake as a result of stimulating endogenous substances that suppress the appetite). Supplemental pancreatic enzymes are included in Premium Insurance Caps and Race Caps Supreme.

Beta-3 Adrenergic Receptor Agonists stimulate the production of brown adipose tissue (BAT) and are currently in the early stages of testing on humans for the prevention or alleviation of obesity. Beta 3 Adrenergic Receptor Agonists have already been proven to stimulate the production of brown adipose tissue in obese mice. The experimental Beta-3 Adrenergic Receptor Agonist code-named BRL 35135 was orally administered to obese rats at the rate of 0.5 mg per kg - this treatment resulted in a 45-fold increase in thermogenesis in brown adipose tissue and a decrease in plasma insulin levels of 50%. Humans receiving the experimental Beta-3 Agonist code-named BRL 26830A for 18 weeks experienced weight loss of an average 15 kg. Adrenaline increases the rate of breakdown of adipose tissue (body fat) into triglycerides (i.e. Via lipolysis) as an energy source (and is therefore involved in facilitating weight loss in persons afflicted with obesity) - this action of adrenaline is mediated via activation of beta-3 adrenergic receptors.

Oleoyl Estrone (a synthetic, fatty ester of Estrone) facilitates weight loss in persons afflicted with obesity. Rats administered oleoyl estrone lost 25% of body weight in 2 weeks: weight loss occurred solely from adipose tissue loss and not from muscle loss.

Insulin-like Growth Factor-1 (IGF-1) is under investigation as a potential therapeutic agent in the treatment of obesity (due its ability to mobilize fatty acids from adipose tissue for the endogenous production of energy).

Supplemental 7-Keto DHEA facilitates weight loss in persons afflicted with obesity (by facilitating the process of thermogenesis).

Cholecystokinin (CCK) helps to prevent obesity (by suppressing appetite). Animals afflicted with obesity are less sensitive to the appetite-suppressant effects of CCK than non-obese animals.

Human growth hormone (hGH) replacement therapy reduces visceral fat and subcutaneous fat in persons afflicted with obesity (in persons with a clear-cut hGH deficiency). Human growth hormone (hGH) also helps to prevent obesity in elderly persons by inhibiting the formation of adipose tissue.

TESTOSTERONE facilitates weight loss in persons afflicted with obesity (primarily by stimulating lipolysis and by inhibiting the activity of lipoprotein lipase in adipocytes). Obesity (of the stomach and hips in women and of the stomach in men) can occur as a result of insufficient endogenous production of testosterone.

Optimal levels of THYROID HORMONES prevent obesity. Caution: exogenous, supplemental thyroid hormones should not be utilized for weight loss purposes unless there is a clear deficiency of thyroid hormones is determined monitored by your physician. Diiodotyrosine (T2) facilitates weight loss in persons afflicted with obesity (due to its ability to increase Basal Metabolic Rate). Thyroxine (T4) (Percutacrine Thyroxinique applied topically) is used in France to stimulate weight loss in specific areas of the body in persons afflicted with obesity and has been reported to be highly effective. Tiratricol (a metabolite/analog of Triiodothyronine) facilitates weight loss in persons afflicted with obesity (due to its ability to mimic the ability of Triiodothyronine (T3) to increase the body's Basal Metabolic Rate). Triiodothyroinine (T3) facilitates weight loss in persons afflicted with obesity (by increasing the body's basal metabolic rate).

FORSKOLIN facilitates weight loss in persons afflicted with obesity (it stimulates the production of cyclic amp (camp) which in turn regulates the process of lipolysis). Forskolin inhibits the endogenous synthesis of fatty acids in adipocytes. Forskolin counteracts the decreased response by adipocytes to adrenaline (which occurs as a result of the aging process).

Gamma-Linolenic Acid (GLA) facilitates weight loss in persons afflicted with obesity (this occurs via the following process: GLA converts to DGLA, which converts to Prostaglandin E1 which stimulates the activity of Adenyl Cyclase resulting in increased levels of cyclic AMP (cAMP); increased cAMP subsequently leads to increased lipolysis.

Medium-Chain Triglycerides (MCTs) help to prevent and treat obesity by stimulating the process of thermogenesis (unlike many other dietary Fats, MCTs are inefficiently stored within the body's Adipose Tissues, due to their rapid conversion to Energy). MCTs are most effective for obesity when used as a replacement for other types of dietary fats (rather than being used in addition to other types of dietary fats such as long-chain saturated fatty acids).

Prostaglandin E1 (PGE1) alleviates obesity (this occurs from PGE1 stimulating the production of Brown Adipose Tissue and from PGE1 stimulating Adenyl Cyclase resulting in increased production of cyclic AMP (cAMP) - a compound that stimulates lipolysis).

Superunsaturated Fatty Acids facilitate weight loss from adipose tissue (due to their ability to induce thermogenesis). Alpha-Linolenic Acid (LNA) facilitates weight loss by increasing the body's basal metabolic rate, increasing oxidation, functioning as an uncoupling agent and increasing Energy production in the body. Docosahexaenoic Acid (DHA) facilitates weight loss from Adipose Tissue (due to its ability to induce thermogenesis via increased uncoupling protein 3 production/activity). Fish oils (6,000 mg per day) facilitate loss of adipose tissue (bodyfat) in persons afflicted with obesity. Menhaden oil helps to control obesity by facilitating the transport of endogenous fatty acids into the mitochondria of cells for use in the production of energy (it achieves this by decreasing the sensitivity of Carnitine Palmitoyltransferase (CPT I form) to inhibition by Malonyl Coenzyme A)

Flax seed oil is a valuable adjunctive treatment for obesity.Flax seed oil helps the kidneys to eliminate excess water and increases the body's basal metabolic rate, oxidation rate and production of energy (due to the alpha-linolenic acid (LNA) content of flax seed oil). In addition the LNA content of flax seed oil functions as an uncoupling agent.

Calcium (1,000 mg per day) facilitates weight loss in persons afflicted with obesity.

Chromium facilitates weight loss in persons afflicted with obesity (by improving the body's utilization of Glucose - due to chromium polynicotinate being a component of Glucose Tolerance Factor).

Iodine facilitates weight loss in persons afflicted with obesity (where obesity is caused by Hypothyroidism).

Magnesium facilitates weight loss in persons afflicted with Obesity (due to its role in the production of Adenosine Triphosphate (ATP)).

Manganese may alleviate obesity.

Hydroxycitric Acid (-HCA) facilitates weight loss in persons afflicted with obesity by preventing the conversion of excess dietary carbohydrates to adipose tissue (by inhibiting the ATP-Citrate Lyase enzyme).HCA is formulated in Appestat Caps.

Metformin facilitates weight loss in persons afflicted with Obesity (by increasing the body's sensitivity to Insulin).

Orlistat is designed for the treatment of obesity (by inhibiting pancreatic lipases, Orlistat prevents the absorption of dietary fats as without pancreatic lipases, fat molecules remain too large to be absorbed by the intestines).

Pharmaceutical appetite suppressants are often prescribed to suppress the appetite in persons afflicted with obesity.

Sibutramine is used to facilitate weight loss in persons afflicted with obesity (by suppressing the appetite).

Preliminary research indicates the Daidzein (found in soy proteins) facilitates weight loss (IN WOMEN ONLY) - this means that Daidzein may be beneficial for women afflicted with obesity.

Epigallo-Catechin-Gallate (EGCG) (90 mg per day) facilitates weight loss in persons afflicted with obesity.

Increasing dietary protein intake to an amount that equals 25% of total calorie intake facilitates weight loss and white adipose tissue reduction in persons afflicted with obesity.

Persons afflicted with obesity are often deficient in Coenzyme Q10 - CoQ10 supplementation accelerates weight loss where CoQ10 deficiency has been established. (Race Caps Supreme is an excellent source of Coenzyme Q-10.)

Bromocriptine facilitates weight loss in persons afflicted with obesity (the speculated mechanism for additional weight loss with bromocriptine is via suppression of appetite).

Choline supplementation helps to prevent obesity (this occurs from choline facilitating the retention of carnitine, a compound with known anti-obesity effects).

Vitamin B5 facilitates weight loss in persons afflicted with obesity (by facilitating the processes of thermogenesis, beta-oxidation and peristalsis).

Vitamin C facilitates weight loss in people afflicted with obesity.

Vitamin D helps to prevent obesity (by lowering the secretion of leptin).

Dumontiaceae facilitates weight loss in persons afflicted with obesity.

Kelp alleviates obesity where obesity is due to hypothyroidism (due to the Iodine in Kelp increasing the body's Basal Metabolic Rate).

Spirulina (8,400 mg per day) facilitates weight loss in persons afflicted with obesity.

Grapefruit (juice) facilitates weight loss in persons afflicted with obesity.

Banaba Leaf facilitates weight loss in persons afflicted with obesity (probably due to the Corosolic Acid content of Banaba Leaf).

Brindle Berry (rind) accelerates weight loss in persons afflicted with obesity (due to the Hydroxycitric Acid content of Brindle Berry preventing the conversion of excessive dietary carbohydrates to adipose tissue).

Chillis are of assistance to persons afflicted with obesity (due to the Capsaicin content of Chilli increasing the body's BMR by stimulating the thyroid and due to the Capsaicin content of Chillis stimulating lipolysis).

Daikon helps to dissolve hard fat deposits embedded in the body's tissues.

Dandelion facilitates weight loss in persons afflicted with obesity.

Ginger facilitates weight loss in people afflicted with obesity (due to the ability of Ginger to increase the body's Basal Metabolic Rate (BMR) which results in greater activation of Beta-3 Adrenergic Receptors on brown adipose tissue resulting in greater thermogenesis).

Green tea (and to a lesser extent, black tea) facilitates weight loss in obesity by increasing the process of thermogenesis (due to the tea polyphenols and theophylline content of tea). Green tea reduces the absorption of dietary fats (by approximately 40%) by blocking the production of digestive enzymes that facilitate the absorption of dietary fats. Green tea suppresses appetite.

Guggulipid facilitates weight loss in persons afflicted with obesity (by stimulating the production of thyroid hormones).

Gymnema sylvestre (a herb) helps to prevent obesity by reducing the appetite (and craving) for carbohydrates.

Korean ginseng is a useful weight loss aid for the treatment of obesity (due to its ability to stimulate the process of thermogenesis).

When used in conjunction with engaging in exercise, maral root causes loss of body weight (including loss of body weight in persons afflicted with obesity) (due to the beta-ecdysterone content of maral root).

Sida cordifolia facilitates weight loss in persons afflicted with Obesity (due to the Ephedrine content of Sida cordifolia).

Willowbark enhances the ability of ephedrine to facilitate (via thermogenesis) weight loss in people afflicted with obesity (when consumed concurrently with ephedrine or ephedra) (due to the salicin content of willowbark).

Yohimbe facilitates weight loss (especially weight loss in areas of the body below the waist, particularly the thighs) in persons afflicted with obesity (due to the yohimbine content of yohimbe stimulating the process of thermogenesis and the process of lipolysis via antagonism of alpha-2 adrenergic receptors).

Maitake Mushrooms enhance weight loss in persons afflicted with obesity (due to the Beta 1,6 Glucan content of Maitake).

Coconut Oil facilitates weight loss in persons afflicted with obesity (due to the high content of medium-chain saturated fatty acids in Coconut Oil).

Mustard seeds facilitate weight loss in persons afflicted with obesity (by increasing the body's basal metabolic rate (BMR).

Psyllium seeds/husks facilitate weight loss in obesity patients (by delaying the emptying of the stomach psyllium seeds/husks suppress the appetite).

Garlic is useful in the treatment of obesity (it increases blood levels of norepinephrine which leads to enhanced thermogenesis in brown adipose tissue).

All forms of exercise facilitate weight loss in persons afflicted with obesity. Clinical studies have shown that the exercise undertaken first thing in the morning prior to breakfast is more effective for weight loss than an equivalent amount of exercise undertaken at other times of the day. Aerobic exercise facilitates weight loss (especially bodyfat loss) in persons afflicted with obesity. Ten minutes of running results in the burning of approximately 150 calories (depending on body size). Endurance exercise facilitates weight loss (especially bodyfat loss) in persons afflicted with obesity. Isotonic exercise (i.e. Weight lifting) facilitates loss of bodyfat (especially in persons afflicted with obesity) - this loss of bodyfat occurs primarily as a result of the increased basal metabolic rate that occurs as a result of isotonic exercise).

Reference

ADDENDUM Question:

What short-term protocol is recommended for losing body fat weight?

For reduction of your appetite cravings take the following for up to 3-weeks then take a week off, before repeating another 3-week session:

Weight loss and reduced appetite occur when an athlete consistently follows the following guidelines:

(1) Reduce normal carbohydrate intake by 50%.

(2) Increase raw food vegetable and fruit intake by 25%.

(3) Drink 8-10 glasses of water per day.

(4) Eat no food after 7:00 PM.

(5) Reduce animal and dairy byproducts to once per week.

(6) Exercise activity is conducted at or below 75% VO2 Max Heart Rate.

(7) Take each of the Appestat Caps product or ingredients:

L-Carnitine Tartrate250-500 mg

5-Hydroxy-Tryptophan<100-200 mg

Garcina Cambogia(Citri Max)200-300 mg

Chromium Polynicotinate (Chromemate)100 Mg

Zinc (Opti-Zinc) 15 Mg

Kelp 40-225 mcg

Rationale:

L-Carnitine Tartrate is a fatty acid carrier in mitochondria.

5-HydroxyTryptophan depresses of brain receptor sugar-cravings.

Garcina Cambogia (Citrimax) suppresses appetite.

Chromium Polynicotinate is a carbohydrate metabolism-balancing substrate.

Zinc releases natural leptin from body fat cells (leptin suppresses appetite).

Kelp enhances efficient thyroid metabolic activity.

Directions: take 2 units of the above 60 minutes prior to eating with 8 ounces distilled water or 100% pure fruit juice (apple, prune, orange, cranberry, or tomato) note: do not use fruit juice that contains fructose or high fructose corn syrup in the ingredients list.

The Appestat Caps protocol is designed for short-term weight reduction in the off-season not to exceed 2 periods of 21 days each nor more than 15 pounds weight loss.Athletes are advised to consult with their physician before attempting a weight loss program and if on either medications or if health concerns are contraindicated to a weight loss supplement protocol. Lifestyle habits form the basis for weight management and healthy natural control of Body Mass Index (BMI); unless the regular dietary habits support weight mass control, fat weight gain will result from caloric excess. Not one temporary diet actually works, rather healthy daily dietary choice does work favorably to control healthy muscle mass to fat weight ratio.

How fat is too fat?

A Body Mass Index (BMI) of 20-25 is regarded as a healthy body weight in ratio to stature. To figure your BMI, divide your weight in kilograms (1 lb = 0.45 kg) by height in meters squared (1 inch = 0.0254 meters).

Classification Overweight & Obese by Body Mass Index

To determine if you are overweight, a measure of male or female androids is called the Gynoid Obesity Ratio (GOF) for significant health risk is:

(A) Males >0.95

(B) Females >0.80

TO DETERMINE GOR FOR SIGNIFICANT HEALTH RISK:

(1) Measure waist circumference at navel relaxed, not pulling in stomach.

(2) Measure girth of buttocks/hips where girth is largest.

(3) Divide waist measure by hip measure.

Examples: Waist (30") ÷ Hips (34") = GOR of 0.88 or less than <0.95.

Waist (36") ÷ Hips (34") = GOR of 1.05 or greater than >0.95.

Percent Body Fat is a 3rd but less accurate measure of excess body fat weight.As men and women age, their body fat tends to increase gradually, silently, weekly, or seasonally. With decrease in metabolic rate as anabolic growth rate ceases and no decrease in food intake or exercise caloric expenditure, an excess of ONLY 218 CALORIES(1 extra Bagel) will add 1 ounce FAT to body adipose structures.

GENERAL STANDARD FOR OVERFAT BODYWEIGHT

Men >20%

Women >30%

FACING THE PROBLEM OF UNWANTED WEIGHT GAIN

If overeating were the major cause of obesity, then cutting back on the amount of food intake or making different food choices would dramatically solve or eliminate the problem, but it does not always resolve fat weight gain. Brouchard (N ENGL J MED;322:1477,1990.) studied 12 pairs of monozygotic twins for 100 days, overfeeding by 1000 kcal per day for 6 days per week to assess the role of inherited characteristics on body fat storage from overfeeding. This study showed that surplus energy intake did not produce similar responses in the outcome variables among twin pairs. Other than overeating, resting metabolic rate, dietary-induced thermogenesis (Example: cayenne pepper), spontaneous movement-fidgeting, basal body temperature, Levels of ATP, Lipoprotein Lipase, Total Enzymes, metabolically active brown adipose tissue, and muscle fiber type makeup/distribution.

Genetics and hormonal factors causing obesity are less than once formerly thought.Genetic factors contribute 25% to percent body fat and fat mass, while cultural habits are blamed for 30%, leaving 45% as nontransmissable factors. (Bouchard, C.,et al., Int J OBES,12:205,1988.)

STRESS and SEDENTARY LIFESTYLE combine to contribute most to the genetic susceptible individual weight gain.

Research has identified a model operant in human adipose tissue gain. A hormone-like protein, Leptin, has been identified for activating the satiety response to stop eating. When Leptin is released from fat tissue cell sites into the bloodstream, it is carried to the ventromedial nucleus of the hypothalamus, the control center for appetite satiety or hunger. This mechanism derives the physiological "Setpoint" for bodyfat. The size of each adipocyte, established before adulthood, may have some hormonal hold on the amount of leptin available to quench the appetite center. Endurance exercise will not reduce the size of the adopocytes, but may reduce the number or congestive storage of adipose tissue.

WHAT IS A GOOD DIET AND WHAT IS NOT?

Starvation is NOT a good practice nor efficient for permanent weight loss/control.When calories are dramatically reduced the resting metabolic response may decrease by as much as -45%! I recommend no less than 1000 calories per day for weight-loss. The 3 week cycle with a 1 week break, then return to the cycle of 21 X 1000 calorie intake per day may be a good way to lose 4-6 pounds every cyclic period.

WEIGHT LOSS WITHOUT COMMITMENT AND TIME DO NOT OCCUR

Endurance exercise enhances mobilization and utilization of body lipid stores and facilitates protein retention in skeletal muscles retarding protein breakdown. During a 21-24 day time period the following observed results occurred during a 1000 kcal per day caloric intake while exercising 2.5 hours per day.

Exercise has an appetite-suppression role in endurance athletes, but only when exercise demands are increased above the present adaptive levels.Off-Season is when these select athletes, who maintain minimum fitness, gain unwanted adipose tissue weight.For health reasons it is wise to apply the above measures of overweight excess once every quarter. Gains in the mid-section (waist) are regarded as dangerous, however minute, and should be monitored often.

Fat content in food is 97% deposited, metabolizing only 3% of its hefty 9 calories per gram, while Carbohydrates, simple or complex, are 77% deposited to muscle glycogen stores, or if in excess of the needs for muscle glycogen are deposited in adipose tissue sites.

Twenty-seven percent (27%) of the dietary "Carbs" are required to metabolize themselves into the system via the bloodstream and liver, but add only 4 calories per gram upon gaining entry.It is, however, the excess dietary sugar, all fat, and some of the complex carbohydrates that contribute to approximately 95% of all stored excess fat.

Advantages males have over female athletes when it comes to weight loss is found in the different ways fat is distributed by gender. Fat stored in upper body areas (stomach etc.) is more responsive to neurohumoral stimulation. Waist and upper body fat stores are preferentially mobilized during exercise far more than the adipose stores below the waist.

COMMENT: I do not advise long term weight loss unless morbid obesity and health are the concerns of you and your family Medical doctor. Of those observed on caloric restriction of 21 days on, 7 days off, success rate is remarkable. As a precaution, weight control or weight loss protocols should only be employed in the off season, since one of the side effects to even mild weight reduction is performance.