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PATHOGENESIS OF OBESITY
Dr. Ann de Wees Allen, N.D.
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PATHOGENESIS OF OBESITY AS RELATED TO INSULIN AND GROWTH HORMONE
OBESITY DEFINED
In Total Body Weight
Women: Body weight 20% or more above normal
Men: Body weight 25% or more above normal
In Body Fat Content
Women: Body fat levels above 30%
Men: Body fat levels above 25%
INSULIN AND HYPOTHALAMIC DISFUNCTION
Oversecretion of insulin results in hypothalamic dysfunction. The metabolic result is obesity. Thyroid hypoactivity in obese subjects is rare.
The Hypothalamus influences:
Insulin release
Fatty acid mobilization
Hepatic glycogen synthesis
CONTRIBUTING FACTORS IN THE PATHOGENSIS OF OBESITY
Hyperinsulinemia stimulating lipogenesis
Reduced sympathetic nervous system (SNS) activity
Reduced thyroid hormone activity
Reduced levels of growth hormone
Impaired insulin-mediated thermogenesis
GROWTH HORMONE AND OBESITY
Obese subjects have depressed growth hormone levels. Normal GH levels in non-obese individuals are four times higher than that of obese individuals and five times higher than that of hyper-obese individuals. Growth hormone increases insulin resistance and glucose tolerance. In the obese, even though their GH levels are low, linear growth is normal. Ability to release GH is impaired in the obese individual. Obese subjects taking typical growth-hormone-releasing-agents (GHRA) will release much less GH than a non-obese subject. Oral administration of L-arginine in a specific formulation increases GH release in the obese to equal two-thirds that of a non-obese, normal weight subject. Said formula can elicit a GH increase in obese women twelve to fifteen times that of their normal levels.
INSULIN AND LIPOPROTEIN LIPASE
Lipoprotein Lipase: Enzyme found in capillary beds of adipose tissue under condition of high blood insulin levels
Higher glucagon/lower insulin = Low LPL = fatty acids from blood triglycerides not released for entry into adipose tissue cells
Higher insulin/lower glucagon = High LPL
Lowered insulin = Reduced glucose transport into adipose tissue cells = Reduced intracellular glucose
ADIPOSE TISSUE LIPASES
Lipoprotein lipase
Intracellular triglyceride lipases
Hormone-sensitive lipase
INSULIN AND ENDOCRINE FACTORS
Norepinephrine and other alpha agonists INCREASE APPETITE
Beta agonists and beta stimulators (like isoprotenol) DECREASE APPETITE
Prostoglandins DECREASE APPETITE
PGI-1, a prostoglandin and alpha receptor blocker, blocks the effects of norepinephrine
Response to norepinephrine is decreased in diabetics
Increased serum INSULIN levels and insulin resistance are associated with obesity.
GROWTH HORMONE VS. INSULIN STIMULATION OF MUSCLE GROWTH
Both GH and insulin stimulate muscle growth. The difference is that insulin is a very poor muscle stimulus while GH is a very powerful muscle stimulus. GH also blocks fat storage while insulin stimulates fat storage. Insulin is requires for muscle growth, but normal persons have totally adequate insulin levels for muscle growth. If growth hormone levels are high enough, insulin fat-storing effects can be mitigated.
MECHANISM OF GROWTH HORMONE STIMULATED BY INSULIN
GH is released by either 1) insulin released in response to high blood sugar or 2) insulin introduced into the blood stream. Either way, a large insulin rush causes the blood sugar to drop to 50% of its normal level, at which point GH is released. The arrival of growth hormone stops the sugar-burning effects of the insulin. This halts the rapid decrease in blood sugar. It is a preventive mechanism the body utilizes to prevent blood sugar from plunging to dangerous levels. Excess blood sugar aided by insulin will then convert to stored fat. When GROWTH HORMONE dominates - Triglyceride storage is reduced. Thus, ratios of GROWTH HORMONE to INSULIN are extremely important in controlling excess body fat.
BIOCHEMICAL RESPONSE TO GROWTH HORMONE
RELEASING AGENTS
Growth hormone (GH) helps determine whether dietary protein is converted to fat or to muscle. Lack of appropriate levels of GH encourage fat storage as a speciation technique. Neanderthal and Cro Magnon man had to stop hunting at age 22-23 as he was then too physically impaired to keep up with the hunt. Without access to adequate amounts of protein (meat), Neanderthal man could not maintain the muscle mass he had during his youthful period (up to age 23). As a result of this and other species-related factors, humans begin to lose GH at age 23. This decline in GH stimulates fat storage and decreases muscle mass, thus ensuring a longer survival/breeding span in our ancestors.
Another contributing factor in the determination of the conversion of dietary proteins and carbohydrates to either fat or muscle is stimulation of Lipoprotein Lipase (LPL). LPL is the gatekeeper for fat storage in the fat cells. Ingestion of any high glycemic ingredient or food OR the ingestion of protein alone can stimulate LPL. Thus, a properly formulated Growth Hormone Releasing Agent (GHRA), with a low glycemic format and GH stimulating properties, exacerbates the conversion of protein into muscle as opposed to fat.
EQUASIONS RELATIVE TO GROWTH HORMONE RELEASE
E + HGH = M and conversely E - HGH = F
Excess amino acids + human growth hormone = muscle mass
Excess amino acids - human growth hormone = adipose tissue
E = Excess amino acids and/or high glycemic carbohydrates
HGH = Human growth hormone
M = Muscle mass
F = Adipose tissue (fat)
GHRA = HGH = M + S + R + V + T + E
GHRA = L-arginine formula protocol
HGH = Human growth hormone
M = Muscle mass
S = Increased strength
R = Reduced adipose tissue
V = increased VO2 Max
T = Reduced recovery time
E = Increased endurance.
Increase in the release of HGH = Increased lean muscle mass, increased strength, reduced adipose tissue, increased VO2 Max, reduced recovery time, and increased endurance.
--------------------------------------------------------------------------------
[ Research Articles | Sports Nutrition Success Stories | The Glycemic Index |
The Glycemic Research Institute | Dr. Allen's Biography | Photo Gallery ]
--------------------------------------------------------------------------------
Dr. Ann de Wees Allen, N.D.
E-mail: [email protected]
Copyright 1997 - 2000 Ann de Wees Allen, N.D. All rights reserved.
Dr. Ann de Wees Allen, N.D.
--------------------------------------------------------------------------------
PATHOGENESIS OF OBESITY AS RELATED TO INSULIN AND GROWTH HORMONE
OBESITY DEFINED
In Total Body Weight
Women: Body weight 20% or more above normal
Men: Body weight 25% or more above normal
In Body Fat Content
Women: Body fat levels above 30%
Men: Body fat levels above 25%
INSULIN AND HYPOTHALAMIC DISFUNCTION
Oversecretion of insulin results in hypothalamic dysfunction. The metabolic result is obesity. Thyroid hypoactivity in obese subjects is rare.
The Hypothalamus influences:
Insulin release
Fatty acid mobilization
Hepatic glycogen synthesis
CONTRIBUTING FACTORS IN THE PATHOGENSIS OF OBESITY
Hyperinsulinemia stimulating lipogenesis
Reduced sympathetic nervous system (SNS) activity
Reduced thyroid hormone activity
Reduced levels of growth hormone
Impaired insulin-mediated thermogenesis
GROWTH HORMONE AND OBESITY
Obese subjects have depressed growth hormone levels. Normal GH levels in non-obese individuals are four times higher than that of obese individuals and five times higher than that of hyper-obese individuals. Growth hormone increases insulin resistance and glucose tolerance. In the obese, even though their GH levels are low, linear growth is normal. Ability to release GH is impaired in the obese individual. Obese subjects taking typical growth-hormone-releasing-agents (GHRA) will release much less GH than a non-obese subject. Oral administration of L-arginine in a specific formulation increases GH release in the obese to equal two-thirds that of a non-obese, normal weight subject. Said formula can elicit a GH increase in obese women twelve to fifteen times that of their normal levels.
INSULIN AND LIPOPROTEIN LIPASE
Lipoprotein Lipase: Enzyme found in capillary beds of adipose tissue under condition of high blood insulin levels
Higher glucagon/lower insulin = Low LPL = fatty acids from blood triglycerides not released for entry into adipose tissue cells
Higher insulin/lower glucagon = High LPL
Lowered insulin = Reduced glucose transport into adipose tissue cells = Reduced intracellular glucose
ADIPOSE TISSUE LIPASES
Lipoprotein lipase
Intracellular triglyceride lipases
Hormone-sensitive lipase
INSULIN AND ENDOCRINE FACTORS
Norepinephrine and other alpha agonists INCREASE APPETITE
Beta agonists and beta stimulators (like isoprotenol) DECREASE APPETITE
Prostoglandins DECREASE APPETITE
PGI-1, a prostoglandin and alpha receptor blocker, blocks the effects of norepinephrine
Response to norepinephrine is decreased in diabetics
Increased serum INSULIN levels and insulin resistance are associated with obesity.
GROWTH HORMONE VS. INSULIN STIMULATION OF MUSCLE GROWTH
Both GH and insulin stimulate muscle growth. The difference is that insulin is a very poor muscle stimulus while GH is a very powerful muscle stimulus. GH also blocks fat storage while insulin stimulates fat storage. Insulin is requires for muscle growth, but normal persons have totally adequate insulin levels for muscle growth. If growth hormone levels are high enough, insulin fat-storing effects can be mitigated.
MECHANISM OF GROWTH HORMONE STIMULATED BY INSULIN
GH is released by either 1) insulin released in response to high blood sugar or 2) insulin introduced into the blood stream. Either way, a large insulin rush causes the blood sugar to drop to 50% of its normal level, at which point GH is released. The arrival of growth hormone stops the sugar-burning effects of the insulin. This halts the rapid decrease in blood sugar. It is a preventive mechanism the body utilizes to prevent blood sugar from plunging to dangerous levels. Excess blood sugar aided by insulin will then convert to stored fat. When GROWTH HORMONE dominates - Triglyceride storage is reduced. Thus, ratios of GROWTH HORMONE to INSULIN are extremely important in controlling excess body fat.
BIOCHEMICAL RESPONSE TO GROWTH HORMONE
RELEASING AGENTS
Growth hormone (GH) helps determine whether dietary protein is converted to fat or to muscle. Lack of appropriate levels of GH encourage fat storage as a speciation technique. Neanderthal and Cro Magnon man had to stop hunting at age 22-23 as he was then too physically impaired to keep up with the hunt. Without access to adequate amounts of protein (meat), Neanderthal man could not maintain the muscle mass he had during his youthful period (up to age 23). As a result of this and other species-related factors, humans begin to lose GH at age 23. This decline in GH stimulates fat storage and decreases muscle mass, thus ensuring a longer survival/breeding span in our ancestors.
Another contributing factor in the determination of the conversion of dietary proteins and carbohydrates to either fat or muscle is stimulation of Lipoprotein Lipase (LPL). LPL is the gatekeeper for fat storage in the fat cells. Ingestion of any high glycemic ingredient or food OR the ingestion of protein alone can stimulate LPL. Thus, a properly formulated Growth Hormone Releasing Agent (GHRA), with a low glycemic format and GH stimulating properties, exacerbates the conversion of protein into muscle as opposed to fat.
EQUASIONS RELATIVE TO GROWTH HORMONE RELEASE
E + HGH = M and conversely E - HGH = F
Excess amino acids + human growth hormone = muscle mass
Excess amino acids - human growth hormone = adipose tissue
E = Excess amino acids and/or high glycemic carbohydrates
HGH = Human growth hormone
M = Muscle mass
F = Adipose tissue (fat)
GHRA = HGH = M + S + R + V + T + E
GHRA = L-arginine formula protocol
HGH = Human growth hormone
M = Muscle mass
S = Increased strength
R = Reduced adipose tissue
V = increased VO2 Max
T = Reduced recovery time
E = Increased endurance.
Increase in the release of HGH = Increased lean muscle mass, increased strength, reduced adipose tissue, increased VO2 Max, reduced recovery time, and increased endurance.
--------------------------------------------------------------------------------
[ Research Articles | Sports Nutrition Success Stories | The Glycemic Index |
The Glycemic Research Institute | Dr. Allen's Biography | Photo Gallery ]
--------------------------------------------------------------------------------
Dr. Ann de Wees Allen, N.D.
E-mail: [email protected]
Copyright 1997 - 2000 Ann de Wees Allen, N.D. All rights reserved.
