Weight loss and dieting is a perennial subject of conversation, TV talk
shows, best-selling books, and even trips to the doctor. And no wonder. In
spite of the widespread introduction of “low fat”, “no fat”, and “reduced fat”
foods and snacks throughout the 1990’s, obesity has reached epidemic proportions
in much of the Western world. Obesity (defined as being 20% or more over “ideal”
or “normal” weight for one’s size) is now estimated to afflict 35-40% of adults
in America. “Common sense” says that the obvious way to avoid or reduce unwanted
weight gain is simply to eat less calories.
Since carbohydrates (sugars and starches) and protein each provide only 4
calories (of energy content) per gram, while fat provides 9 calories per gram,
and since it’s those unsightly bulges of fat we want to avoid or rid ourselves
of to begin with – then just reduce the fat in one’s diet, and slimness is “just
a bite away.” Unfortunately, this “common sense” approach to weight (fat) loss
misses the mark in many ways. One hint should be obvious from the way that
cattle, hogs and other livestock are fed to rapidly fatten them up at feedlots
just before slaughter. Are they fed lard, dairy fat, vegetable oil, margarine,
etc.? No. They are fed corn to rapidly fatten them up! Yet corn contains less
than 5% fat – it is almost 90% carbohydrate. And what about those “low fat”
foods widely introduced during the very 1990’s decade when America’s incidence
of obesity increased by a whopping 30-40%? While some were lower fat dairy
products and leaner cuts of meats, most of these nouveau “foods” were
low-fat cereals, pasta, cookies, snack bars, corn and potato chips, cakes, ice
creams, etc. Virtually all of these (high profit) manufactured “foods” are high
in sugar/starch and low in protein.
Then there is the so-called “French paradox.” The French are significantly
less afflicted than America with heart disease and obesity – both conditions
allegedly produced by an excessive fat intake, yet the French eat comparable
amounts of meat and fish, four times as much butter, and twice as much cheese
(all fat-rich foods) as Americans. Interestingly, the French consume only about
18% as much sugar as Americans. (1)
By now, dear reader, you should be getting the hint that obesity is far more
related to carbohydrate consumption than fat intake. Yet even obese people have
only 1-2 pounds of carbohydrate stored in their body, as glycogen – a
muscle/liver – stored starch. So how can a high carbohydrate, reduced fat diet
promote weight gain among Americans, while a high fat, low sugar diet doesn’t
fatten Frenchmen nearly as much?
The answer lies not with the dietary ingredients themselves, but rather in
the hormonal and biochemical reactions these metabolically different food
categories (fat, carbohydrate, protein) elicit in the human body. And the chief
hormonal culprit in promoting excess body fat (technically called “white adipose
tissue”) is – Insulin.
THE INSULIN – GLUCAGON FAT CONNECTION
Insulin is a large polypeptide hormone secreted by the beta-cells of the
pancreas. Insulin release is directly controlled by dietary factors. “Glucose
[blood sugar] is the principal stimulus to insulin secretion in human beings….
Insulin lowers the concentration of glucose in blood by inhibiting hepatic
[liver] glucose production and by stimulating the uptake of glucose by muscle
and adipose tissue…. Under normal conditions, insulin inhibits lipolysis [the
breakdown of stored body fat for use as organ/muscle fuel], stimulates fatty
acid synthesis [from both sugars and fats]… and decreases the hepatic
concentration of carnitine [carnitine “shuttles” fatty acids into mitochondria
in most cells for use as ATP energy fuel].” (2)
“Insulin stimulates the fat cells to take up fat and sugar from the blood and
store it away as body fat, especially in the middle of the body, within the
abdomen and around the vital organs.” (3) “Overweight people tend to have higher
basal [baseline] levels of insulin; hyperinsulinemia [high blood insulin] which
promotes lipogenesis [fat-formation].” (4)
Insulin is the chief hormone the body uses to lower excessively high blood
sugar. The entire bloodstream of a normal, non-diabetic human contains less than
5 grams – a level teaspoonful – of glucose at any one time. It is thus
relatively easy to stimulate a rapid rise in blood sugar through sugar – food
ingestion. Eating a candy bar or drinking a soft drink will normally raise blood
sugar – and blood insulin – within minutes. And while starch foods (starches are
chains of sugar molecules, broken down during digestion) may be slightly slower
to raise blood sugar and insulin, the modern industrialized starches, such as
white flour and finely ground corn meal, used to make pasta, bread, cakes, corn
chips and tortillas, crackers, cookies, etc., are digested and absorbed almost
as quickly as simple sugar foods.
Insulin has a hormonal partner in regulating and fine-tuning blood sugar
levels – glucagon, also secreted by the pancreas. “The secretion of glucagon is
regulated by dietary glucose, insulin, amino acids, and fatty acids; glucose is
a potent [glucagon] inhibitor…. [The metabolic effects of glucagon] are
normally opposed by insulin, and when equivalent equations of both hormones are
present, insulin is predominant.” (2) “Glucagon levels are largely determined by
the amount of incoming dietary protein, just as insulin levels are strongly
related to the amount of incoming carbohydrate.” (7) Just as insulin lowers high
blood sugar, glucagon raises low blood sugar – especially important when we skip
meals, exercise severely, fast, starvation diet, etc.
Insulin and glucagon also have opposing actions on two key enzymes which
control the fate of fat in the body (stored body fat, dietary fat, or fat made
in the liver/fat cells from carbohydrates under the stimulus of insulin).
“Residing on the surface of the fat cells are two enzymes – both regulated by
insulin and glucagon – responsible for herding fat into or out of the fat cells.
The first, lipoprotein lipase [LPL], transports fatty acids into the fat cell
and keeps them there…. The other, hormone-sensitive lipase [HSL], does just
the opposite – it releases the fat from fat cells into the blood [where it is
then transported to other cells to be “burned” as fuel]…. insulin stimulates
the activity of lipoprotein lipase, the fat-storage enzyme, and glucagon
inhibits it; glucagon stimulates the fat-releasing hormone [HSL], and insulin
inhibits it.” (3) “The adipose tissue enzyme [LPL] is highly sensitive to
variations in the metabolic state, being rapidly increased by oral glucose, by
high carbohydrate diet and after usual meals. On the other hand, the LPL
activity in adipose tissue decreases when plasma insulin is low as in diabetes
and during caloric restriction [and on a low carbohydrate diet].” (5)
As the Drs. Eades note in their book Protein Power: “By altering the ratio of
insulin to glucagon – which we can do through our selection of foods -we can
determine which pathway predominates. Instead of allowing our [fat] biochemistry
to control us, we can control it…. In the insulin-dominant mode, fat storage
prevails. In the glucagon-dominant mode…, fat flows away from the fat cells.
Fat released from the fat cells enters the other cells and gets shuttled into
the mitochondria, where it is completely burned for cellular energy. Along with
this fat from the fat cells any dietary fat – whether consumed as fat or
converted from carbohydrate or protein – also flows into the mitochondria for
oxidation instead of into the fat cells to be stored.”
The chief dietary stimulant for insulin release is carbohydrate (CHO); the
chief stimulant for glucagon release is protein. The chief activator of body fat
– promoting LPL is insulin; the chief LPL-inhibitor is glucagon. Without high
insulin/LPL activity, dietary fat will not end up as stored fat. To get a clear
sense of the central necessity of insulin to promote fat storage, consider the
fate of the untreated Type I diabetic, whose pancreas has (more or less)
completely ceased secreting insulin. Even on a high CHO/fat diet, such a
diabetic will continually lose fat (and muscle, as well), and may even lose
30-40 pounds in a month. Without insulin, even a high fat/high CHO diet will not
cause fat gain, nor will a high fat diet even prevent loss of existing fat
stores. But when dietary fat is combined with large amounts of dietary CHO which
activates both insulin and LPL, then much of both the fat CHO ends up as stored
body fat.
The National Research Council (USA) reported in 1985 that the average
American diet (see chart 1) was 46% CHO calories, 43% fat calories, and only 11%
protein. (3) Thus it should be obvious that the typical American diet is also an
optimal diet for promoting obesity.
Even though all CHOs have some tendency to stimulate insulin release, some
are worse than others. CHO-research expert Sheldon Reiser has reported that when
human volunteers were given drinks or meals calculated to contain 50 grams of
glucose, “… glucose and insulin responses were 35-65% lower when starch was
the carbohydrate source than when either glucose or sucrose [white sugar] was
the carbohydrate source…. The undesirable effects of sucrose… appears to be
due, at least partly, to the metabolic properties of the fructose moiety. [One
sucrose molecule is one glucose bonded to one fructose]…. Fructose infusion in
humans and rats has been shown to produce large decreases in the ATP content of
the liver. [The liver-chief metabolic organ of the body uses 12% of the body’s
total ATP energy supply to do its hundreds of metabolic tasks. Anything that
seriously lowers liver ATP is by definition a metabolic poison.]…. Neither
fructose nor glucose, when given [alone], stimulates insulin as potently as
glucose and fructose combined. Since diets rarely contain fructose in the
absence of glucose or glucose polymers, small amounts of fructose reaching the
general circulation [after meals] could greatly affect insulin secretion….
Numerous studies have shown a relationship between insulin levels… and blood
triglyceride levels…. Studies in both rats and humans have demonstrated that
fructose is more readily converted into lipogenic [fat-forming] substrate than
is glucose….
As might be expected on the basis of its more lipogenic metabolism, fructose
appears to be incorporated into blood triglycerides more rapidly than is
glucose…. In human studies in which the intake of sucrose has been either
eliminated or reduced, significant decreases in fasting serum triglycerides
[normally made under the prodding of insulin] occurred…. The feeding of
sucrose also appears to produce greater increases in blood triglycerides than
does the feeding of glucose or partial starch hydrolysates.” (6)
Thus, natural unrefined starches (especially vegetables) will tend to cause
less hyperinsulin responses than sugar-rich foods such as candy, cake, pie,
doughnuts, soft drinks, sports drinks, etc., as well as natural sugar foods such
as dates, figs, dried pineapple, etc.
INSULIN: ACCELERATOR OF AGING
In his 1999 book The Anti-Aging Zone, Barry Sears proposes that there are
four chief “pillars of aging” that promote ever-worsening hormonal regulation of
and communication between cells, ultimately leading to aging, disease and death.
Sears’ four pillars (7) are:
1) Excess insulin.
2) Excess cortisol.
3) Excess blood
glucose.
4) Excess free radicals.
Many researchers in the past several decades have uncovered evidence
supporting insulin’s role as the “chief pillar of aging.” Gerald Reaven is known
for his research on “Syndrome X.” This is a syndrome common among sedentary
modern Western humans, which involves the strong clustering of hypertension,
insulin resistance, hyperinsulinemia, hyper-triglyceridemia, glucose
intolerance, obesity, low HDL cholesterol and heart disease. (1) Reaven has
shown that the common denominator of the syndrome is hyperinsulinemia and
insulin resistance. As Western peoples age, they tend to develop the condition
of insulin resistance, wherein the target cells of insulin – especially
the muscle cells – become even more resistant to “hearing the message” of
insulin. This in turn lessens the blood sugar-lowering effect of insulin, so
that even-smaller amounts of sugar lead to ever-higher blood glucose levels –
i.e. glucose intolerance. As cells become more resistant to “hearing” the
insulin in an attempt to “bludgeon” the cells into accepting glucose- i.e.
hyperinsulinemia.
Insulin is known to cause sodium retention with consequent water retention –
hence the hypertension (high blood pressure) connection. As already noted,
insulin promotes fat storage in fat cells – i.e. obesity. Insulin
stimulates the liver to convert sugar and dietary fats into triglycerides – the
form of fat that circulates in the blood and is stored in fat cells – i.e.
hyper-triglyceridemia. And as R.W. Stout noted in 1985: “The arterial wall
is an insulin-sensitive tissue. Insulin promotes proliferation of arterial
smooth muscle cells [a beginning phase of atherosclerotic [plaque formation] and
enhances lipid synthesis and low-density lipoprotein [LDL] receptor
activity. Insulin also promotes experimental atherosclerosis in a number
of species.” (1) Insulin-injecting diabetics typically develop
atherosclerosis 10 – 20 years earlier than non-insulin-injecting diabetics.
In a 1989 article, “The Deadly Quartet,” M.D. Norman Kaplan reviewed the
standard theory that upper-body obesity typically precedes hypertension, glucose
intolerance and high triglycerides. Kaplan demonstrates that
hyperinsulinemia is the more likely root cause of all four conditions – obesity,
glucose intolerance, high triglycerides and hypertension. (1,3)
Two of the other “pillars of aging” – excess cortisol and excess blood
glucose – are also intimately tied to excess insulin. As Heleniak and
Aston report, “A consequence of obesity is the development of insulin resistance
as weight is gained…. Insulin resistance has been induced in normal human
subjects by overfeeding. The onset of glucose intolerance may be due to
frequent snacking on high energy density foods which prevent insulin levels from
returning to normal fasting levels keeping insulin circulating in the blood for
a better part of the 24-hour day.” (4) If levels edge chronically higher,
cells must become somewhat insulin resistant.
Why? Because most cells can burn either fat or glucose for fuel, but
the brain (under non-fasting conditions) can only burn glucose and typically
needs 400 – 500 calories/day of glucose – i.e. about one half the normal total
circulating blood sugar. The brain doesn’t need insulin to absorb glucose,
giving it a competitive edge over the other 100 – 200 pounds of tissue – unless
insulin levels are frequently high.
Thus in order to safeguard the brain’s minute-by-minute blood glucose
delivery, other cells must develop insulin resistance when insulin levels
are frequently or chronically high, so that they don’t “snatch” all the blood
glucose from the hungry brain. The primary hormone that should raise blood
sugar to adequately feed the brain is glucagon. But “insulin can act as a
glucagon release-inhibiting paracrine hormone,” (2) especially at high
concentrations. So then the body goes to “Plan B”: the release of
cortisol.
THE INSULIN-CORTISOL CONNECTION
Cortisol comes to the brain’s rescue in two ways. (8) It increases
gluconeogenesis – the making of glucose by breaking down proteins from
skin, muscle and organ tissue and converting them to glucose in the liver.
“Cortisol also causes a moderate decrease in the rate of glucose utilization by
cells everywhere in the body” (8) – i.e. cortisol causes insulin
resistance!
Thus Sears’ first three pillars of aging – excess insulin, cortisol and blood
glucose – are all interlocking and mutually enhancing. And not only does
cortisol cannibalise precious body protein to make blood sugar, it also weakens
the immune system and damages hippocampal neurons – the very one’s lost in
Alzheimer’s disease. (7)
Cortisol also contributes mightily to obesity. “Adrenal corticosteroids
also play a role in the development of hypothalamic obesity, gold thioglucose
obesity, and dietary obesity. Thus, the substrate for essentially all
forms of obesity rests on a foundation of glucocorticoid [i.e. cortisol]
secretion from the adrenal gland” (4).
Cortisol will also be secreted to raise blood sugar in those who frequently
skip meals, are fasting, practice “starvation dieting”, or are under severe
stress.
INSULIN, cAMP, & EFFECTIVE HORMONAL COMMUNICATION
Most hormones deliver their “message” by interacting with specific receptors
on outer cell membrane surfaces, although some do penetrate directly into the
cell as well. When hormones bind to their appropriate cellular receptors, they
normally activate substances inside the cell known as “second messengers” (the
hormone [Ed.- hormone is Latin meaning chemical-messenger] is the first
“messenger”). These second messengers actually induce the hormonal biological
effect inside the cell. Insulin acts through the second messengers inositol
triphosphate (IP3) and diacylglycerol (DAG).
Perhaps the commonest second messenger, however, is cyclic AMP (cAMP). “Many
hormones do appear to utilize cAMP as a second messenger, including calcitonin,
chorionic gonadotrophin, corticotrophin, epinephrine [adrenalin],
follicle-stimulating hormone [FSH], glucagon, luteinizing hormone [LH],
lipotrophin, melanocyte-stimulating hormone [MSH], norepinephrine
[noradrenaline], parathyroid hormone, thyroid-stimulating hormone [TSH], and
vasopressin.” (9)
Thus, not only are insulin and glucagon opposite in their basic physiologic
actions, they were opposing second messengers: IP3/DAG vs. cAMP. Sears points
out that “…if a cell has multiple hormone receptors, then the final biological
response of the cell depends on which second messenger system (cAMP or IP3/DAG)
predominates at that point in time.” (7) When hormones such as noradrenaline or
glucagon bind to their cell membrane receptors, they activate an enzyme called
“adenylate cyclase.” This enzyme then produces the cAMP second messenger inside
the cell.
Unfortunately insulin opposes cyclic AMP production by adenylate cyclase. (9)
Now you can begin to see why Sears considers excessive insulin as the basic
pillar of aging. Insulin is one of the few hormones (cortisol being the other
major one) which increases with age – most others, such as thyroid, DHEA,
testosterone, estrogen, growth hormone, etc. decrease with age.
Now look again at the long list of hormones (and not all of them are listed)
which use cAMP as their second messenger, most of which hormones suffer
decreased secretion with aging. Since insulin generally increases with age, but
opposes cAMP, while most hormones that act through cAMP decrease with age, it is
obvious that hyperinsulinemia will tend to distort the overall “symphonic
orchestra” of hormone interactions, and thus promote “low fidelity” hormonal
communication.
Thus hyperinsulinemia will tend to damage our entire metabolism, because the
sum total of the myriad biochemical reactions in our trillions of cells is under
the control of our (ideally) tightly synchronized and integrated hormonal
“symphonic orchestra.” Imagine the sound of a symphony played by an orchestra
where one instrument (e.g. the trumpet) is highly amplified while the other
instruments are being muted in their sound volume, and you have a crude metaphor
for the metabolic dysregulation induced by excessive CHO-consumption – caused
hyperinsulinemia.
INSULIN, EICOSANOIDS & CAMP
Eicosanoids are a biologically powerful group of quasi-hormones (technically
called “autocrine hormones”) derived from a unique group of polyunsaturated
fatty acids containing 20 carbon atoms. Prostaglandins, thromboxanes,
leukotrienes, lipoxins and hydroxylated fatty acids are just some of the
subclasses of eicosanoids. Autocrine eicosanoids, unlike endocrine hormones, are
not secreted by glands, nor do they travel through the bloodstream to reach
distant target tissues. Rather they are continuously being produced, in minute
quantities, at the local cellular level, “living” and “dying” in seconds.
Eicosanoids are powerful local “biological response modifiers,” or feedback
modulators, helping to coordinate/fine-tune cellular reactions. Prostaglandins
(PG) of the one-series, derived from the fatty acid gamma-linolenic acid (GLA),
are generally considered “good PGs,” while PGs of the two-series (PG2) are
considered “bad PGs” – at least when present beyond some bare minimum necessary
levels. PG2s are derived from the fatty acid arachidonic acid (AA), which in
turn can either be made from GLA or gotten preformed from the diet. (See charts
1 & 2.)
A key property of PGs is their ability to modulate intracellular cAMP
levels. “The PGs of the E series are those most implicated in adipose tissue
regulation…. PGE1 stimulates adenylate cyclase. The resulting increase in cAMP
production ultimately leads to accelerated lipolysis…. PGE2 has an inhibitory
effect on adenylate cyclase resulting in a decrease of intracellular
cAMP.” (4) “…cyclic AMP is the same second messenger used by a great number of
endocrine hormones to translate their biological information to the appropriate
target cell. By maintaining adequate cellular levels of [PGE1], you are
guaranteed that a certain baseline level of cyclic AMP is always present in a
cell. When an additional burst of cyclic AMP is generated by the endocrine
hormone interacting with its receptor, it’s now far more likely that the overall
cyclic AMP levels in the cell will be high enough to ensure that the appropriate
biological response (i.e. better hormonal communication) is produced…. In some
ways, the levels of cyclic AMP generated by “good eicosanoids” are like a
booster signal to ensure that fewer [cAMP-using] endocrine hormones are
necessary to deliver [their] appropriate biological message…. Thus, even with
decreasing levels of endocrine hormones, hormonal communication can be
maintained….”(7)
Not only does PGE1 boost hyperinsulinemia-suppressed cAMP levels, it also
helps control insulin itself. “PGE1 has been found to play a role in insulin
secretion and glucose tolerance. The [pancreatic] beta-cell regulation of
insulin release is influenced by PGE1. PGE1 inhibits insulin secretion, perhaps
by normalizing insulin receptor sensitivity. Low levels of PGE1 have been found
in diabetics.” (4)
Considering the pivotal importance of PGE1 and PGE2 for controlling insulin
levels, cAMP levels, and for modulating the effect of the age-decreasing levels
of most cAMP-using hormones, how then can we gain greater control over our
PGE1/PGE2 levels? We can exert dietary/nutrient influence over PGE1/PGE2 at
three key points in their production pathways. The first control point involves
increasing the effectiveness of the conversion of cis-linoleic acid (a fatty
acid common to many vegetable oils) into GLA. The second control point rests
upon influencing the fate of the GLA metabolite dihomo-gamma-linolenic acid
(DGLA). DGLA can end up either as “good” PGE1 or “bad” PGE2, depending on
whether or not the conversion of DGLA to AA is successfully blocked. The third
control point comes from restricting the dietary intake of preformed AA.
Cis-linolenic acid (CLA) is the chief polyunsaturated fatty acid found in
most vegetable oils, such as sunflower, safflower, corn, soy and sesame oils.
Yet its only two known functions in the human body are to be burned for fuel
(like any fatty acid), or to serve as the substrate to produce GLA. The
conversion of CLA to GLA is catalyzed/controlled by the activity of the enzyme
delta-6-desaturase (D6D). According to the world’s premier GLA researcher, Dr.
David Horrobin, the activity of D6D can be blocked by a host of factors
(10):
1) Trans-fatty acids (common in hydrogenated oils, margarine’s and
shortenings).
2) High saturated fat
intake.
3) Cholesterol.
4) Deficiencies of zinc, pyridoxine
(vitamin B6), or magnesium.
5) Diabetes – i.e. severe insulin
deficiency.
6) Excessive alcohol
intake.
7) Aging.
8) Oncogenic viruses.
9) Chemical
carcinogens.
10) Ionising radiation.
Thus avoiding hydrogenated oil/margarine-based “food” products; eating only
low-fat meat, poultry and dairy products; minimizing alcohol intake; avoiding
chemical additive-containing processed/manufactured (i.e. junk) foods; and
taking supplements of zinc (15mg/day), vitamin B6 (10-50mg/day) and magnesium
(200-500mg/day), will tend to maximize D6D activity, at least somewhat
increasing conversion of CLA to GLA. Vitamin B6 may also aid the conversion of
GLA to DGLA for conversion to cAMP-enhancing PGE1. (10) Vitamin C and niacin
(vitamin B3) are needed to convert DGLA to PGE1 (10); so supplements of C
(300-500mg/day, minimum) and B3 (50-100mg/day) may also aid PGE1 formation.
For those who don’t wish to trust their PGE1 manufacture to “temperamental”
D6D, supplements of preformed GLA from evening primrose oil, borage oil, or
blackcurrant oil may be helpful. Barry Sears claims that over time GLA
supplements may become counter-productive, gradually increasing AA and anti-cAMP
PGE2 more than PGE1. (7) Sears doesn’t mention the need for C and B3 to aid DGLA
to PGE1 conversion – this may have affected his clinical results. My own
decades-long clinical experience has not generally shown GLA supplements to be
problematic, and there is a vast human clinical literature of successful use of
GLA in many areas of disease, including showing significant results in treating
obesity. (11)
DGLA can be converted to AA by the enzyme delta-5-desaturase – normally a
reaction better suppressed than permitted. This is the critical control point in
nutritional attempts to enhance PGE1 and reduce PGE2. And it turns out that the
primary activator of D5D is – insulin! (3,7) The primary hormonal suppressor of
D5D is glucagon, (3,7) while the fish-oil fatty acid EPA (eicosapentaenoic acid)
is also a significant inhibitor of D5D. (3,7) (I take 2-3 capsules twice daily
of the sardine oil-derived Kyolic(r)-EPA as part of my own personal anti-D5D
regimen.)
Each Kyolic(r)-EPA cap provides 280mg EPA (also 120mg DHA and garlic extract,
along with 10mg unesterified vitamin E to prevent rancidity).
The third control point in lowering excessive levels of PGE2 production
involves eliminating as much red meat fat as possible from our diets. Feed-lot
beef, pork, etc. is rich in AA; low-fat range-fed beef, poultry, etc. is low in
AA, and contains some EPA.
GROWTH HORMONE, TESTOSTERONE, ESTROGEN: THE INSULIN
CONNECTION
Growth hormone (GH) and insulin have both complementary and antagonistic
properties. GH and insulin are both anabolic – they facilitate the growth of
lean body mass – i.e. muscle, organ tissue, tendons, bones, etc. When animals
are surgically deprived of both hormones, growth ceases. Giving either GH or
insulin alone causes virtually no increase in growth, but giving them both
together restores normal growth. (8)
In other ways, these hormones are opposites: GH promotes fat burning/loss,
while insulin opposes fat burning and promotes fat gain. “Increased insulin
levels and decreased GH levels are characteristic of obesity.” (4) PGE1
suppresses insulin release while PGE1 increases pituitary GH release. (4) Aging
pituitaries may still produce adequate GH – it’s the releasing of GH that seems
to become problematic with age. Perhaps not surprisingly, GH-releasing hormone
requires adequate pituitary cAMP levels to perform its GH-releasing “magic.” (7)
Also, a factor that can decrease pituitary GH-production is elevated insulin,
which may inhibit GH synthesis. (7) Thus lowering insulin through a low-CHO diet
combined with GLA/EPA supplements to enhance PGE1/cAMP levels is a natural way
to restore age-declining GH function.
While GH can stimulate fat-burning by itself, it helps to build muscle mass
when combined with its normal synergist – testosterone. (7) In both men and
women, testosterone is produced through the combined action of
pituitary-released follicle-stimulating hormone (FSH) and luteinizing hormone
(LH), acting on the ovaries in women and Leydig cells of the testes in men.
Yet both FSH and LH act through the second messenger cAMP. (9) Thus
obesity/high CHO diet-elevated insulin will tend to inhibit the
testosterone-producing activity of FSH/LH.
The problem doesn’t end there, however. In both men and women, testosterone
may be converted to estrogen through an aromatase enzyme. And the aromatase
enzyme exists and functions primarily in body fat! Furthermore, estrogen is
itself a powerful pro-fat hormone: “In addition to deposition of fat in the
breasts and subcutaneous tissues, estrogens cause the deposition of fat in the
buttocks and thighs….” (8) Indeed, insulin, estrogen and cortisol are the
three primary pro-fat hormones of the human body.
Another threat to normal male testosterone levels is severe, chronic stress.
Both testosterone and cortisol are made from the precursor protohormone
pregnenolone. Normal daily male testosterone production is 5mg, while 10-20mg of
cortisol is produced daily under non-stressed life conditions. (7) The amount of
cortisol produced under stress may double, perhaps “stealing” scarce
pregnenolone needed for (decreasing with age) testosterone production. As noted
earlier, cortisol is extremely pro-fat, and is the chief agent of muscle
catabolism (breakdown), directly opposing testosterone’s anabolic
muscle-building action.
THE INSULIN – EXERCISE CONNECTION
The late twentieth century Western world has achieved the most sedentary
lifestyle for the mass of humanity in all human history. Our sedentary modern
world also provides a glutton’s feast of cheap sugar-and starch-rich breads,
chips, pastas, cakes, cookies, candy, etc. so abundantly available that even
those on welfare can afford to feast on these hyperinsulinemia-promoting
carbo-riches. It is perhaps no coincidence that in order to rapidly (and
cheaply) fatten cattle and hogs before slaughter, they are confined in crowded
feed-lots where the animals have virtually no room to move, while being fed all
the CHO-rich grain they can eat.
Modern obese humans routinely suffer from the unique twentieth century
“disease” – hypokinesis – i.e. too little bodily movement. The late twentieth
century Western epidemic of obesity is as much due to widespread chronic
hypokinesis, as it is to the CHO/caloric excess typical of modern humans. Thus
Thompson and colleagues note: “Body fat is significantly affected by a program
of prescribed exercise in both sexes at all age levels…. Exercise has been
shown to produce body fat loss without caloric restriction in both animals…
and humans…, although the loss is usually more pronounced with caloric
restriction.
In fact, reductions in activity level are strongly correlated with body fat
increases, even if caloric intake is significantly reduced…. In addition,
exercise decreases storage fat rather than LBM [lean body mass], whereas dietary
interventions [i.e. dieting[ tend to reduce both [body fat and LBM].” (12)
Studies done in the 1970’s with both men and women found that significant
body fat loss could be produced simply through a regular (i.e. at least four
days/week) long-term walking program, without any dieting. (13,14) “Vigorous
regular walking has resulted in reduced body fat stores, reduced… insulin
requirements (a 36% decrease in the ratio of insulin/glucose concentration
occurred), and [spontaneously] reduced food intake.” (4) A key feature of
the essentiality of moderate aerobic exercise, i.e. walking (the primary
“natural” form of “exercise” engaged in of necessity by virtually all of
humanity prior to the twentieth century) to preventing/reducing obesity is that
“exercise increases insulin sensitivity and decreases insulin resistance)….”
(15)
The reason for this is quite simple. Actively exercising muscles may take in
up to 30 times more blood sugar than they do when at rest, and this cellular
uptake of glucose occurs without insulin! (7,8) Thus walking provides the body
with an alternative method to remove excess glucose from the bloodstream without
the usual need for insulin secretion. Taking a brisk long walk 30-60 minutes
after a large meal may help blunt the otherwise inevitable massive insulin surge
large (CHO-rich) meals normally induce.
THE ANTI-INSULIN PROGRAM
1) Seriously reduce (better yet, eliminate) from the diet all processed,
refined, junk food, high sugar (sucrose, fructose, glucose), high white flour
“foods”: bread, pasts, cake, pie, candy, ice cream, crackers, cereal,
corn/potato chips, snack bars, waffles/pancakes, soft drinks, doughnuts, sweet
syrups, ad infinitum.
2) Minimize intake of salt, especially salty
CHO-foods: pretzels, chips, crackers, etc. “Salt increases plasma glucose and
insulin response to starchy foods.” (4)
3) Increase glucagon –
stimulating with lean protein: low-fat (ideally range-fed, organic) beef, lamb,
chicken. turkey, fish etc.
4) Reduce CHO-intake from the typical
American/British levels of 250-400 grams/day to 75-150 grams/day. These
carbohydrates should be mainly vegetables, with small amounts of brown rice,
millet, beans, almonds, pumpkin seeds and other unrefined, high-fibre natural
foods.
5) Take 40-60 minute brisk walks, 4-6 days/week. Avoid walking in
highly polluted areas and/or times of day, as toxins from auto exhaust may
inhibit mitochondrial burning of fuel (i.e. fat) for energy.
6) Take
various supplements discussed in this article – e.g. C, B6, B3, Zinc, Magnesium,
GLA, EPA, etc.
ADDITIONAL NUTRITIONAL/PHARMACOLOGIC AIDS TO FAT LOSS/INSULIN
REDUCTION
1) Chromium Picolinate. This form of chromium is well absorbed, and has
been shown in various animal and human studies to aid in fat loss while at least
modestly enhancing lean body mass. (16) “The ability of chromium picolinate to
enhance insulin responsiveness has been demonstrated in rat myoblast cell
cultures. 72-h pre-incubation with chromium picolinate (50ng Cr/ml)
resulted in a 60% increase in insulin binding, and markedly enhanced glucose and
leucine uptake….” (16) Dosage: 200mcg Chromium (as picolinate) two or three
times daily for women; 200mcg three times daily or 400mcg twice daily for
men.
2) Obesity, aging, chronic dieting, genetics, lack of exercise and
lack of cold exposure may all lead to “subclinical” hypothyroidism, often
involving deficient conversion of less active T4 to T3. T3 decreases the
activity of D5D, reducing pro-insulin PGE2, just as do glucagon and EPA. (7) T3
also stimulates fat burning. (4) Ideally one should use T3 (Cytomel) only under
a physician’s care and guidance, but those who fit the low-thyroid profile and
suffer from chronic obesity and fatigue, and who are willing to take practical,
moral and legal responsibility for their own actions, may wish to experiment
with modest doses of T3 – i.e., 2-3 mcg once or twice daily, taken morning
and/or early afternoon. T3 is fast/short-acting, and most effects will be gone
within 24 hours or less. Nonetheless, there is some risk here – caveat emptor!
Heart palpitations, excessive sweating, racing thoughts, headaches,
irritability, and insomnia are all hints – it’s not for you! Those with known or
suspected (past or present) hyperthyroidism, even if obese, should not use T3
without a doctor’s care. Similarly those with any other serious disease states –
especially heart arrhythmia’s/heart disease – should be extremely cautious in T3
use.
3) Anti-cortisol states. Since cortisol levels tend to increase
with age (and stress), and since cortisol promotes both obesity and insulin
resistance, this is a key strategy to normalize weight/insulin levels. DHEA, (7)
and high dose vitamin C (17) may all help lower elevated cortisol levels. DHEA:
10-50mg A.M. Gerovital-H3: 100mg A.M. Dilantin (Phenytoin) 25-50mg at bedtime.
Vitamin C: 500-1000mg 3-4 times
daily.
4) L-Tryptophan/5-Hydroxytryptophan (Oxitriptan). Several human
studies with 5HTP, the precursor of serotonin, have found good weight loss
results with 5HTP. (18,19) There is evidence that some humans compulsively
snack on CHO foods to feel better. The large insulin releases generated by such
“carbo-bingeing” preferentially increase tryptophan/serotonin in the brain,
temporarily reducing anxiety and depression in such people. (20) By providing an
alternative, non-insulin-driven way to increase brain serotonin, L-Tryptophan,
supplements may help reduce weight not only by reducing total caloric intake,
but especially by reducing CHO intake, thus lessening hyper-insulinemia/insulin
resistance. In the 1992 Italian study (19), 300mg/5HTP supplements may help
reduce weight not only by reducing total caloric intake, but especially by
reducing CHO intake, thus lessening hyperinsulinemia/insulin resistance. In the
1992 Italian study, (19) 300mg 5HTP 3 times daily before meals reduced women’s
caloric intake over a twelve week period from 3232 cal/day to 1273 cal/day,
while reducing CHO intake from 350gm/day to 150gm/day. Weight dropped an average
of eleven pounds. (The study did use special enteric-coated 5HTP capsules to
prevent gut irritation) Ed [IAS provides same Italian 5HTP]. Taking 1000-1500mg
L-Tryptophan at bedtime, or 50-100mg 5HTP before meals may reduce CHO-craving
and intake.
5) Pro-GH supplements. As noted earlier, PGE1 may enhance GH
release. so all the PGE1-enhancing nutrients (GLA, EPA, B3, B6, C, zinc,
magnesium) may be helpful here. Hydergine has been shown to increase GH-release
in the elderly with long-term usage at 1.5mg every 6 hours. (21) The authors of
this study also note that bromocryptine (Parlodel) may also enhance adult
GH-release. They also note that the enhanced pituitary GH-release from hydergine
seems to be related to an increase in brain (hypothalamic) dopamine status,
which normally declines (often precipitously) with age. Thus the
dopamine-enhancing agent Deprenyl may also be useful as part of a GH-restoration
program.
6) Mitochondrial energizers and protectants. In a healthy
human, storage fat is at a minimum and sooner or later all fat-dietary,
body-manufactured, and storage fat – ends up as “fuel for the furnace” – i.e.
the trillions of mitochondrial “power plants ” found in most of our cells.
Vitamins B1, B2, B3, B5 (pantothenic acid), and biotin, as well as NADH,
alpha-lipoic acid, CoQ10/Idebenone, magnesium and manganese are all necessary
“spark plugs” to facilitate burning fat and sugar for energy. 10-100mg B1, B2,
B3, 50-200mg B5, 1-10mg biotin, 5-20mg NADH, 50-300mg alpha-lipoic acid,
60-300mg CoQ10 and/or 45-135mg Idebenone, 200-500mg magnesium, and 3-10mg
managanese may optimize mitochondrial energy cycles. Since the mitochondrial
structures inevitably generate massive amounts of free radicals in turning fuel
into energy, and since these structures are rich in easily rancidified
polyunsaturated fatty acids, a panoply of antioxidants – e.g. 100-400 IU vitamin
E, 500-2000mg vitamin C, 100-200mcg selenium, 50-300mg alpha-lipoic acid,
500-1000mg N-acetylcysteine, 2mg copper as copper sebacate (SOD-mimetic),
50-100mg grape seed extract/pycnogenol, 300-500mg silymarin – may help protect
the essential “fat burning furnaces.” In addition, 1gm L-carnitine twice daily
on an empty stomach may facilitate fat burning – carnitine is the “shuttle
molecule” that “escorts” fatty acids into mitochondria where they are then
oxidized. (22) ALC (acetyl-L-carnitine) may also be a useful mitochondrial
regenerator – mitochondria become progressively deformed and dysfunctional with
aging. Dosage: 1-3gms/day. Ward Dean suggests this dose can be half L-carnitine
and half ALC to achieve successful mitochondrial regeneration.
(23)
7) Caffeine. Caffeine, whether from coffee or as a “drug”, has many
benefits for aiding fat loss. However, excessive doses (probably 300mg/day and
up, on average) may pose risks of “caffeinism”, with such symptoms as headaches,
restlessness, irritability, insomnia, anxiety, excessive urination, gut
irritation, heart palpitations, and muscle tremors. (15) A thermogenic/fat
burning dose is probably 100-200mg daily – i.e. the equivalent of one to two
cups of coffee/day, or two to four cups made with half decaf and half regular.
Caffeine taken with a meal may induce increased thermogenesis – burning fat to
make heat. (15) It may increase resting metabolic rate – our resting metabolism
burns 60-70% of our total daily energy consumption. (15) Caffeine
preadministration 45-60 minutes before exercise has been shown to spare
liver/muscle glycogen and to enhance fatty acid burning in humans. (24) Caffeine
taken after at least an eight hour fast, i.e. in the morning after arising, may
be especially effective when combined with a 40-60 minute brisk walk, to enhance
burning of stored body fat. (24)
NOTE
This review of anti-aging weight loss has of course only scratched the
surface of this amazingly complex and multi-pronged issue. Nonetheless, it is my
deeply-held belief, derived from clinical and personal experience combined with
a 30 year continuous reading of the medical/scientific literature, that the
combination of hypokinesis, excessive CHO consumption (especially of the sugar
and white flour junk food variety), hyperinsulinemia/insulin resistance,
excessive PGE2/inadequate PGE1 and hypo-cAMP status, is the core of the modern
epidemic of refractory, chronic obesity. The interested reader is strongly urged
to read references 1, 3, 7, and 15 for a much more detailed coverage of these
and other related issues.
Copyright 2003. This article may not be reproduced for public
broadcast in any form, without the written permission of: International Antiaging Systems
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