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 cannibalize 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 counterproductive, 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
