Blended excerpts from Potential Within A Guide to Nutritional Empowerment
Authored by Franco Cavaleri ISBN 0-9731701-0-7
This article is composed of multiple excerpts to result in tone and content shifts and reference numbering that may be out of order.
Herbs like coleus forskohlii and ginseng can only elicit long-term benefits if a functional nutritional foundation is in place. Our cells can’t perform without adequate calcium, and so our bodies will always fulfill this primary requirement to keep us alive even at the expense of bone mass.
Caffeine has an effect similar to coleus in that the former blocks an enzyme called phosphodiesterase. Phosphodiesterase enzymes
have various functions in the cells, one of which is to “chomp” on cAMP, reducing the “excited” status of the cell. Caffeine interferes with phosphodiesterase activity and raises the cellular response rate and intensity to signals (20).
With higher cAMP levels, cells respond more quickly to hormone and other signals characterized by the hypersensitization caffeine promotes. Calcium is vital to this process, which means chronic caffeine use or abuse can result in the depletion of this valuable mineral.
Colon cancer, too, is associated with inadequate dietary calcium (21, 22). Excess dietary sodium, poor dietary protein quality, and abundant caffeine consumption can inhibit calcium absorption and status and indirectly magnify the risk of cancer. Supplementation with calcium will thwart this danger as will the elimination of the factors inhibiting positive calcium status in the body.
Caffeine has a compounding negative influence on biological calcium status. It promotes urinary excretion of calcium and induces its expulsion from the intestinal tract, resulting in fecal loss of the mineral. Moderate alcohol consumption further exacerbates poor calcium status as well as magnesium excretion (23). An individual consuming alcohol and caffeine abundantly, relying on the typical processed, mineral-stripped, sodium-enriched diet, is at tremendous risk for calcium deficiency and its associated physical fallout. Again, osteoporosis is only one of the clinical risks. The underlying mess that occurs concurrently festers until other metabolic disasters are developed.
Earlier we saw that prostaglandin from the Type 2 series of autocrine hormones (PGE2 from arachidonic acid) inhibits the activation of thermogenic brown fat cells, the cells that help us burn away excess dietary and body fat (8, 9). When our natural hormone chemistry tries to activate thermogenesis in response to a fat load in the blood from a meal, PGE2 gets in the way and blocks activation. This, in fact, is where ASA in the common ECA stack (Ephedrine, Caffeine, Aspirin formula) works its thermogenic potential. Ephedrine has a noradrenergic effect on the neuron that controls or communicates with the fat-burning brown fat cell. This noradrenergic activity is the ability to induce secretions of noradrenalin, or norepinephrine, from the neuron. In essence, noradrenalin/norepinephrine contact on the brown fat cell membrane receptor is the signal that actually turns the brown fat cell on, stimulating thermogenic activity and triggering the natural fat furnaces.
When fat accumulates in the blood, this very system is set off naturally—noradrenalin is secreted, activating the brown fat cell that chomps on fat and rids the body of excess calories from the meal as heat. PGE2, the hormone most of us overproduce due to our North American lifestyles, blocks the neurotransmitter, noradrenalin, from contacting the brown fat cell. It competes with noradrenalin, and the brown fat cell never gets the signal to turn on the furnace. ASA simply impedes PGE2 production to allow ephedrine (an active factor in the herb ephedra) to stimulate the brown fat cell on the surface through that norepinephrine secretion (9). Today ephedrine has been replaced in this common combination with a safer noradrenergic herb, citrus aurantium (CA). Caffeine supports the stimulation by blocking other inhibitive enzymes (phosphodiesterase) and promoting noradrenalin/norepinephrine activity inside the cell (10, 11, 12).
The multiple blocks in this system are why ephedrine doesn’t work well on its own as aweight-loss agent. Caffeine must be made available to obstruct the phosphodiesterase enzyme. Then again the system is further enhanced by the addition of ASA, which blocks more than just PGE2.
Recent interviews of centenarians revealed that each one consumed coffee starting at a young age. Scientific data, on the other hand, has linked the overindulgence of coffee to endocrine disturbances, primarily those associated with impaired androgen activity in men. In these studies it was shown that avid coffee consumption could actually affect sperm count and testosterone secretion. More recent studies demonstrate, however, that sperm count isn’t affected but sperm quality is. Motility of sperm might be enhanced by caffeine, but the sperm’s ability to fertilize is reduced (47, 48).
Lower testosterone levels in men and higher estrogen potential in women are also somehow coffee-related (49). Increased sex-hormonebinding globulin (SHBG) levels and associated higher risks of breast cancer, endometriosis, and fibrocystic breast disease in female coffee drinkers have been identified in these studies. Higher SHBG levels, as we’ve seen, are connected to elevated estrogen activity in the body. Studies indicate increased cortisol production with coffee consumption, which might nominally reduce testosterone production (50). However, very little research points to significantly compromised testosterone levels due to coffee consumption.
There might be an explanation for the hormone and sperm anomalies that has little to do with caffeine.
The University of Guelph in Ontario recently released new findings on coffee. This novel research identifies coffee as a contributor to the high rate of insulin resistance plaguing society. The study revealed that two cups of coffee consumed after a high-glycemic-index meal can induce insulin resistance to prolong the clearance of blood sugar (51). If these findings prove conclusive, the ill effects of coffee might include significant heightening of oxidative stress, promotion of insulin resistance, interference of hormone synthesis, and an increased risk of most of our epidemic diseases.
But what explains the apparent resistance of those coffee-indulgent centenarians to these new coffee-related disorders? Once again, as we’ll see, the explanation can be found in how we grow our food and how we treat our environment today in comparison to what these centenarians experienced when they were younger. The cultivation of coffee and cocoa beans takes place primarily in countries where spraying with toxic pesticides is poorly, if at all, regulated.
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