PPA has a long history of relative safety. Few adverse effects are reported about this chemical, despite an estimated 16 billion doses taken annually. Yet, if you look at how PPA works, the danger potential is clearly evident. PPA directly stimulates alpha-adrenergic receptors, as well as the beta-adrenergic receptors linked to the thermogenic effect. The stimulation of alpha-adrenergic receptors promotes vasoconstriction, or a tightening of blood vessels in the respiratory lining, which in turn results in a shrinkage of swollen tissue. This explains its use in nasal decongestants. Unfortunately, this blood vessel constriction effect isn’t just limited to the respiratory area, but affects the entire body.
As such, it’s possible that the increased blood vessel “tightness” induced by PPA or norephedrine may increase blood pressure. The increased blood pressure, in turn, can increase the risk of strokes and heart attacks. To be fair, such untoward effects of PPA are rare. Most often they occur only when too large a dose is used, or if it is taken too often. Still, most doctors suggest that people with pre-existing heart disease, diabetes, or high blood pressure avoid using either PPA or ephedrine.
What about people free of any evidence of cardiovascular disease? Is using PPA safe for this population? The existing medical literature shows that it is safe, but as the adage says “Only the dose determines the poison.” This is evident in a recently published medical report about a 34-year-old woman who increased the dose of a PPA-based nasal decongestant. The particular formula that she used contained 75 milligrams of PPA with 400 milligrams of guifenesin (an ingredient used to thin mucus secretions, often also found in ephedrine formulations). She had no prior history of any type of cardiovascular problems, didn’t smoke or use any drugs, and had no signs of high blood pressure, elevated blood cholesterol levels, or diabetes.
The prescribed dose of the nasal decongestant she used was one tablet every 12 hours. However, this woman reasoned that taking the drug more often would likely maximize symptom relief, so she took another dose just 2 hours after ingesting the initial dose. Her unexpected symptoms began 30 minutes after the second dose. She felt a squeezing pain radiating across her chest and down both arms, along with excessive sweating, heart palpitations, light-headedness, and shortness of breath. These are all classic symptoms of a myocardial infarction or heart attack.
While this woman’s normal systolic blood pressure reading was 100, it now shot up to 198! Her heart rate, recorded as soon as she showed up at a local emergency room, was 52 beats a minute. Blood tests for various drugs, such as cocaine and amphetamines (both of which are capable of causing similar effects) was negative. She was given an aspirin tablet and transdermal nitroglycerin paste. The aspirin may prevent heart muscle damage if provided as soon as symptoms become apparent, while the nitroglycerin dilates coronary arteries, also helping to prevent excessive heart damage.
This treatment worked, since she was free of her previous frightening symptoms in 30 minutes. Her blood pressure also was normal within an hour. Blood chemistry tests revealed that she had suffered a small heart attack, what physicians call a “microinfarct.” She was discharged from the hospital 2 days later. Tests done 15 months later showed no recurring cardiac symptoms or disease.
As noted, side effects from PPA are rare, but when they do occur they usually are caused by a rapid increase in blood pressure. In the heart, however, PPA overdose leads to a potent blood vessel constriction effect that may deprive the heart of blood--which is precisely what occurs during a typical heart attack. While catecholamines, such as epinephrine, are also capable of constricting coronary arteries, the usual medical treatment for that effect, beta-blocking drugs, is dangerous for those who’ve taken an overdose of PPA. The proper treatment involves giving specific alpha-adrenergic blocking drugs, such as phentolamine. This type of treatment, however, should only be administered by a qualified medical professional.
The point of all this isn’t that PPA or norephedrine is inherently toxic or dangerous to normal people free of cardiovascular disease, but as illustrated by the case described here, could be highly dangerous if abused. If you opt to use any supplement containing PPA for fat-loss purposes, heed the dosing instructions, and don’t be tempted to increase the dose for faster results. Don’t be fooled into thinking that just because something is available without a prescription means that it’s innocuous.
Growth hormone and testosterone
Looking at competitive bodybuilders today compared to 20 years, it’s apparent that today’s competitors appear to have a lot more muscle than their earlier counterparts. Some ascribe these noticeable size and muscularity differences to improved dietary techniques and training equipment. Others just write it off to more athletes with better genetics. While all of these factors do play a role in the appearance of current top professional bodybuilders, jaded skeptics often point to newer combinations of anabolic drugs.
Perhaps the foremost combination of anabolic drugs to explain the rash of monstrous physiques that rule the posing platforms of today is that of testosterone, growth hormone, and insulin. The interesting thing about this particular combination is their synergistic effect. None of them alone provides the massive anabolic boost that many seek, yet when they are combined, the effect is dramatic for some people. The flip side of this incredible muscle size increase is side effects, some of which are more apparent than others.
For example, many competitors show bloated midsections. This is not from any accumulation of visceral fat deep in the gut (the usual cause of “beer bellies”), but may result from a combination of internal organ growth and increased thickness of the abdominal wall. The net effect is an abdominal area that protrudes like a pot belly at rest, yet transforms into a sculpted “six pack” when flexed. The suggested cause of this abdominal anomaly is thought to be the same anabolic combination of drugs; that is, growth hormone, testosterone, and insulin. My feeling is that the main offenders are growth hormone and insulin.
The active product of growth hormone is insulinlike growth factor-1 (IGF-1). The name derives from the structural similarity between IGF-1 and proinsulin, which is a storage form of insulin. The point here is that both insulin and IGF-1 are capable of interacting to a certain extent with their respective cellular receptors. These receptors induce cellular growth changes, and are located in abundance in the gastrointestinal area of the body. Thus, under the stimulation of exogenous insulin and growth hormone (by way of IGF-1), these hormones induce the growth of internal organs--hence the bloated abdominal appearance.
One question often asked concerns the relationship between growth hormone (GH) and testosterone. This is relevant because hormones tend to have interactions, and lowering one type of hormone may increase the release of another and vice-versa. For example, GH is known to blunt levels of cortisol in the body. GH does this by inhibiting cortisol production, most likely at the level of the adrenal glands. This would have an anticatabolic effect, since cortisol is the chief catabolic hormone in humans. On the other hand, cortisol is also a steroid hormone, albeit a catabolic one. If GH blocks cortisol synthesis, could it also adversely affect testosterone production?
Testosterone, similarly to cortisol is also a steroid, although an anabolic steroid. The same researchers who established the cortisol-blocking effects of GH tested the effects of GH on testosterone synthesis. This study involved 7 healthy men, ages 23-34 who were injected with 4 units daily of GH for a week. The test results showed that GH has no effect on testosterone production rates, either good or bad.
But how does testosterone affect GH release? This effect was examined in a study of the both testosterone and its byproduct, dihydrotestosterone (DHT) in a group of 12 boys with apparent GH deficiency. The study showed that giving the boys testosterone injections for 3 months increased GH secretion from the pituitary gland, while DHT did not. The explanation for this is that testosterone is converted into estrogen by way of the enzyme aromatase, and estrogen promotes the release of growth hormone-releasing hormone in the brain. DHT, because it cannot be converted into estrogen, has no effect on GH release.
One lesson to be learned from this study is that any drugs that inhibit the conversion of testosterone into estrogen will also blunt GH release in the body. This is, of course, a moot point if you’re already using exogenous growth hormone. Many athletes will prefer this route of taking direct GH injections and will use another drug to block testosterone conversion into estrogen. The latter effect produces side effects such as gynecomastia or excessive male breast tissue. Judging by the apparent preponderance of gyno seen in many competitors today, the estrogen-blocking drugs aren’t potent enough to completely block the aromatization process.
What about taking GH alone, without other anabolic drugs--will this promote increased muscle size and strength? A recent review of past studies involving the use of GH for anabolic effects in healthy athletes examined this subject. The study noted that in animals, providing GH increases muscle size, but not strength. The same holds true for people with acromegaly, a disease characterized by excess GH release caused by a tumor on the anterior pituitary gland of the brain. Such people often show large, but weak muscles. In one case, the man still listed in the Guinness Book of World Records as being the tallest man ever, 8-foot-11 inch Robert Wadlow, suffered from myopathy or weakness of his legs to such an extent that he had to wear leg braces. He eventually acquired an infection from those braces that killed him at age 23.
Studies with athletes who’ve used only GH show that these people do not seem to get any stronger or bigger than they would from weight-training alone. Any fat-free mass that does result from using GH usually turns out to be either an increase in connective tissue or fluid retention. While both insulin and testosterone favor the incorporation of amino acids into muscle (promoting muscle protein synthesis), GH does not. Nor does GH alone show any anticatabolic effects in muscle, despite the fact that it does inhibit cortisol synthesis. The muscle contractile proteins, actin and myosin, aren’t affected by GH administration. This is significant because an increase in contractile muscle proteins produces strength increases.
On the other hand, testosterone inhibits bodyfat synthesis by blocking the activity of a fat-synthesizing hormone called lipoprotein lipase. This effect is dramatically increased when GH is combined with testosterone. Thus, in this respect, GH is clearly synergistic with testosterone in blunting bodyfat accretion. Evidence shows that these hormones also boost each other’s activity in an anabolic sense. Add it all up and you have massive muscularity--and often, bloated bellies.
For more information see www.appliedmetabolics.com
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
