Sugar Ray Robinson held the middleweight title of the world five times and won the welterweight title once. Considered by most boxing experts the best pound-for-pound fighter ever, Robinson was untouchable in his younger days. His punches came fast and hard, and by the time his opponent realized what hit him, Sugar Ray had danced away, often leaving his opponent lying on his back.
Financial pressures, however, made Sugar Ray stay in the ring too long. He was still fighting at 40 and began to lose to men who wouldn’t have lasted three rounds with him in his younger days. Ray took a lot of punches in those last fights, and the resulting head trauma may have contributed to the severe case of Alzheimer’s disease that eventually caused his death.
A more recent example of the effect boxing can have on the brain is Muhammad Ali, who may be the greatest heavyweight champion ever and who was voted second to Robinson in an Associated Press poll of the greatest boxers of the 20th century. Ali doesn’t have Alzheimer’s, but it’s clear from his slurred speech and slow gait that the once lightning-fast fighter is suffering. In his case it’s Parkinson’s; the brain cells that produce the neurotransmitter dopamine have been severely damaged.
Ali was born with an abnormally small substantia nigra, the area of the brain where dopamine is produced, and that area seems to have been selectively damaged by blows to the head. Of course, Ali didn’t realize that, and it certainly didn’t affect his earlier boxing skills. Like Robinson, however, Ali fought past his prime and consequently took many head punches that would never have landed in his younger days.
Traumatic brain injury (TBI) can lead to severe damage to the pituitary gland. Located just behind the nose in the brain, the gland produces many vital hormones, including growth hormone, thyroid-stimulating hormone and gonadotropins such as luteinizing hormone, which controls testosterone synthesis.
Statistics show that more than 1.5 million Americans have suffered some form of TBI. Often it’s the result of head trauma, as from a violent car accident, but anything that violently hits the head can lead to TBI. About 40 percent of patients with moderate or severe head injury show damage to the pituitary gland. The hormones most affected by TBI are growth hormone and gonadotropins, the two primary anabolic hormones in the pituitary.
In some cases the damage is caused by direct injury to the pituitary gland. Or the damage may ensue from vascular injury, which limits blood flow to the gland, leading to the death of cells. A common cause of TBI is a concussion, an injury to the brain that often involves a temporary loss of consciousness and that has occurred in 40 percent of people diagnosed with TBI. The injury is common in contact sports, such as boxing, football and ice hockey. In fact, a boxer’s primary objective is to induce a concussion, which usually means knocking out the opponent.
No boxer walks away from the sport without suffering some form of brain injury. While a series of knockouts results in the greatest degree of brain damage, even being hit in the head repeatedly causes a shearing effect in the brain—because brain tissue is thrust violently against the skull—leading to an actual loss of brain cells. The cumulative effect can be devastating and may take years to show up. Early symptoms include slurred speech and slowed movement.
The worst aftermath of being hit in the head repeatedly, as in boxing, is a type of dementia that looks like Alzheimer’s disease: pugilistica dementia. Jerry Quarry, a great heavyweight of the ’70s who fought Ali, died from it, as have countless other fighters.
All fighters know the risk of brain damage, and most try to end their ring careers before they lose their marbles. But a lesser known consequence of years spent in the ring has recently been recognized. Since boxing is a definite risk activity for the development of TBI and since TBI is known to lead to damage in the pituitary gland, researchers tested 11 recently retired or still competing boxers to check their growth hormone levels.1
None of the boxers could be considered bums, since all were current or former world champions. Their average age was 38, with an age range of 18 to 55. None reported any serious illness, and none were taking any type of medication. But seven of the fighters complained of memory impairment, while another four complained about fatigue. None showed any symptoms that would suggest pituitary gland problems, such as a tendency to sleep, cold intolerance, low blood pressure, low blood glucose levels, reduced body hair, decreased sex drive, excessive urination and thirst.
Even so, 45.4 percent of the subjects had a growth hormone deficiency—rare in men that young. In another 36.4 percent the status of their growth hormone release was uncertain. Based on that finding, the authors suggest that GH deficiency is probably a common occurrence in boxers at all levels and occurs at a significantly younger age than it normally does.
Many readers are probably thinking that while this information is interesting (or maybe not), it doesn’t apply to them since they aren’t boxers. But consider the fact that any type of concussion, which always involves some brain injury, can damage the pituitary gland and result in a permanent loss of GH release. That could happen to an 18-year-old engaged in some form of martial arts, where head trauma results in a knockout. Or a car accident in which you get knocked out. That can injure the brain enough to cause pituitary trauma, either as a result of direct injury to the gland or through damage to the blood vessels that serve it.
Another aspect to consider is that the product of growth hormone, insulinlike growth hormone 1 (IGF-1), is known to be vital for the maintenance of neurons, the functioning cells of the brain. Recent studies show that GH itself exerts a protective effect on brain cells. A lack of adequate GH may promote brain degeneration.
Restoring Growth Hormone:
A New Method?
Growth hormone and IGF-1, which is stimulated by GH, drop about 14 percent with each decade of life. By age 60 many people are deficient in GH, a condition that’s called “somatopause.” Changes in the body that occur with a GH deficiency are typical of the physical decline associated with aging. They include a reduction in skeletal muscle mass and strength; increased bodyfat, especially in the abdominal area; an increase in low-density-lipoprotein cholesterol, which is the type most linked to cardiovascular disease; impaired blood clotting, which also predisposes them to heart attacks and strokes; increased blood pressure; reduced heart power; lowered immune response; and lower bone mass.
A lack of GH and IGF-1 is also associated with mental decline, including the loss of memory common with age. IGF-1 is involved in maintaining energy processes in the brain, the formation of new neurons, nerve stimulation reactions and other vital brain functions. Without GH and IGF-1 a toxic metabolite of the essential amino acid methionine, homocysteine, increases in the brain, resulting in further degenerative changes.
Knowledge that those adverse effects are linked to a deficiency of GH and IGF-1 has led to the concept of GH therapy. As a peptide hormone, GH must be injected. Another possible alternative treatment features the use of growth hormone secretagogues. When GH-replacement therapies are provided to people deficient in the hormone, the effects of GH deficiency diminish.
Providing GH therapy presents some formidable problems, however, starting with its high cost—potentially thousands of dollars. Since it’s not an officially accepted form of therapy, it isn’t covered by medical insurance. Side effects are also common, most often with higher-than-normal physiological replacement dosages: edema, or water retention, muscle pain and carpal tunnel syndrome, which pinches nerves in the wrists and hands. In addition, the long-term life-extension effects of GH remain speculative at best. Some scientists even suggest that long-term use of GH may shorten life span, though the evidence for that is sparse.
The reason GH declines with age has to do with the two hormones that control its release in the brain, growth-hormone-releasing hormone and somatostatin. GHRH promotes GH release, while somatostatin blocks it. With age somatostatin becomes dominant. The pituitary gland still continues to synthesize GH and exhibits no defects unless affected by trauma. That explains why drugs such as GH secretagogues work in older people; they bypass somatostatin.
GH release is also affected by brain neurotransmitters, which are the chemicals that regulate nerve impulses in the brain. One neurotransmitter linked to GH release is acetylcholine, which is also linked to memory and learning functions. In Alzheimer’s disease, nerve cells that synthesize acetylcholine are destroyed, which results in the intellectual deficit characteristic of Alzheimer’s disease.
The present medical treatment of Alzheimer’s involves drugs that inhibit the primary enzyme that degrades acetylcholine in the brain. But since acetylcholine also promotes GH release, a group of researchers looked at whether the same drugs used to treat AD could also promote GH release.2
For eight weeks 24 older men were put on either a placebo or the drug donepezil, trade name Aricept, which is used to treat Alzheimer’s disease. They took a five-milligram dose for the first four weeks, 10 milligrams for the second.
There was a 53-percent increase in GH and a 31 percent increase in IGF-1 in the drug group. That change equals a shift to hormone levels typically seen in men 20 years younger, or about age 40. Still unclear is whether that level of GH increase would reverse some the negative effects seen with a GH deficiency. If this drug does work, it would dramatically reduce the current cost of GH therapy and also produce little or no side effects.
One point to consider is that the drug therapy would be useful only for those with a full-blown GH deficiency. For all others, using it would have little or no effect on GH release.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
