by Gary L. Taylor, Technical IT, etc.
Proanthocyanidins are also known under several other names, among the most common: OPC, pycno-genols, and leukocyanidins. Proanthocyanidin is a name for a class of bioflavaniods. In 1936, this bioflavinoid was classified and referred to as Vitamin P, although it didn't gain official vitamin category status. The common link between the bioflavaniods, of which there are about 20,000 different ones, is that they contain a benzene-pyran-phenolic acid molecular nucleus (referred to as flavin) as part of their much larger molecular structure. Proanthocyanidins have been sold as nutritional/therapeutic supplements in Europe for almost a quarter of a century. Their introduction to the United States has been relatively recent.
The discovery of proanthocyanidins can be attributed to Professor Jacques Masquelier. Dr. Masquelier spent almost a half century researching proanthocyanidin. He also invented the extraction techniques by which proanthocyanidins are obtained from plants rich in these substances.
Much of the research and documentation for the known and suspected effects/benefits of proanthocyanidins comes from many of the European research institutes and universities.
The most noted individuals involved in proanthocyanidin research are Dr. Jacques Masquelier, Dr. Morton Walker, and Dr. Richard Passwater. The institutions that have been noteworthy for this same research include: The Pasteur Institute, Horphag Research Ltd., The Huntington Institute, and the University of Bordeaux. Information contained in this article is derived from research documented by the above.
What are the natural sources rich in proanthocyanidins? Proanthocyanidins are found in high concentrations from such sources as: cranberries, grape skins, grape seeds, pine bark, lemon tree bark, and hazelnut tree leaves. The two most common and richest known sources are grape seed extract and pine bark extract. It has been indicated that grape seed extract may be a better choice because: 1) It yields a 10% higher concentration of proanthocyanidins. 2) Grape seed extract contains a specific proanthocyanidin with a higher degree of oxygen free radical scavenging potential. This proanthocyanidin is designated as Proanthocyanidine B2-3'-0-gallate.
There is little doubt as to the powerful antioxidant properties of proanthocyanidins. In vitro research has confirmed that they are 50 times more effective than vitamin E and 20 times more powerful than vitamin C. Proanthocyanidins also prevent the oxidation of vitamin C to dehydroascorbate by providing hydrogen ions which reduce glutathione - keeping the levels of the active for of vitamin C (ascorbate) higher. One aspect, relating to oxygen toxicity effects on the brain and CNS, which proanthocyanidins have, is they can penetrate the blood-brain barrier better than certain other antioxidants.
Many technical divers take aspirin to help decrease the probability of platelets adhering to capillary walls and reduce the probability of blood clotting. Proanthocyanidins have the same effects as well as protecting the platelets from free radical damage - all without some of aspirin's side effects as experienced by a few people.
Leukotriene oxidation produces powerful bronchioconstrictors. This oxidation can take place when a diver breathes oxygen at high partial pressures. This class of bronchioconstrictors are not blocked by the endogenous antihistamines of the body and could increase the risk factor of technical dives. Proanthocyanidins, by their antioxidant properties, help prevent the formation of these compounds and reduce the levels of any that are present.
Anyone who is involved with dives where high partial pressures of oxygen are encountered, should know that one of the physiological concerns is lipid peroxidation and the attending effects on the diver. Proanthocyanidins reduce the level of lipid peroxidation.
The protection from free radicals which proanthocyanidins offer helps to increase efficiency of the circulation by preventing free radical damage to the walls of the capillaries, strengthening the walls of blood vessels, maintaining healthy permeability of the blood vessel walls, and ensuring elasticity of the arteries and veins. The diver depends on a healthy circulatory system, with all the demands diving puts on it - at times extreme demands.
DOSAGE:
Although there is no official established dosage for proanthocyandidins, the research indicates that maximum benefits are indicated with daily dosages of 60 mg.CONTRAINDICATIONS:
None documented at the present time.TOXICITY:
No known toxic effects - research from the Pasteur Institute and Huntington Institute as well as others.OTHER CONFIRMED, INDICATED, OR POTENTIAL BENEFITS:
Boost immune system
Protection from arteriosclerosis
Enhance connective tissue health
Reduces lipid peroxidation
Boosts the effects of vitamin C
Lower cholesterol levels
Reduces inflammation & edema
Reduced cancer risk
Reduced risk of stroke and heart attack
Effective antioxidant for brain & nerve tissue
Possible arthritis reduction and relief
Helps prevent inflammation of lung tissues
Potential anti-aging benefits
Reduction & repair of UV damage to cells
Reduction of muscle cramps
Potential for reduction of diabetic retinopathy
*** Appears to enhance and augment the antioxidant properties of vitamins E, C, and A. I'm sure there will be much more on-going research on proanthocyanidins as the potentials they hold for health benefits appear to be great. Next article will continue with some of the lesser known antioxidants.
Until next time - Bon appetit & stay healthy!
ProPlanner is a multi stage, multi gas decompression planning aid. PROPLANNER is a professional, proven decompression management system, based on the in depth research carried out by the late professor A.A. Bühlmann and his model ZH-L16C. This proven program has been most popular amongst both recreational and technical divers on a worldwide scale for many years.
The new 2002 version is available!
ProPlanner Software is available in three upgradable versions:
- Air / Nitrox.
- Air / Nitrox / Trimix.
- Air / Nitrox / Trimix / Rebreather.
Other features include:
- Altitude diving.
- Gas mixing calculations and printouts.
- Storing and printing of decompression schedules.
- Oxygen toxicity calculations.
- Tissue loading graphs.
- Mission run time calculations.
- Metric or imperial use.
- Safety factor.
- Gas volume calculations.
- Multi level, multi dive capability.
- Mission planning and appending of new dives to a stored dive sequence.
- Easy to use on-screen graphics.
- IBM compatible.
- Any dot matrix and most laser printers supported.
Aquatronics strongly recommends that proper training is sought before any dives using the ProPlanner are undertaken.
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by Robert F. Millott, Ed.D., I#265, Milledge Murphey, Ph.D., Mary Beth Horodyski, Ph.D., and Neil Delude, Ph.D.
Scuba divers are sometimes admitted to the hyperbaric chamber complaining of symptoms of decompression illness even when accepted table guidelines were strictly followed. The determination of the cause of such a "hit" remains unanswered. Decompression illness (DCI) or "bends" occurs when the elimination of gas from the body's tissues is inadequate to parallel the rate of external pressure decrease resulting in the supersaturation of gas in the tissues. This supersaturation of the tissues may permit the gas to come out of solution in the form of bubbles (or increasing proportions of free phases grow). The bubbles are primarily formed from nitrogen (Weinke, 1991).
In many situations such bubbles are small in size and considered subclinical. If the size and concentration remain below the critical set point, the diver should remain asymptomatic. However, reports of divers suffering from DCI in situations when the disorder would normally not be displayed has led to interest in reviewing other possible causes. It has been suggested that the diver may have been dehydrated, thus leading to the agglutination of the normally sub-clinical bubble and the resultant DCI (Bennet & Elliot, 1975). Although dehydration has been found to be related to DCI, some divers will vehemently deny dehydration, (stating they took necessary precautions) regarding proper hydration.
In a recent case, a diver using the Canadian DCIEM tables sustained an episode of DCI. A review of related factors which he reported to have controlled, including rate of ascent, hydration level, repetitive dives, age, temperature, level of personal fitness and regular diving activities, failed to identify contributing factors to DCI. However, it was determined that he was under a great deal of "pressure" or stress. The question raised herein is whether physiological changes resulting from psychological stressors can be a contributing factor in DCS. The purpose of this article is to suggest that the physiological effects of stress have possible ramifications of this stress on divers.
Thus divers who suffer decompression illness may do so despite diving within the "no-decompression limits" of the tables they choose to use. "Bends" or decompression illness (DCI) as it is more properly called, is a malady attributed to bubbles of an inert gas (nitrogen) coming out of solution or exceeding some critical ratio in the body. In many situations, these bubbles are micro bubbles - too small to cause a problem - yet existent. Such bubbles may be detected with "Doppler" devices. If the size and concentration of such remain below a critical set point they will be asymptomatic. The purpose of this article is to explore one factor often overlooked in varied hypothesis which suggest what circumstance might render these bubbles problematic - that factor is the physiological consequences of stress.
Stress, first described by Selye (1947), is a state produced within an organism subject to a stimulus perceived as a stressor (threat). He further defined stress as a state brought on by a specific syndrome (General Adaptation Syndrome -GSA) inducing changes within the biological system. Increased stress may result in impaired (or in some cases, enhanced) performance due to a number of psychological and physiological changes.
Two types of stress encountered by divers are physical and psychological stressors. Physical stressors are usually found to be related to environment, equipment or fitness level. Environmental physical stressors include water temperature, animal life, visibility, and currents. Equipment-related stress is often the result of poor adaptation of the diver to the equipment being used, and/or poorly maintained equipment. Inefficient swimming skills and lack of physical fitness can increase the stress level experienced sub-aquatically by a diver.
Psychological stressors encountered by the diver can be related to levels of competency or training of the diver. Time pressure and peer pressure are common psychological stressors (Sharr, 1989, p.68). Divers may also have increased stress levels related to thoughts of possible underwater dangers. Other psychological stressors may be unrelated to diving (family tensions, work overload, interpersonal problems,) but might play a role in the status of the diver at the time of the dive. These stressors may in turn, cause a number of recognized psychological problems (perceptual, cognitive, response, mental narrowing and ultimately Panic; and behavioral aberrations such as the wild-eyed, white-knuckled look, jerky erratic or unrhythmic movements, irritability, fixation or repetitive behavior and increased error rates and judgmental errors.) Finally, psychological stressors are known to produce physiologic reactions that in turn cause added stress by way of a feedback loop mechanism. However, it is the physiological effects or responses of the body that may provide a clue to why stressed individuals are more prone to DCI than non-stressed persons.
Wilson and Schneider (1981) report that stress can result in over 1,400 physicochemical responses in the body. (Asterita, 1985). Many of the physiologic responses of stress are the body's effort to resist change and maintain homeostasis. Most physiologic responses identified occur to the autonomic nervous system with changes in endocrine responses.
The most common physiologic responses to stress include increased arterial pressure, increased blood flow to active muscles, decreased blood flow to organs not directly related to the stress issue, increased rates of cellular metabolism, increased blood glucose concentrations, increased glycolysis in muscles, increased muscle strength, increased mental activity, and increased rate of blood coagulation (Allen 1986). Under normal circumstances these responses to stress may impart a positive effect to the diver, increasing the physical response to a threatening situation. However, as stress is increased, the physiologic responses may progress to a psychological panic syndrome, resulting in hyperventilation, excessive muscle tension and cramping, excessive heart rate increase, and breathing difficulties (Sharr, 1989, p.66) - a negative and destructive state.
As previously mentioned, the two main physiological pathways affected by stress are the autonomic nervous system (most specifically the sympathetic branch) and the neuroendocrine system. The sympathetic branch of the autonomic nervous system originates in the posterior hypothalamus and traverses down the spinal cord to the effector organs, such as the heart, systemic and peripheral blood vessels, bronchi of the lungs and the adrenal medulla and cortex (Asterita & Guyton). Sympathetic stimulation of the heart results in increased heart rate, contraction strength and myocardial cell metabolism. Peripheral vasoconstriction, as a result of sympathetic stimulation, redirects blood away from the periphery to provide increased circulation for central body functions (perhaps this is relevant to type I DCS in joint and skin. However, within the respiratory system the resultant effects of the sympathetic nervous system include the dilation of the bronchi and constriction of local blood vessels. The cumulative effects of increased heart rate, dilation of the bronchi, and constriction of local (lung) blood vessels potentially reduces the efficiency of the lungs for the removal of nitrogen bubbles.
Sympathetic stimulation of the adrenal medulla causes the release of large quantities of epinephrine and norepinephrine into circulation. The effects of epinephrine and norepinephrine are similar to those of the sympathetic nervous system. However, the effects of these two hormones extend approximately 10 times longer due to their slow removal rate from the circulating blood (Guyton 1981). Epinephrine causes a decrease in the coagulation time of blood with concomitant increases in the red blood cell count (Asterita, 1985). Additionally, physical activity results in increased release of epinephrine and norepinephrine. Thus the effects of epinephrine and norepinephrine are enacted through both physiologic (exercise) and psychological (Stress) activities.
Cortisol, also called hydrocortisone, is secreted from the adrenal cortex. In situations of emotional or physical stress, neural responses act on the hypothalamus causing the secretion of the corticotrophin releasing factor which stimulates the anterior pituitary to release ACTH (anterior corticotropin hormone). ACTH causes the release of cortisol into circulation (Mcardle, Katch, Katch). Cortisol has many effects on the body, most notably are increased liver gluconeogenesis, enhanced amino acid transport, increased protein metabolism, increased mobilization of fats for utilization in energy production, and changes in amounts of blood cell constituents (Guyton, Asterita). Cortisol also decreases plasma levels of eosinophils and lymphocytes with a resultant diminished level of immunity. (Allen, p.82) The potential for blood clotting is increased by these changes. The smooth muscle activating factor (SMAF) causes inflammation and can induce decompression sickness in animals. Anti-SMAF causes inflammation of capillary walls and leaks of blood fluids into the tissues causing blood thickening. Anti-bodies C3a and C5a too may contribute immunological implications, and the nitrogen bubbles in contact with the White blood cell release a toxin called Oxygen radical with resultant inflammation which may accelerate bubble formation. This points to blood as a active participant in DCI in the context mentioned by Brylske (1994) the disorderly blood flow.
Thus this review of the impact of stress on physiological parameters reveals that several important homeostatic control mechanisms are affected. When combined with the natural stresses of diving, impairment of these control mechanisms may result in increased likelihood of a diver sustaining DCS.
Stress is recognized as having an impact on the body chemistry/physiology. Stress impacts human internal chemistry by increasing the concentrations of several compounds which may make one more susceptible to DCI. The potential for clotting of the blood is increased by these changes. The immune system is also altered. Chemical such as acetylcholine, corticoid, cortisone, are among those which are suggested as instrumental to these effects.
Since stimulation of the sympathetic branch of the autonomic nervous system causes a number of chemical changes within the muscular system, it appears quite possible that these changes may make the body more susceptible to decompression illness. An increase perspiration, heart rate, blood sugar and body temperature re-noted. Effects including peripheral vasoconstriction or shunting the blood away from the periphery to make more blood available to the central functions such as brain and muscle. The same system dilating the bronchi may constrict the blood vessels leading to the lungs - thus reducing the efficiency of the lungs in transmitting nitrogen (inert gas) bubbles to capillaries where offgassing may occur.
Two active hormones introduced in this process are secreted by the medulla, noradrenaline and epinephrine (adrenaline), both which exhibit effects lasting 10 time longer than the previously discussed sympathetic activity. (Asterita, 1985)
Other physiologic effects include - increased blood pressure, increased heart rate, increased respiration, and blood sugar levels. These effects are routinely ascribed to the physiological changes resultant from sympathetic nervous system activation during the stress response.
Both epinephrine and norepinephrine cause the bronchi and bronchioles to dilate. Epinephrine causes a lowering of the cosinophil count in the blood and decreases the coagulation time of the blood with concomitant increases in the red cell count. These chemicals may increase the hemoconcentration as well. Norepinephrine may constrict blood vessels of the peripheral systems. The spleen contracts and adds volume and red blood cells to the blood stream. Simultaneously the coagulability of the blood increases. The lymphatic system also produces more lymphocytes which specifically protect the body against foreign agents by engulfing any foreign matter.
Acute Adrenocortical insufficiency results in pallor and cold sweat, muscular weakening, tachycardia, hypotension, hypovolemia, hemoconcentration, hypoglycemia, hypochloremia, hyperkalemia, leukopenia, anuria and gastrointestinal ulceration.
Adrenocortical response - results in increased blood pressure, increased blood volume, decreased hematocrit, increased blood sugar, increased nitrogen secretion, increased leukocytes, decreased eosianophiles, decreased size of thymus and lymph nodes, hypertrophic of the adrenocortex with discharge of lymph granules.
The outward or visible physiological symptoms of stress may include hyperventilation, dilated pupils, and muscle tension. Additional responses may be apparent to the diving instructor or diving partner prior to embarking on a dive. These responses include irritability, simple mental errors, negligence, forgetfulness, extreme cockiness, garrulousness, lack of attentiveness to completion of tasks in preparation for the dive (Crotts, 1994). These signs should not be ignored. Instead, they should be addressed immediately so as to put the diver at ease or enable one to cancel the dive if signs and symptoms of stress warrant such action.
Several methods of stress reduction may be employed to alleviate stress symptoms prior to and during a dive (Sharr, 1989). These methods include clearly describing dive procedures, accentuating the positive aspects of preceding dives, use of a buddy system, practice of stress reduction protocols such as deep breathing, imagery, and muscle relaxation techniques. The use of 5 to 10 minutes of meditation and breath control techniques has been advocated by one dive instructor (Mount, 1993). While diving, he stresses a need for the diver to monitor his breathing and to use this as a means of controlling reactions to the stress of the dive. Such practices may well provide a vehicle for stress management.
Stress can impart positive or negative effects on divers. One's reaction to stress is an individual response. Divers encounter stress as a result of environmental, physical and/or psychological factors. Regardless of the source, such stress may manifest itself physiologically. It has been shown that the physicochemical responses evoked through stress are too numerous to list for the scope of this article. However, any physiological response due to stress effects homeostatic control mechanisms, which may render a diver more susceptible to developing DCS. Thus it is important to identify any outward physiological or psychological symptoms of stress prior to and during a dive so that steps can be taken to prevent DCS. The resultant physiological responses to stress could render a diver more susceptible to DCI. Further research is needed to document coping strategies of divers and a possible cause/effect relationship of stress and DCI.
Allen, R.J., (1986), Human Stress: Its Nature and Control, Burgess Pub. Co. Minn, MN.
Asterita, M.F., (1985), The Physiology of Stress, Human Sciences, Press, Inc. NY.
Bachrach, A.J, & Egstrom, G.H., (1987), Stress and Performance in Diving, Best Publishing, San Pedro, CA.
Bennett & Elliott, (1975), The Physiology and Medicine of Diving and Compressed Air Work, McMillian Publications Inc.
Brylske, A., (1994) Diving Medicine Controversies, Diver Training, 12(4):18-22.
Clark, L.K. (ed), (1990), Stress & Rescue, Concept Systems Inc.
Crotts, D., (1994) Diver Stress, Sources, 94:5:50-51.
Fulton, J.F. (ed), (1951), Decompression Sickness, W.B. Saunders Co. Philadelphia, PA.
Guyton, A.C., (1981). Textbook of Medical Physiology. (6th ed.) Phil. W.B. Saunders Co.
Mount, T. & Gillian, B. (1992), Psychological Aspects in Diving, pg.60 in Mixed Gas Diving, Watersports Publishing Inc., CA.
Sharr, P, (1989), 'Deep Diving' in Graver, D. (ed) Advanced Diving: Technology and Techniques, National Association of Underwater Instructors, Monteclair, CA.
Wienke, B.R. (1991), Basic Decompression Theory and Application, Best Publishing Co., Flagstaff, AZ.
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