Examples of Phase I and Phase II Optimizers in Pro Phase™ are ellagic acid from pomegranate, catechins from green tea extract and glucosinolates from watercress powder. Ellagic acid can bind directly to DNA to protect it and bind directly to some toxic substances to promote their excretion.* In addition, ellagic acid induces Phase 2 enzymes at the gene level and makes sure these are not over-induced by its modulation of CYP1A activities. The catechins in green tea, besides being strong antioxidants, also can bind directly to toxic substances. They have the ability to modulate Phase 1 enzymes, moderately up-regulating them when carcinogens are not present and limiting the enzyme production when toxic substances are encountered. Glucosinolates are precursors to isothiocyanates. In particular, watercress is metabolized by gut flora into phenylethyl isothiocyanates (PEITC) which like the other ingredients above, can selectively inhibit Phase 1 enzymes and induce the activities of phase 2 enzymes.

As the liver is one of the main organs for detoxification, silymarin (milk thistle seed extract), artichoke leaf extract and alpha lipoic acid have been added to the formula because they are hepatoprotectant.* They also increase glutathione and provide potent antioxidant protection.

The remaining ingredients in this formula are present to support the various Phase 2 detoxification pathways.* Vitamins B6, B12 and folate, along with MSM support methylation. Calcium D-Glucarate has been added to support glucuronidation.

The sulfate donors, sodium sulfate and NAC are especially important in cases of heavy metal burden because they support glutathione production and the sulfation pathway.*

Click here to purchase Pro Phase™.

Ultracore daily detox contains rice protein which is an easily-digestable protein source that helps maintain healthy metabolic and liver function.* It contains key amino acids that support the production of glutathione. Glutathione is a powerful antioxidant required for both phase I and phase II detoxification processes.* N-Acetyl Cysteine (NAC) is a derivative of the amino acid cysteine and been shown to have antioxidant properties, which help protect against the free radicals generated during phase l detoxification.* It’s also a precursor to the production of glutathione, a powerful antioxidant that is needed to breakdown pollutants and toxins and it contains sulphur, which is needed by the phase II detoxification pathway.

Ultracore daily detox also contains various antioxidants such as Ellagic Acid and Green Tea catechins which help protect against free radicals and oxidative damage that can happen during both phases of detoxification.* MSM is included because it supports the production of sulphur based amino acids that offer antioxidant activity. DL-Methionine is a sulfur based amino acid that metabolizes fats, this helping to reduce their buildup in the liver (it is a lipotropic).* Methionine is also a powerful antioxidant, and is used by the liver to manufacture glutathione, the body’s master antioxidant and heavy metal chelator.*.

Ultracore daily detox also includes many substances to help in the removal of heavy metals and various environmental toxins.* Glycine is an amino acid that is required for the synthesis of bile salts, and is used by the liver to detoxify chemicals in the phase II detoxification pathways.* Chlorella aids the body in the breakdown of hydrocarbons and metallic toxins such as DDT, PCB, mercury, cadmium and lead as well as supporting immune response.* Potassium d-glucarate is a source of glucaric acid, which helps support the removal of carcinogens, toxins, and steroid hormones from the body by strengthening the glucaronic pathway.* Milk Thistle is an herb that contains a group of active flavonoids known to protect the liver by supporting the structural strength of the outer cell membranes of liver cells, reducing the ability of toxins to enter.* It also supports improved glutathione synthesis. Dandelion Root helps the body to clear toxins and cleanse the liver and Watercress is included to enhances phase two liver detoxification pathways.*

Ultracore daily detox can be mixed in any cold beverage. It has a light strawberry and vanilla flavor.

Ultracore daily detox is a convenient way to support optimal health.*

Prozyme Blend chewable is beneficial for geriatric individuals because as we age, enzyme secretion decreases.* It is especially beneficial for those with jaw or teeth problems as improper chewing decreases enzyme secretion. People under stress or those who overuse antacids need digestive enzymes as the over use of antacids can decrease enzyme effectiveness and secretion.* People who eat a lot of fried, grilled, or baked foods require digestive support as those foods are prepared at hightemperatures for long periods of time which causes them to lose naturally occurring enzyme activity.

prozyme blend chewable is an orange flavor vegetarian chewable tablet.

prozyme blend chewable is a comprehensive, vegetarian supplement designed to support digestive tract health and nutrient absorption in people of all ages.* It contains non-dairy probiotics and a broad spectrum of digestive enzymes. Each chewable tablet provides 2.25 billion beneficial microorganisms along with amylase, bromelain, lactase, lipase, protease and cellulase to aid the body in digesting and absorbing food nutrients that are not easily assimilated such as fats, proteins and dairy products.

WEDNESDAY, April 13 (HealthDay News) — The brains of people diagnosed with Alzheimer’s disease start shrinking up to a decade before symptoms appear, a new study finds.

Researchers from Rush University Medical Center in Chicago and Massachusetts General Hospital in Boston did brain imaging tests on older adults with no signs of memory loss.

Of the 33 people in the Mass General group, eight developed Alzheimer’s over the course of 11 years. In the Rush group, seven of 32 people followed for an average of seven years developed the disease.

About 55 percent of those whose brains were in the upper tertile (third) of atrophy developed Alzheimer’s, while none of those whose brains in the bottom tertile (little or no atrophy) developed Alzheimer’s.

Among those with moderate amounts of atrophy, about 20 percent developed the disease.

“We could differentiate those who would decline from those who would remain healthy,” said senior study author Leyla deToledo-Morrell, director of the graduate program in neuroscience at Rush University Medical Center.

Based on the atrophy measurements, “we could even determine how quickly they were going to develop Alzheimer’s disease,” she added.

The study is published in the April 13 issue of Neurology.

Doctors have long known that Alzheimer’s is an insidious disease, and that changes in the brain begin long before the first symptoms become evident, said Dr. Jeffrey Burns, director of the Alzheimer and Memory Program at University of Kansas Medical Center.

“This suggests, along with other studies, that Alzheimer’s pathology is likely present years, if not decades, before the emergence of symptoms,” Burns said.

What’s probably happening is that biochemical changes in the brain that are only partially understood cause degeneration of brain cells, said Dr. Steven DeKosky, vice president and dean of the University of Virginia School of Medicine. Over time, the cells begin to die off, leading to structural changes in the brain tissue, or atrophy.

Specifically, people in the study who would later be diagnosed with Alzheimer’s disease were more likely to show cortical thinning, or shrinkage, in several brain regions, including the medial temporal lobe, temporal pole and the superior frontal gyrus, which prior research has implicated in the early stages of Alzheimer’s.

“The amount of atrophy was much, much, much less than in a person with Alzheimer’s disease,” deToledo-Morrell said.

“But because each one who developed Alzheimer’s disease showed it, the results are extremely significant,” she added.

Eventually, the hope is that one day there will be drugs to slow the progression of the disease — there are none currently available — and being able to diagnosis Alzheimer’s early would mean people could start treatment before they have experienced significant declines, she said.

“If we can identify people at risk of the disease, they would be at much greater benefit from receiving treatment, rather than people who have already developed Alzheimer’s, who already have a certain amount of cell death and you can’t really rescue those cells,” she said.

Though the number of participants in the study was small and the findings need to be repeated in larger populations, it is “remarkable they saw changes this clear with this small number of cases,” DeKosky said.

Still, it’s doubtful that such a technique is specific enough to be used to predict Alzheimer’s on an individual basis, the experts said, because not everyone who had higher levels of atrophy got Alzheimer’s. “It’s a ways away from being clinically useful,” Burns said.

But, a second study from the same journal may have practical applications immediately. The study found that vascular disease risk factors, such as hypertension, diabetes, cardiovascular disease and high cholesterol, may raise the risk of Alzheimer’s disease.

The good news is that treating those conditions lowered the risk of Alzheimer’s.

Chinese researchers followed 837 people over age 55 with mild cognitive impairment, which is often a precursor to Alzheimer’s, for five years.

During that time, 298 developed Alzheimer’s, while the others still had mild cognitive impairment but had not progressed to Alzheimer’s.

People who were treated for all of their vascular disease risk factors were less likely to progress to Alzheimer’s disease than those who weren’t treated or who only had some of their risk factors treated, according to the study.

“That’s a terrific study,” Burns said. “It says vascular disease has a real effect on the manifestation of Alzheimer’s disease. The vascular disease is damaging your brain and is probably causing you to have lowered resistance to the pathological effects of Alzheimer’s disease.”

Vascular disease can damage the blood vessels leading to and within the brain, he added. “With vascular disease, the brain is under attack two ways, so you develop Alzheimer’s disease sooner.”

Cholesterol-lowering medications, blood pressure medications and lifestyle changes such as losing weight and exercising can all help lower vascular disease risk factors, DeKosky said.

“If you aggressively treat vascular disease factors, you can delay the breakthrough of clinical symptoms of Alzheimer’s,” DeKosky said. “That’s a pretty exciting finding.”

More information

The U.S. National Institute on Aging has more on Alzheimer’s.

The potential of antioxidants to reduce the cellular damage induced by ionizing radiation has been studied in animal models for more than 50 years. The application of antioxidant radioprotectors to various human exposure situations has not been extensive although it is generally accepted that endogenous antioxidants, such as cellular non-protein thiols and antioxidant enzymes, provide some degree of protection. This review focuses on the radioprotective efficacy of naturally occurring antioxidants, specifically antioxidant nutrients and phytochemicals, and how they might influence various endpoints of radiation damage. Results from animal experiments indicate that antioxidant nutrients, such as vitamin E and selenium compounds, are protective against lethality and other radiation effects but to a lesser degree than most synthetic protectors. Some antioxidant nutrients and phytochemicals have the advantage of low toxicity although they are generally protective when administered at pharmacological doses. Naturally occurring antioxidants also may provide an extended window of protection against low-dose, low-dose-rate irradiation, including therapeutic potential when administered after irradiation. A number of phytochemicals, including caffeine, genistein, and melatonin, have multiple physiological effects, as well as antioxidant activity, which result in radioprotection in vivo. Many antioxidant nutrients and phytochemicals have antimutagenic properties, and their modulation of long-term radiation effects, such as cancer, needs further examination. In addition, further studies are required to determine the potential value of specific antioxidant nutrients and phytochemicals during radiotherapy for cancer.

This is an abstract from an article from the journal Toxicology. For the whole article click here.

Along with consuming Cruciferous Vegetables, Dr. Pressman recommends these quality nutrients to help reduce cellular damage caused by exposure to radiation:

Glutaplex
Alpha Lipoic Acid
Complete Orange Blend
Organic Reds
Biomega Fish Oils
Biocore Multi

For questions, please contact Dr. Pressman at healthradio@aol.com

biocore daily detox is an advanced supplement designed to support the body’s natural phase III elimination mechanisms.* It also combines powerful amino acids, antioxidant and herbs to support both phase I and phase II detoxification processes.*

biocore daily detox contains rice protein which is an easily-digestable protein source that helps maintain healthy metabolic and liver function.* It contains key amino acids that support the production of glutathione. Glutathione is a powerful antioxidant required for both phase I and phase II detoxification processes.* N-Acetyl Cysteine (NAC) is a derivative of the amino acid cysteine and been shown to have antioxidant properties, which help protect against the free radicals generated during phase l detoxification.* It’s also a precursor to the production of glutathione, a powerful antioxidant that is needed to breakdown pollutants and toxins and it contains sulphur, which is needed by the phase II detoxification pathway.

biocore daily detox also contains various antioxidants such as Ellagic Acid and Green Tea catechins which help protect against free radicals and oxidative damage that can happen during both phases of detoxification.* MSM is included because it supports the production of sulphur based amino acids that offer antioxidant activity. DL-Methionine is a sulfur based amino acid that metabolizes fats, this helping to reduce their buildup in the liver (it is a lipotropic).* Methionine is also a powerful antioxidant, and is used by the liver to manufacture glutathione, the body’s master antioxidant and heavy metal chelator.*.

biocore daily detox also includes many substances to help in the removal of heavy metals and various environmental toxins.*
Glycine is an amino acid that is required for the synthesis of bile salts, and is used by the liver to detoxify chemicals in the phase II detoxification pathways.* Chlorella aids the body in the breakdown of hydrocarbons and metallic toxins such as DDT, PCB, mercury, cadmium and lead as well as supporting immune response.* Potassium d-glucarate is a source of glucaric acid, which helps support the removal of carcinogens, toxins, and steroid hormones from the body by strengthening the glucaronic pathway.* Milk Thistle is an herb that contains a group of active flavonoids known to protect the liver by supporting the structural strength of the outer cell membranes of liver cells, reducing the ability of toxins to enter.* It also supports improved glutathione synthesis. Dandelion Root helps the body to clear toxins and cleanse the liver and Watercress is included to enhances phase two liver detoxification pathways.*

biocore daily detox can be mixed in any cold beverage. It has a light strawberry and vanilla flavor.

biocore daily detox is a convenient way to support optimal health.*

Benefits:

Supports liver detoxification*
Provides powerful antioxidants
Available in a great tasting easy to mix powder
Provides a hypo-allergenic easy to digest source of protein

biocore daily detox is an advanced supplement designed to support the body’s natural phase III elimination mechanisms.* It also combines powerful amino acids, antioxidant and herbs to support both phase I and phase II detoxification processes.*

biocore daily detox contains rice protein which is an easily-digestable protein source that helps maintain healthy metabolic and liver function.* It contains key amino acids that support the production of glutathione. Glutathione is a powerful antioxidant required for both phase I and phase II detoxification processes.* N-Acetyl Cysteine (NAC) is a derivative of the amino acid cysteine and been shown to have antioxidant properties, which help protect against the free radicals generated during phase l detoxification.* It’s also a precursor to the production of glutathione, a powerful antioxidant that is needed to breakdown pollutants and toxins and it contains sulphur, which is needed by the phase II detoxification pathway.

biocore daily detox also contains various antioxidants such as Ellagic Acid and Green Tea catechins which help protect against free radicals and oxidative damage that can happen during both phases of detoxification.* MSM is included because it supports the production of sulphur based amino acids that offer antioxidant activity. DL-Methionine is a sulfur based amino acid that metabolizes fats, this helping to reduce their buildup in the liver (it is a lipotropic).* Methionine is also a powerful antioxidant, and is used by the liver to manufacture glutathione, the body’s master antioxidant and heavy metal chelator.*.

biocore daily detox also includes many substances to help in the removal of heavy metals and various environmental toxins.*
Glycine is an amino acid that is required for the synthesis of bile salts, and is used by the liver to detoxify chemicals in the phase II detoxification pathways.* Chlorella aids the body in the breakdown of hydrocarbons and metallic toxins such as DDT, PCB, mercury, cadmium and lead as well as supporting immune response.* Potassium d-glucarate is a source of glucaric acid, which helps support the removal of carcinogens, toxins, and steroid hormones from the body by strengthening the glucaronic pathway.* Milk Thistle is an herb that contains a group of active flavonoids known to protect the liver by supporting the structural strength of the outer cell membranes of liver cells, reducing the ability of toxins to enter.* It also supports improved glutathione synthesis. Dandelion Root helps the body to clear toxins and cleanse the liver and Watercress is included to enhances phase two liver detoxification pathways.*

biocore daily detox can be mixed in any cold beverage. It has a light strawberry and vanilla flavor.

biocore daily detox is a convenient way to support optimal health.*

Benefits:

Supports liver detoxification*
Provides powerful antioxidants
Available in a great tasting easy to mix powder
Provides a hypo-allergenic easy to digest source of protein

Avoiding all food that contain wheat, rye, and barley gluten. Bread, bagels, pasta, pizza, malted breakfast cereals, and crackers are all examples of foods that contain gluten. Although some foods are labeled wheat-free, this does not mean that they are gluten- free.

Avoiding oats, at least initially. Oats may cause symptoms in some people, perhaps as a result of contamination with wheat, barley, or rye during processing. But many people who have celiac disease can eat moderate amounts of oats without having symptoms. Health professionals vary in long term recommendations regarding eating foods with oats. But most agree it is best that people newly diagnosed with celiac disease not eat oats until the condition is well controlled with a gluten free diet. Then, up to of oats may be eaten daily as long as no new symptoms arise. You should eat only oats known not to be contaminated with wheat, barley, or rye during processing.

Avoiding or limiting milk products in the beginning of treatment if they cause or aggravate symptoms. After symptoms improve and the small intestine heals (about 2 to 6 months), you may gradually reintroduce milk products in your diet.

Avoiding all beer products, alcoholic and non-alcoholic, including lagers, ales, and stouts.

Reading ingredient levels carefully and being aware of types of hidden gluten. Gluten can be in things like medicines, vitamins and other nutritional supplements, lipstick and lip balm, and various food additives. Products whose label have the phrase “modified food starch” or hydrolyzed protein” may contain gluten.

On a gluten free diet, you can still have:

Eggs and dairy products such as cheese. But you may need to avoid milk and milk products at the beginning of treatment.

Flours and starches made from rice, corn, buckwheat, potatoes, soybeans, or tapioca.

Fresh, frozen, and canned meats. Read labels for additives that may contain gluten.

Fresh, frozen, dried, or canned fruits and vegetables if they do no contain thickening agents or other additives containing gluten.

Certain alcoholic beverages, including wine, liquor (including whiskey and brandy), liquers, and ciders.

Note: The information on this website is  not a substitute  for the advice of  & treatment by a qualified professional.

The study of appetite regulation is primarily concerned with attempting to find a way to alter the inherent biological drive to eat. For several decades, researchers have been trying to pinpoint a primary mechanism within the body governing hunger and satiety in order to ascertain whether the selection of food has any specific physiological origin, or if there is even an overall caloric homeostasis in man. The outcome of work to date indicates that hunger is not the result of one single factor, but is instead elicited by many factors involved in a final common pathway.

In certain primitive societies, greater or lesser body mass was essential to survival. A long canoe trip across miles of ocean required that the traveler store food in his own body in the form of adipose tissue. In the African veldt, leanness was essential for the required quickness of running down and capturing prey on foot. In our modern, basically sedentary society, however, optimal weight is almost irrelevant for physical survival. It is instead involved with our concepts of health and longevity-and very often societal or cultural preferences. So-called normal weight, therefore, seems to be a concept dependent on the context to which it is applied.¹

Today, fat people, although continuously preoccupied with food and eating, often do not know when they are hungry.² For many, overeating and obesity serve the important function of avoiding emotions. Situations that provoke overeating and concomitant obesity resemble those that are usually accompanied by grief or severe depression.³ An individual who experiences every tension as a need to eat instead of feeling appropriate emotions such as anxiety or anger progressively gains weight. Disturbed hunger awareness is the main psychological deficit in some overweight individuals while others may have distorted feelings of sell-awareness. Attempts at weight reduction not only fail to solve their physical problems, but may induce additional feelings of frustration and stress. Many who attempt to reduce without inner emotional readiness eventually abandon the effort as too stressful. Others succeed without resolving their underlying psychological conflicts and become, as Hilde Bruch’s explains, “thin fat people,” the extreme of which is anorexia nervosa.⁴

The word anorexia is misleading since there is not true loss of appetite; the underlying disturbance is related more to not acknowledging hunger.⁵ In the advanced stages of emaciation, however, true loss of appetite may occur, similar to the disinterest in food during late stages of famine. Metabolically, the body goes into low gear, reverting to its pre-pubertal state, with many changes in metabolic and neuroendocrinal functioning.⁶ The effect on the psyche of severe undernutrition is largely responsible for the drawn-out course of the illness, sustaining it in many ways and making recognition and resolution of the underlying psychological issue difficult.⁷

Hunger and appetite are not solely behavioral phenomena since they have physiological bases as well. The integration of myriad impulses involved in appetite regulation takes place mainly in the complex structure sometimes called the brain’s brain, the hypothalamus. The signals transmitted to the hypothalamus include information about the circulating levels of various nutrients and feedback concerning the quantity of food present in the gastrointestinal tract. In addition, stimulation of the hypothalamus by a variety of physiological and psychological factors causes the autonomic nervous system to set off a chain of reactions that alter the functions of many glands and organs.

The hypothalamus performs its tasks through a complex pattern of many neurotransmitter substances including serotonin, the catecholamines (dopamine, norepinephrine, epinephrine), endogenous opiates and neuropeptides.⁸ The series of events which regulate food intake involves a delicate balance between these neural substances as well as the nutritional status of the organism. Research has shown that we obtain several precursor substrates from dietary sources, therefore many metabolic pathways are ultimately under nutritional control.⁹ Eating certain foods can raise the levels of these chemicals and actually increase the amplitude of the message sent, with behavioral consequences. In addition, diet-induced changes in plasma amino acids may directly alter the functional activity of brain neurons that mediate feeding behavior. Thus, the brain both controls and is controlled by an individual’s nutritional status.¹⁰

A well-known syndrome found in both animals and man is stress-induced eating. In the laboratory, stress-induced eating involved activation of the endogenous opioid systems.^11,12 Various studies have shown that both exogenous and endogenous opiates can stimulate food intake.^13,14 Opiate peptides have been shown to modulate responses to amino acid neurotransmitters. The implication is that dietary proteins, upon digestion, generate neuroactive peptides. In addition, alterations in carbohydrate metabolism have been shown to alter sensitivity of other receptors (e.g., dopoamine) thought to be involved in feeding. Dome neuropeptides released prior to or after a meal regulate temperature. This phenomenon explains the interrelationship between external temperature regulation and food intake (the thermostatic hypothesis)¹⁵ and why a person with a fever has little desire to eat.

It has been reported that obese mice and rats have an increased level of B-endorphin within the pituitary as well as being more sensitive to naloxone-induced suppression of feeding. (Naloxone is a specific opiate antagonist.) Opiates, moreover, appear preferentially to stimulate the intake of foods with a high energy content.¹⁶ After ten days with several episodes of stress-induced eating per day, there is a withdrawal syndrome similar to that seen after opiate addication, which supports the concept that obesity may result from autoaddiction to endogenous opioid peptides.¹¹

Changes in circulating glucose levels modulate the response to opiate antagonism of feeding, which relates to Mayer’s well-known glucostatic theory.¹⁷ Glucose interacts directly with the opiate receptor, altering its ability to bind the endogenous opiates. Animals with high blood sugar levels are extremely sensitive to naxolone-induced suppression of food intake. On the other hand, feeding brought about by insulin-induced hypoglycemia is resistant to the suppressive effect of naxolone.^18,19

Another important factor in the understanding of appetite regulation in stress-induced eating is the isolation of the neuropeptide. corticotrophinreleasing factor (CRF). CRF releases adrenocorticotrophic hormone and B-endorphin and increases heart rate, mean arterial blood pressure and is therefore involved in stress-related phenomena. CRF seems to fulfill Han Selye’s criteria for the central mediator of his general adaptation-to-stress syndrome. As we have seen, stress can result in either increased feeding or anorexia. Anorectics are know to have overactive hypothalamic-pituitaryadrenal functions, which might mean that the defect is an increase in CRF. Depressed patients, many of whom are arnorectic, also have a non-supressible pituitary-adrenal axis, suggesting the possibility of increased CRF function.²⁰ Thus, it seems stress can produce either overeating through activation of the endogenous opioid system or decreased eating through a rise in CRF activity.

Several different types of abnormal eating patterns have been observed in stressed individuals.²¹ One is the night-eating syndrome, characterized by evening hyperphagia and morning anorexia. It occurs during periods of life stress and disappears with relief of that stress, and is sometimes related to the development of obesity. Interestingly, studies on the circadian variation in endogenous opiate levels due to fluctuations in normal rhythmic biologic cycles in rats have shown that the highest levels occur during the nocturnal feeding phase with lowest levels during the daytime phase of the cycle.²²

Another abnormal eating pattern is binge eating, which also occurs during periods of life stress. It is characterized by the ingestion of large amounts of food in a short period of time, typically followed by feelings of self-condemnation and guilt and self-induced vomiting. Binge eating occurs more in people who keep their weight at an abnormally low level than in overweight people; many binge eaters are anorectic. Such periods of active overeating are associated with extreme degrees of inactivity.²¹

Obesity and anorexia are the two pathological and opposite poles of stress-related eating. More common eating variations are conscious attempts to lose weight by fasting and overeating in certain cultural milieus. Occasionally, fasting and overeating go hand in hand, as observed in the night-eating and binge eating syndromes.

Some recent studies have focused on the role of the sympathetic nervous system in the metabolic adaptation to fasting and overfeeding. Contrary to expectations, researchers found that fasting suppresses sympathetic activity and conserves calories by diminishing metabolism and heat production, resulting in a resistance to weight loss during therapeutic fasting.^23,24

Conservation of fuel and energy during fasting is an important biological survival mechanism; therefore stimulation of metabolic processes by catecholamines would be detrimental to overall metabolic homeostasis when available calories are limited. Catecholamines mobilize fuels in situations associated with an increase in total energy use, but are not responsible for fuel mobilization in the fasting state when total energy use is reduced.²⁵

Some researchers have cautioned that it is potentially dangerous to enforce weight reduction in people with circulatory disorders. If overweight individuals maintain the weight they have lost, the ensuing restoration of weight places a damaging burden on circulation.²⁶ Changes in sympathetic activity may partly explain the relationship between cardiovascular disease and nutrition. Increased sympathetic activity may account for some of the increased incidence of arrhythmias, angina and hypertension in populations in which overeating is common. Arrhythmias are fatal in some patients during post-fast refeeding.²⁷ In patients with underlying heart disease, arrhythmias could result from an abrupt increase in sympathetic activity to the heart. Conversely, hypotension and poor resistance to a variety of pathophysiological stresses that occur in chronic starvation may result from suppression of the sympathetic nervous system.²⁸

Stress is an unavoidable fact of life in contemporary society. Stress related problems are exacerbated in people whose diets fail to provide the extra nutrients their bodies need to deal with the heavy demands of stressful situations. Just the normal biochemical needs of uncomplicated daily living can often provoke severe symptoms when nutritional deficiencies have compounded over the years. And abnormal neural or glandular functions can result from long-standing deficiencies.

Stress nutrition is a program specifically designed to combat stress dysfunction and attempts to meet individual biochemical requirements by providing the right amount of each nutrient in proportion to every other nutrient. It is important to determine not only what vitamins and minerals a person is deficient in and to what degree, but also if there are any problems on the neuroendocrinal level. Not only is it essential to curtail intake of sugar, fats, carbohydrates, processed foods, refined foods, alcohol, cigarettes and pharmaceuticals, but equally important is consuming a diet balanced to the individual’s particular nutrient requirements. People under stress are often deficient in the B vitamins, particularly pyrodoxine and pantothenic acid, as well as vitamin C and the minerals calcium, magnesium and zinc. Stress nutrition not only deals with diet in its program, but might include exercise, behavior modification or biofeedback.

In a complex biochemical system such as man, many factors are involved in the acquisition and consumption of food. Diverse signals can originate in the brain, in the periphery, or they can develop as a habit. In addition, factors such as emotions, perceptual differences and eating disorders can play a role in modifying the signals used to initiate feeding. Though each separate factor can be manipulated to initiate eating, there appears to be no one single primary mechanism that can be called the “hunger” mechanism.

REFERENCES

1. Cahill, G.F., Jr. (1978): Obesity and diabetes. In. Recent Advances in Obesity Research, 11, Proceedings of 2nd International Congress on Obesity, edited by G. Bray. Newman Publishing Co., London.

2. Stunkard, A.J. (1959): Obesity and the denial of hunger. Psychosom. Med.. 21:281-290.

3. Kalucy, R.S., and Crisp, A.H. (1974): Some psychological and social implications of massive obesity. I A study of some psychosocial accompaniments of major fat loss occurring without dietary restriction in massively obese patients.] J. Psychosom. Res., 18: 465-473.

4. Bruch, H. (1973): Thin fat people. [at Eating Disorders: Obesity, Anorexia Nervosa and the Person Within, pp. 151-174. Basic Books. New York.

5. Bruch, H. (1973): Hunger awareness and Individuation. In: Eating Disorders: Obesity, Anorexia Nervosa and the Person Within, pp. 44-65. Basic Books. New York.

6. Vigersky, R., and Loriaux, D.L. (1977): Anorexia nervosa as a model of hypothalamic dysfunction. Ins Anorexia Nervosa, edited by R. Vigersky, pp. 109-121. Raven Press, New York.

7. Bruch, H. (1978): The Golden Cages The Enigma of Anorexia Nervosa. Howard University Press, Cambridge, Mass.

8. Morley, JE: The neuroendocrine control of appetite; the rule of the endogenous opiates, cholecystokinin, TRH, gamma-amino butyric acid and the diazepam receptor. Life Sci 1980; 27:355-68.

9. Kissileff HR, van Itallie TH. Physiology of the control of food intake. Ann HeN Nutr 1982; 2:371-418.

10. Growdon. J.H. (1979): Neurotransmitter Precursors in the Diet: Their Use In the Treatment of Brain Diseases. In: Nutrition and the Brain, Vol. 3, edited by R.J. Wurtman and J.J. Wurtman. Raven Press, New York.

11. Morley JF. Levine AS. Stress Induced eating Is mediated through endogenous opiates. Science 1980; 209: 1259-61.

12. Vaswani KK, Tejwani GA. Opiate mediated, stress Induced Increase In the Intake of high fat diet. Soc Neurosci Abstr 1982; 8:224.

13. Morley JE, Levine AS. The role of the endogenous opiates as regulators of appetite. Am J. Clin Nutr 1982; 35:757-61.

14. Sanger DJ. Endorphinergic mechanisms In the control of food and water intake. Appetite 1981; 2:193-208.

15. Brobeck JR: Food intake as a mechanism of temperature regulation. Yale J Biol Med 211:545-52, 1948.

16. Marks-Kaufman, R, Kanarek RB. Morphine selectively influences macronutrient uptake in the rat. Pharntacol Biochem Behav 1980; 12:427-30.

17. Mayer. J: Regulation of energy Intake and the body weight; the glucostatic theory and lipostatic hypothesis. Ann NY Acad Sci 1955: 63:15-43.

18. Levine AS, Morley JE, Brown DM, Handwerger BS. Extreme sensitivity of diabetic mice to naloxone-induced suppression of food intake. Physiol Behav 1982; 28:987-89.

19. Levine AS, Morley JE. Peptidergic control of Insulin-induced feeding. Peptides 1981; 2:261-64.

20. Morley JI . Levine, AS. Corticotroplln releasing factor, grooming and ingestive behavior. Life Sci 1982; 31:1459-64.

21. Stunkard, A.. d’Aguile., Fox. S., and Filion, R.D.L. (1972): Influence of social class on obesity and thinness in children. J. A.M.A., 221:579-584.

22. Morley, JE 1981.- The endocrinology of the opiates and the opiold peptides. Metabolism 30:195-209.

23. Young JB, Landsberg L: Suppression of sympathetic nervous system during fasting. science 196:1473-1475, 1977.

24. Young JB. Landsberg L: Stimulation of the sympathetic nervous system during sucrose feeding. Nature 269:615-617, 1977.

25. Young JB, Landsberg L: Fasting, Feeding and Regulation of the Sympathetic Nervous System. New England Journal of Medicine 298:1295-1301, 1978.

26. Keys. A. (1955): Obesity and heart disease. J. Chronic Dis., 1:456-461.

27. Garnett FS. Barnard DL. Ford J, et al: Gross fragmentation of cardiac myofibrils slier therapeutic starvation for obesity. Lancet 1:914-916, 1969.

28. Pickering G: High Blood Pressure. Second edition. New York, Grune and Stratton,

The NMI research conducted on the US general population showed that 44 percent of the over US adult population have memory loss and losing brain capacity as their biggest fear. More than half of the females (52 percent) reported memory loss/ and losing brain capacity as their biggest fear about aging, significantly more than the males (36 percent).

“We have known of the escalating memory loss problem for a long time and were very interested to see this research from NMI,” says Mark Underwood, President and co-founder of Quincy Bioscience. “We have been conducting very exciting studies in the area. We are working with a new paradigm of a jellyfish protein to help with memory loss and we have released in a brain supplement with this protein called Prevagen.”

“Too much calcium within a brain cell impairs its function. The jellyfish protein apoaequorin is remarkably similar to the calcium-binding proteins found in the human nervous system which become depleted in the mental aging process and can lead to cell death,” continues Underwood. “Unfortunately, we lose our ability to regulate brain cell calcium as we age. Starting at about forty, our brains produce fewer calcium-binding proteins. This causes calcium levels to rise throughout the nervous system. Neurons are flooded with dangerous levels of calcium and our brains slow down. The jellyfish apoaequorin which is the key ingredient in Prevagen works to regulate this imbalance.”

Research studies have shown that Apoaequorin, with its ability to bind to and balance calcium levels, can be used to help replace missing calcium-binding proteins and thereby slow age-related memory loss, loss of cognitive function, and alertness. Additional studies are planned.

Prevagen is manufactured by Quincy Bioscience, a Madison, Wisconsin based biotechnology company, focused on the discovery, development and marketing of new compounds to fight the mental aging process. The company’s products focus on restoring calcium balance related to neurodegenerative disorders and other destructive age-related mechanisms. Quincy Bioscience is developing health applications of the jellyfish protein apoaequorin for dietary supplement and pharmaceutical products.

Click here to buy Prevagen.