Monthly Miracles

by Michael Gerber, MD, HMD

Nevada Homeopathic and Integrative Medical Association (NHIMA) 2012 Fall Conference: Part 3

Robert Rowan MD

Julia Ross, MA, MFT

Paul Ling Tai, DPM, FACFS, ABAARM, DACBM

DVDs of this conference are available from Tiffany at

www.nevadahomeopathy.org

.

Robert Rowan, MD

The Toxic Impact of Heat on Food

Dr. Rowan is a well-known integrative medicine practitioner, author, and lecturer from Santa Rosa, California. He has been the editor-in-chief of Second Opinion, an international, monthly medical newsletter, for the last 12 years.¹

Tracing his personal dietary history from carnivore/omnivore to a vegan/raw foods diet, he shared his exceptional personal improvements in physical fitness such as hiking Mt. Whitney without injury as had befallen him on a previous attempt. Also improved were his blood parameters and blood pressure.

Were We Meant to Eat Meat?

Rowan noted that carnivore teeth are sharp for cutting. Herbivore: flattened for grinding. Human molars are for grinding. Carnivore jaws move vertically for tearing. Herbivores move horizontally for grinding. Human jaws grind. Carnivore intestines are short, three times torso length for eliminating the toxic byproducts of protein digestion quickly. Herbivore intestines are far longer, up to 30 feet in length. Carnivores cool by panting, herbivores cool through perspiration. Humans perspire. He concluded that there are many other parameters which prove the point that we should be vegetarian.

Pottenger’s Cats

From 1932 to 1942, Francis M. Pottenger Jr., MD, of the famous Price-Pottenger Nutrition Foundation, studied experimental diets and physical characteristics of 900 unwanted cats. Their diets were identical in two groups except that one group was fed 2/3 raw meat with 1/3 raw milk and cod liver oil and the other was feed 2/3 cooked meat with 1/3 raw milk and cod liver oil. In every imaginable parameter, the raw meat cats did much better through several generations of litters. Skull configuration, distinctive sex characteristics, tissue tone, quality of fur, bone makeup, resistance to infection from fleas and parasites, signs of allergy, and friendly, predictable, behavior were much better in the raw-food group. Miscarriages were rare and the litters averaged five kittens with the mother cat nursing her young without difficulty. In the cooked-food group there were great differences in size and skeletal patterns; even second and third generations of cats found many differences in dental and facial structure. In the third generation, some of the bones became soft and spongy or overly brittle. They had heart problems, nearsightedness and farsightedness, underactivity of the thyroid gland, infections of the kidney, liver, testes, ovaries, and bladder, with arthritis and inflammation of the joints, nervous system with paralysis, and meningitis. Abortions in females were rampant running 25% in the first generation to as high as 70% in the second. The cooked-meat group had increased intestinal parasites, skin lesions, allergies, pneumonia, empyema, and diarrhea, leading to death. There was a high perinatal mortality of both mothers and kittens, with the kittens weighing 19 grams less than those in the raw-meat group. It required four generations for the deficient cats to regenerate to a state of normal health after the raw diet was reinstituted. A female cat subjected to a deficient diet for a period of 12 to 18 months caused her reproductive efficiency to be so reduced that she could never again bear normal kittens. An interesting rebuttal to the applicability of Pottenger’s study to humans is “Lesson Of the Pottenger’s Cats Experiment: Cats Are Not Humans”

(http://www.beyondveg.com/tu-j-l/raw-cooked/raw-cooked-1h.shtml

), especially as to cats’ inability to synthesize taurine, which can be destroyed by heat and deficiency of which causes neurological damage.

Rowan thinks that Pottenger’s experiment mirrors modern experiments on epigenetics (alterations in DNA expression) using nutrition deficiencies and environmental xenobiotics which may promote epidemics of autism, immune defects, cancer, allergy, suicide, violent behavior, and chronic disease.²

Maillard Reaction, AGES, Acrylomides, Pentosidine

The Maillard reaction imparts the unique taste and smell of cooked foods; however, it creates compounds not found in nature, such as acrylamides, now known to be carcinogens. The browning of meats, toasted bread, biscuits, malted barley or spirits, fried onions or any fried food, dried or condensed milk, and roasted coffee are all examples of the Maillard reaction. It also occurs in the human body. It is a step in the formation of advanced glycation end products (AGEs). This process can be tracked by measuring pentosidine. While studied in foods, it has shown a high correlation in different aging diseases, particularly degenerative eye diseases. AGEs accumulate on nucleic acids, proteins, and lipids. They can form from pathological oxidation reactions. AGEs are now correlated with a wide range of human degenerative conditions such as diabetes complications, pulmonary fibrosis, and neurodegeneration.

In experimental trials a group of 344 rats was split into a control diet and a thermolyzed diet with short exposure of 122 ºC for 30 minutes in an atmosphere devoid of oxygen. Hence oxygen could not be the culprit in findings, but heat. The experimental group became thiamine deficient measured by transketolase with increased oxidative stress measured by reduced GSH. The experimental group had increased markers of Maillard reactions measured by the presence of α-oxoaldehydes (glyoxals and methyl glyoxals). The protein adducts of these carbonyls and protein oxidation levels were increased. The experimental diet also increased oxidative stress biomarkers in livers and colons and increased macrophage infiltration into colons by 4-fold. This infiltration was believed to be caused by AGEs interacting with cell surface receptors. AGEs were believed to be signaling inflammatory cytokines such as TNF alpha. Nitrotyrosine is formed by the reaction of tyrosine and peroxynitrite (formed by NO reacting with superoxide). Nitrotyrosine adducts were increased in the plasma, liver, and colon of the experiment group with the highest concentration (3.6x) found in the colon. The same research group previously found that a thermolyzed diet leads to non-beriberi thiamine depletion, which increases oxidative stress and aberrant crypt foci (ACF), a forerunner of colon cancer.³

What about Heated Fats?

Heating oils creates an alphabet soup of damaged, oxidized, and carcinogenic by products that are implicated and proven to disrupt cell membranes and create disease. Nonesterified fatty acids are an independent risk factor of sudden death in middle-aged males as well as PVCs and ventricular tachyarrhthmias.⁴ Dr. Rowan gave in-depth documentation of the nomenclature of all the adducts of thousands of individual new compounds and explained the poor information on the cell membranes and intracellular membranes that causes extremely toxic reactions for our body economy.

Metabolic Rate, Membrane Composition, and Lifespan

Membrane damage via vulnerable fatty acids means that saturated and monounsaturated fatty acyl chains (SF and MUFA, respectively) are essentially resistant to peroxidation while polyunsaturated fatty acids (PUFA) are damaged. Furthermore, the greater the degree of polyunsaturation of PUFA, the more prone it is to peroxidative damage. Holman empirically determined (by measurement of oxygen consumption) the relative susceptibilities of the different acyl chains.⁵ Docosahexaenoic acid (DHA), the highly polyunsaturated omega-3 PUFA with 6 double bonds, is extremely susceptible to peroxidative attack and 8 times more prone to peroxidation than linoleic acid (LA), which has only 2 double bonds. DHA is 320 times more susceptible to peroxidation than the monounsaturated oleic acid (OA). Thus lipid peroxidation should not be perceived solely in a “damage to lipids” scenario, but also considered a significant endogenous source of damage to other cellular macromolecules, such as proteins and DNA (including mutations). In this way, variation in membrane fatty acid composition, by influencing lipid peroxidation, can have significant effects on oxidative damage to many and varied cellular macromolecules. For example, peroxidized cardiolipin in the mitochondrial membrane can inactivate cytochrome oxidase by a mechanism similar to hydrogen peroxide. Because the PUFAs are more vulnerable to free radical attack, they experience greater lipid oxidative damage, and lipid peroxidation products have been shown to contribute significantly to membrane rigidity. Lipid peroxidation products and peroxidized lipids are likely dominant factors in creating age-related membrane rigidity.

Experimental mammals of similar size show differences in longevity related to the content of DHA in their cell membranes, with the high DHA animals being shorter lived. The relationship between human longevity, membrane composition, and dietary DHA in humans may be complex and is still to be fully elucidated. For example, humans with severe coronary atherosclerosis have erythrocyte membranes with more PUFAs and particularly more DHA.

Cholesterol Oxidation Products (COPs – Oxysterols)

COPs (damaged cholesterol) occur from nonenzymatic conversion (via reactive pro-oxidants such as metals) or enzymatic catalysis as well as heating.⁶ The toxicity of COPs has been well studied and may induce apoptosis and necrogenic effect on vascular cells, and is pro-inflammatory and highly atherogenic, while cholesterol itself if not. Oxidized lipids form easily in heated food, occur spontaneously in vivo (membrane peroxidation), and result in cleavage of the cholesterol molecule creating ketones and aldehydes (highly teratogenic) and polymerization of molecules akin to boiled linseed oil.

In a recent study, Chien et al. studied the kinetics of cholesterol oxidation during heating of cholesterol at 150 ºC for up to 30 minutes.⁷ The COPs concentration was found to increase with increasing heating time. Routine cooking of meat (beef, veal, and pork) was done in an electric skillet (135 ºC) for 10 minutes each side and compared with raw. The COPs levels of cooked beef, veal, and pork increased by 1.7-, 2.3-, and 2.5-fold respectively. When beef, pork, and veal were oven-cooked at 220 ºC for 60, 80, and 90 minutes, respectively, the COPs levels increased by 3.5-, 5.4-, and 4.2-fold.

The three-dimensional structure of protein is destroyed by heating. Rowan likens this process to the effect of a tornado on a city. All the components of the homes are still present – but three-dimensional structure is gone.

He lists typical nutrient losses from heating and concludes by stating his “Rowan Theory.”⁸ Cooked foods are adding molecular compounds to human biological systems never before seen in our evolution. Is it possible that these “foreign” and unmetablolizable compounds are gumming up our cell membranes and cellular machinery? He postulates that this is so, and is at least in part responsible for cellular damage and adverse epigenetic effects in our modern population, compounded by toxic chemical excess and nutritional deficiencies.

Julia Ross MA, MFT, NNTS

21st-Century Sugar Addiction: Defeating the Greatest Dietary Crisis of All Time

Julia Ross is executive director of Recovery Systems, Mill Valley, California. She directs an outpatient program that treats eating disorders and addictions, as well as mood problems more generally, with therapeutic nutritional protocols along with counseling, education, and holistic medical care. She has received many honors, awards, and appointments and has authored several publications, including her very successful books The Diet Cure and The Mood Cure.^9,10

After demonstrating the differences in average dietary composition before and after 1970, she shows the pictures of the new malnutrition from fast food and vastly increased sugar consumption. She cites the recent publication by Robert Lustig, MD, pediatric endocrinologist at UCSF School of Medicine, who delineates the metabolic pathway of sugar and especially fructose in causing liver damage and obesity, particularly childhood obesity.¹¹

Recent annual worldwide deaths due to tobacco use were calculated at 5.3 million and deaths due to sugar consumption at 35 million. Another study revealed that 15 million US binge eaters and many more overeaters comprise our 60% overweight population. Subjects in the study who were provided unlimited sweets one hour/day became binge eaters in 2 weeks, consuming 4 times more food than controls.

A University of Bordeaux study in 2007 found that sugar and sugar substitutes are 4 times more addictive than cocaine. She asserts that sugar is an addictive drug. The definitions of addiction: loss of control, continued use despite adverse consequences, withdrawal symptoms and relapse.

Addiction and Neurotransmitter Deficits

Ross focuses on the deficient neurotransmitters of serotonin, GABA, catecholamines (norephinephrine and dopamine), and endorphin as causes of sugar addiction. Richard Wurtman from MIT and other researchers have documented sugar dependency via insulin-mediated serotonin activation since the 1980s. Multiple studies from1982–2012 document that sweets addict via endorphin (opiate) pathways. Hypoglycemia creates well-documented cravings for sugar to relieve the danger to the brain caused by glucose crashes.¹² Like cocaine, sugar can “reward” by stimulating dopamine activity.¹³

Addictive Foods

Ross lists addictive foods as sucrose (glucose and fructose), high-fructose corn syrup (HFCS) (glucose and fructose), refined starch, chocolate, gluten, and casein (cow’s milk protein). Fructose in HFCS is twice as sweet as glucose and generates equal amounts of triglycerides lasting 12 times longer in the blood and is equal in liver damage to alcohol. HFCS has increased in soda intake by 135% since 1970, and powerful satiety factors are specifically dysregulated by fructose: insulin, leptin, ghrelin, as well as glucose. Our modern diets that skip meals, with low protein, low good fats, caffeine, diet foods, sodas, appetite suppressants, and artificial sweeteners can cause overeating and bulimia. Voluntary starvation can cause drops in blood sugar, serotonin, and thyroid levels within 8 hours and creates rebound cravings, overeating, negative moods, weight gain, eating disorders, and health decline.

Amino Acid Therapy

In Ross’s patients, amino acid supplements take effect in 10 minutes in over 80% of clients to stop compulsive eating. Over 6 to 18 months they permanently correct the brain’s neurotransmitter deficit symptoms, including sugar craving, when combined with adequate dietary protein, fat, healthful carbs, and calories. In a 2-year study of amino acids and overeating, those given a blend of 4 amino acid precursors were compared to controls. The treatment group had 70% less craving and binge eating than controls.¹⁴ The low-potency amino acid blend used contained 5-HTP (5-hydroxytroptophan, the immediate precursor of serotonin) to optimize serotonin levels, DLPA (D,L-phenylalanine) to raise endorphin levels. and L-glutamine to stabilize blood sugar levels. Raising serotonin helps to stop sweet and starch cravings.

Symptoms of Low Serotonin

• afternoon/evening carbohydrate cravings

• negativity, depression

• worry, anxiety

• low self-esteem

• obsessive thoughts/behaviors

• winter blues (SAD syndrome, seasonal affective disorder)

• panic attacks, phobias

• fibromyalgia, TMJ, suicidal feelings, thoughts

• irritability, rage, (PMS)

• hyperactivity

• night owl, hard to get to sleep

• insomnia, disturbed sleep

Glutamine, Tyrosine

Glutamine 500 mg (1–3) 3 or 4 times per day between meals offers an alternative to glucose in the brain. Sublingually it can stop sugar, starch, and alcohol cravings in 3 minutes. Ross also recommends adding chromium from 800 to 1200 mcg with meals. When food is used to reduce stress, the inhibitory neurotransmitter amino acids GABA, taurine, or the amino acid L-theanine soothe naturally. Adrenal stress hormone testing (salivary) and nutrition correction often give benefits. When sugar, chocolate, and caffeine are used for energy and focus, as well as reward, the precursor amino acid tyrosine is needed.

Neurotransmitter Testing: Problems and Alternatives

After Ross’s extensive experience in neurotransmitter testing, she believes strongly that blood platelet testing is the best evaluation technique. She has found urinary neurotransmitter testing to be at odds with clinical symptoms in patients over the years and that the gold standard of spinal fluid evaluation is more difficult to do routinely. Published in 2005, a formal study of 18 human subjects compared the levels of serotonin and the catecholamines found in CSF, BP, urine, and plasma.¹⁵ The study was performed by Tappan Audhya, PhD, professor of nutritional biochemistry at New York University Medical School and director of the Vitamin Diagnostics Laboratory in Cliffwood Beach, New Jersey. His study found that blood platelet testing results corresponded very closely to CSF (cerebral spinal fluid) testing results, but that neither urine nor plasma testing results did. He explains that the levels of serotonin and the catecholamines are known to be stable and abundant in the blood platelets, but not in blood plasma, the levels of which are extremely reactive to stress (even the stress of the blood draw!). He also notes that the levels of neurotransmitters in urine vary rapidly in reaction to both stress chemistry and diet-related (especially pH) changes.

Prof. Dr. Paul Ling Tai, DPM, FACFS, ABPS ABAARM, DACBN

Fat-Burning Weight Loss and Mitochondria Energy

Dr. Tai gave us three memorable lectures. He has had a vast influence in teaching not only in Michigan and the US but around the world, lecturing from Beijing to Brazil and Istanbul to Uzbekistan, among many other countries. An accomplished author as well as speaker his latest books are the Golden Book of Anti-Aging and Regenerative Medicine, volumes 1 and 2. He is president and chairman of the Brazil Academy of Anti-Aging and Regenerative Medicine and A4M Brazil conferences. Dr. Tai is a knighted physician and the grand physician general of the Supreme Council of the Sovereign Medical Order of Knights Hospitaller and a member of the Royal College of Papal Knights in the Americas.

His first lecture focusing on obesity begins with health related statistics such as 400,000 people die each year caused by overweight and obesity.¹⁶ Women who drink one soda per day increase chances of type 2 diabetes by 85%. Fat used to be viewed as merely a place to store extra calories; however, the new changed view of fat is that of a major leptin hormone-producing organ which effects the satiety center, thyroid gland, adrenal gland, and sex hormones.¹⁷ Leptin resistance was discovered in 1994. Since leptin promotes satiety, leptin resistance means that leptin does not enter the brain.¹⁸ High triglycerides in the blood from excess eating block leptin entry into the brain and the body thinks that is is starving. Fat cells also expand and get clogged. Two studies in the Bariatrician in 2008 evaluate the Bauhinia plant from the Amazon which normalizes liptin hormone, satiety regulation, and abnormal sugar metabolism. In clinical studies 100% lost weight. One or two Bauhinia caps 30 minutes before meals 3 times per day were used and he postulates that they unblock leptin receptors in the hypothalamus. Leptin also slows thyroid function even though a person is overweight.¹⁹ He also promotes mozuko extract, special sea kelp found in the coastal water of Okinawa, Japan, to help with metabolism resistance as well as a novel 7-Keto DHEA cream for topical application to reduce fat in fatty areas.

New Technology and Natural Protocol for Gynecomastia, Male Feminization and Low Testosterone

In his second lecture Dr. Tai reviews the impact of testosterone on the body economy. Testosterone (T) affects libido, mood, muscle strength and volume, stimulation or erythropoietin production, accelerated linear bone growth, and syntheses of serum proteins. In the Massachusetts Male Aging Study, the authors demonstrated a substantial decline in testosterone levels in men in three decades beginning in the 40s.²⁰ General symptoms of low testosterone included decreased sexual desire, erectile dysfunction, difficulty achieving organs, reduced intensity of orgasm, low energy and increased fatigue, loss of motivation, and depressed mood. Additionally T is associated with increased body fat, reduced muscle bulk and strength, loss of body hair, and reduced shaving. The prevalence of risk factors in the HIM study increased from 52% down to 32% for the following conditions: obesity, diabetes, hypertension, rheumatoid arthritis, hyperlipidemia, osteoporosis, asthma/COPD, prostatic disease/disorder, chronic pain and headaches.²¹

Andropause is a Lethal Disease

Increased levels of diabetes, metabolic syndrome, brain and heart disease, frailty syndrome, bone loss/osteoporosis, inflammation, and cancer are associated with low testosterone. Aging males with low T may not live as long.^22–24 Eight hundred men, 50 to 91 years of age, were followed for 18 years with 1/3 having low testosterone. Men with low T vs. those with higher T had: increased levels of inflammatory cytokines, increased waist girth, 3 times higher chance of having metabolic syndrome, and 40% greater risk of death.

What is Aromatization?

Aromatase is the enzyme responsible for a key step in the biosynthesis of estrogens, and aromatization is the conversion of androgens into estrogens.²⁵ Estradiol has a 100-fold higher molar potency than testosterone. Cytochrome P450 type 19 (CYP-19) is aromatase and facilitates the production of estradiol in human cells. An increase in aromatase in younger individuals demonstrates gynecomastia, decrease in libido, and erectile dysfunction. It is also associated with poor testosterone treatment response, increased clearance of androgenic hormones, and elevated estrogen production rates.²⁶ Testosterone replacement complications can cause direct negative feedback to the anterior pituitary gland and becomes less responsive to GnRH, which limits its own production of T and can cause testicular atrophy.

Natural Treatments

Dr. Tai has accumulated many herbal and nutritional treatments for andropause, gynecomastia and erectile dysfunction. He first reviews Butea superba (Red Kwao Krua), which gives strength and power and increased male sexual performance. Each of the constituents of the tuber and stem contain inhibitory effects toward cAMP phophodiesterase. Butea superba also increases levels of acetylcholine, which is involved with erectile function and memory. In a three month randomized, double-blind trial in men aged 30 to 70 years, the authors found an 82% improvement in erectile function in impotent patients without apparent toxicity.²⁷

Eurycoma longifolia increased testosterone, muscle strength and penile size, prevents age-associated androgen deficiency, and increased psychological parameters of mood, energy, and sense of well-being.²⁸ It also increased fat free mass, muscle strength/mass, and athletic performance.²⁹

Calcium fructoborate interferes with physiology and reproduction of cancer cells in prostate, breast, cervical, and lung cells. One treated patient had a 50% increase of testosterone.³⁰

Chrysin decreases aromatization, body fat and helps to reduce alcohol consumption.³¹

Indole-3-carbinol partially blocks estrogen receptor sites on cell membranes and converts highly active estrogen forms and their by-products to much safer compounds. It enhances 2 hydroxy estrone metabolites over 4 hydroxy estrone metabolites. I3C also blocks anti-cancer enhancing receptor sites directly killing cancer cells.³²

Diindolmethane (DIM) is another cruciferous vegetable extract that decreases effects of estradiol. It is an estrogen receptor beta agonist and exerts its effects through nonligand protein kinases.^33,34

Pueraria mirifica (White Kwao Krua) has the phytoestrogen miroestrol, which is similar to estriol. The local Thais who consume it are devoid of hormone-related degenerative diseases such as breast cancer and prostate cancer. Pueraria mirifica isn’t just for women. This plant estrogen activates receptors that suppress tumors. The miroestrol is 3000 times more active on beneficial receptors than phytoestrogens in soy.³⁵

L-citrulline, a precursor to arginine, has a well-known ability to increase nitric oxide production with a wide variety of health benefits. It has been well studied for its ability to enhance sexual satisfaction. Both men and women report longer and more intense orgasms with increased intake of arginine.³⁶

Powerful Treatment and Prevention for Alzheimer’s Disease and Memory Loss

In his third lively and entertaining lecture, Dr. Tai reviewed the prevalence and alarming statistics of Alzheimer’s disease (AD). Five million people in the US have AD. Forty percent of people age 85 and older are at risk for AD. AD is the 7th leading cause of death in the US. The prevalence of AD is expected to double by 2050.³⁷

Pathophysiology of AD includes low levels of the neurotransmitter acetylcholine. Low levels of acetylcholine in brain are associated with AD, and restoring levels may slow progression. Beta-amyloid deposition, oxidative stress, and inflammation may also contribute to the etiology of AD. Beta-amyloid clusters into amyloid plaques on the blood vessels and outside surface of neurons of the brain and ultimately cause neural degeneration.³⁸ In susceptible regions of the brain, inflammatory mediators in glial cells from inflammatory cytokines are increased and may contribute to amyloid plaque formation.³⁹ Oxidative stress from AGEs can damage the brain and may contribute to progression of AD.⁴⁰

Pregnenolone

Pregnenolone, the mother hormone for the adrenal gland, keeps brain functioning at peak capacity. It has its highest levels in the brain and enhances mental function, repairs brain and nerve tissue, protects cerebral function, and guards against neuronal injury. Pregnenolone exerts effects through different hormones such as DHEA, progesterone, estrogens, testosterone, cortisol, and aldosterone. Optimum levels of pregnenolone occur around age 35 and by the age of 75, 65% of pregnenolone is lost.⁴¹ Pregnenolone is neuroprotective.^42-43 It improves memory and learning and is a new biomarker of cognitive aging.^44-45 Supplementation improves memory and cognition and increases mental performance under stressful conditions.⁴⁶ Pregnenolone improves release of acetylcholine (Ach) and modulation of Ach neurotransmission and may alleviate AD.^47,48 Mechanisms of pregnenolone include stimulation of layout of new brain connections, improved neurogenesis or neuroplasticity, excitatory effect due to affinity for two types of receptors by activation of NMDA receptors, and occupying GABA receptor sites.⁴⁹

Acetylcholine, Glycerophosphocholine (GPC)

Glycerophosphocholine (GPC) is vital for survival and provides unique protection to all cells. It is abundant in mother’s milk and occurs naturally in all living things; it is an orthomolecule and is a direct precursor to Ach. GPS is effective in attention improvement, concentration, and memory formation. GPC taken daily showed impressive neuron growth-promoting effects in the brain.⁵⁰ GPC proved superior to placebo to the smart drug aniracetam and the synthetic antioxidant idebenone. GPC can give measureable neuronal protection against losses that occur between middle and old age.⁵¹ GPC and Alzheimer’s was studied in a double-blind study of 261 probable Alzheimer’s patients and were given GPC (1200 mg/day) vs. placebo for 6 months. Using measurement scales of MMSA, GDS (Global deterioration scale for cognitive decline), ADAS (Alzheimer’s Diseases Assessment Scale-Total, Cognitive, and Behavioral), GIS (Global Improvement Scale) and CGI (Clinical Global Impression) GPC proved significantly superior to placebo in all clinical assessment scales. GPC significantly improved behavior, activities of daily living without a single dropout due to side effects for GPC.⁵²

Notes

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