Patient Treatment Success Photos!

These are only a few of the many thankful patients that have been “given their life back” after Dr. Sponaugle’s Treatment at Florida Detox & Wellness Institute!

]]> http://floridadetox.com/before-and-after-photos-of-dr-sponaugles-grateful-patients/feed 0 http://floridadetox.com/mold-toxicity-blog-post http://floridadetox.com/mold-toxicity-blog-post#comments Mon, 10 Oct 2011 03:28:04 +0000 drrick http://floridadetox.com/?p=6725 Mold Toxicity

Dr. Rick Sponaugle, Medical Director of Florida Detox® & Wellness Institute has treated over 1,000 patients suffering from undiagnosed Mold Toxicity!

Mold Toxicity – Advanced Treatment for Mold Toxicity

Mold Toxicity is the excessive accumulation of mold mycotoxins in the brain and body.

Hidden mold is always present in water damaged buildings. Most of the time, we are unaware that mold trapped behind the shower tile or above the ceiling tile is producing harmful mycotoxins.

Dr. Sponaugle’s research has compared the SPECT brain scans, brain chemistry patterns and patterns of hormonal suppression in mold toxic patients to those of healthy individuals.

This research has proven that Mold Toxicity, especially Trichothecene toxicity, can cause severe distortion of brain chemistry patterns in addition to severe suppression every hormone in the body.

Mycotoxin-induced changes in Brain Chemistry and hormonal production are the underlying causation of many psychological and medical disorders in Americans including;

Addiction – Anxiety – OCD -Chronic Fatigue – Depression – Fibromyalgia – Insomnia – Multiple Sclerosis – Panic Disorder – Bipolar II – Paranoia & Schizoid Syndrome!

Excito-neurotoxicity

The mold toxic brain suffers from excessive production of two powerful electrifying or ““excitatory” brain chemicals, Glutamate and PEA. This causes a phenomenon called excito-neurotoxicity, in which patients develop an “over electrified” brain. Scientists suggest that brain cells are actually electrified by the excessive electrical current flowing through the brain. Excito-neurotoxicity is thought to be the primary cause of early Alzheimer’s Disease.

Dr. Sponaugle has successfully reversed Alzheimer’s in several patients, see Alzheimer’s page.

He has found undiagnosed mold toxicity as one of the many undiagnosed medical disorders in every Alzheimer’s patient he has successfully treated.

Addiction

Mold toxic patients need something to relax their anxious brains. Mold toxic patients often use opiate pain medication like Oxycontin or even Heroin, to “turn down” the excessive electrical current running through their brain – they use drugs and alcohol to calm the anxiety and panic caused by excessive accumulation of mold toxins in their brain.

Physicians unknowingly cause tremendous addiction when they prescribe benzodiazepines like Xanax and Klonopin to mold toxic patients. They are unaware that the severe anxiety and insomnia disorders their patients suffer with are often derived from toxic gases, mycotoxins, produced by the hidden mold in their work place or home. These patients often find their way to Dr. Sponaugle after they have spent hundreds of thousands of dollars having gone through 5 – 10 Rehab Programs for Xanax or Klonopin addiction.

Anxiety – Insomnia – Panic Disorder – Bipolar Disorder

Excessive Glutamate and PEA

Increased activation of Glutamate and PEA brain receptors produces an “over electrified” brain and an “over electrified” peripheral nervous system – thus the symptoms of Fibromyalgia. For obvious reasons, fibromyalgia is usually accompanied by insomnia, anxiety, panic disorder, and in the most severe cases, Bipolar symptoms.

Mold toxic patients experience a gradual progression of psychological symptoms from their “over electrified brain.”

Insomnia

Initially, mold toxic patients may only notice insomnia. As they accumulate more mycotoxins in their brain, they notice daytime anxiety in addition to their night time insomnia.

Anxiety & Panic Disorder

With continued exposure to hidden mold at work or home, mold toxic patients accumulate higher levels of mold toxins in their brain, they typically progress from an annoying anxiety disorder to a frightening panic disorder.

Bipolar Disorder

At Florida Detox & Wellness Institute, we have seen hundreds of patients who were misdiagnosed as having Bipolar Disorder when in fact, they were suffering from undiagnosed Mold Toxicity, specifically Trichothecene toxicity.

These misdiagnosed patients fortunately found their way to Florida Detox because they were seeking addiction treatment for Oxycontin addiction, Xanax addiction or Alcoholism. They were using drugs in their attempt to self-medicate the excessive electrical current running through their brain, excessive brain “voltage” derived from undiagnosed Mold Toxicity. Many of these patients had developed rage issues and were subsequently diagnosed with Bipolar Disorder.

Psychiatrists and Rehab Doctors at other Addiction Treatment Centers blamed their drug addiction as causation of their Bipolar Disorder when in fact, their undiagnosed mold toxicity caused the Bipolar Disorder that the mold toxic patients were attempting to self-medicate, as best they could with relaxing drugs or alcohol.

America’s Addiction Treatment Centers are full of mold toxic patients. These unfortunate patients will continue to relapse to drugs and alcohol the rest of their life until they are properly diagnosed.

Dr. Sponaugle has diagnosed Mold Toxicity as the true causation of Bipolar Disorder in over 200 patients. All of these patients were previously treated with Anti-Psychotic medications by unknowing psychiatrists with no expertise in Mold toxicity.

One of these patients, a 20 year old male, had undergone arrest and “Baker Act” to the University of Miami Psychiatric Unit 6 times in just 9 months. He was charged with Road Rage for ramming cars, something he had never done before age 20 when he moved into a mold toxic condo on Miami Beach. It only took 6 months of breathing mold toxins for his personality to change.

When these Bipolar patients were properly diagnosed with Mold Toxicity by Dr. Sponaugle, they underwent outpatient treatment for just two weeks with our Brain Wellness Program in addition to an Intravenous Mold Toxin Removal Program Dr. Sponaugle designed specifically for Mold toxic patients.

All of these “Bipolar” patients were weaned off their “Bipolar and Psychotic” medications within weeks.

Depression and Chronic Fatigue

Mycotoxin Suppression of the Brain’s Adrenaline Factory – The A -5 Nucleus

Norepinephrine Deficiency

Dr. Sponaugle’s research has proven that mold toxicity, especially Trichothecene toxicity, suppresses Norepinephrine output from the brain’s A 5 Nucleus, the brain factory that makes 90 percent of our norepinephrine. This is one of the many mechanisms by which Mold Toxicity causes severe depression and severe chronic fatigue.

Normal Norepinephrine levels on Neurotransmitter testing average a level of 40, Trichothecene toxicity can suppress these adrenaline levels to 10! These patients feel like someone has attached a 20 pound cement block to each leg, they often get dizzy for half a second when they stand up quickly from a sitting position.

Mycotoxin Suppression of the Brain’s Pituitary Gland

Excessive accumulation of mold toxins in the brain shuts down production of pituitary hormones – the brain’s pituitary gland becomes “too sick” to produce vital levels of pituitary hormones. Therefore, mold toxic patients suffer from severe pituitary hormone deficiencies and as well, they suffer from downstream hormonal deficiencies. The brain’s “sick” pituitary gland fails to produce the hormones that stimulate the thyroid gland, adrenal glands and sex organs.

Hormone Deficiency Thyroid – Cortisol – Testosterone

Epinephrine [Adrenaline], Norepinephrine [Noradrenaline] and Dopamine are first cousins. All three belong to the adrenaline family and are called catecholamines.

The catecholamines cannot activate their respective nerve receptors in the brain or body without the hormones cortisol, thyroid and testosterone. Mold toxin induced deficiencies of Thyroid Hormone, Cortisol and Testosterone causes severe depression, lethargy and chronic fatigue.

Fibromyalgia

As stated above, the accumulation of mold mycotoxins in the brain, causes excessive production of the two most powerful excitatory or “electrifying” brain chemicals, Glutamate and PEA!

Mold toxic patients suffer from “total body pain” secondary to the excessive production of brain Glutamate and PEA. This results in up regulation of electricity in the body’s electrical system [nervous system]. Dr. Sponaugle diagnoses Mold Toxicity in the majority of his fibromyalgia patients.

Many of these middle-aged women have been to 8 or more University Medical Centers seeking help with their debilitating fibromyalgia symptoms where physicians lacking expertise in Mold Toxicity failed to properly diagnose the underlying cause of their fibromyalgia – they usually prescribe addicting Opiate pain medication or medications like Lyrica that simply treat the symptom, but, not the cause.

HLA DRBQ Genetics

Patients with HLA DRBQ genetics cannot effectively remove mold toxins or other fatty toxins like the aromatic solvent toxin Benzene from their body like “normal” people. They suffer much more from indoor mold toxins in water damaged buildings while others are not affected. Dr. Sponaugle finds HLA DRBQ genetics in all races and nationalities, however, the highest prevalence is in Northern Europeans with light colored skin – blonds and redheads.

The highest incidence appears to be in English, Irish and Welsh – Dr. Sponaugle is convinced that the recent diagnosis of Bipolar II in Catherine Zeta Jones is secondary to neurotoxicity that her doctors have failed to diagnose. She most likely could undergo two weeks of Dr. Sponaugle’s all-natural Intravenous detoxification protocol and her Bipolar symptoms would go away as they have in hundreds of other patients.

Multiple Sclerosis

If mold mycotoxicity, especially Trichothecene Toxicity, remains undiagnosed and brain accumulation of Trichothecene goes on for too long a period of time, the Trichothecene destroys the myelin sheath on brain neurons causing the classic “white spots” of Multiple Sclerosis on MRI of the brain.

Dr. Sponaugle has diagnosed many mold toxic patients, addicted and non addicted, with Multiple Sclerosis. His research has demonstrated that those patients who have a combination of high Trichothecene levels and severe “brain fog” are likely to demonstrate classic “bright spots” on their MRI. Some of these patients were still in their young thirties.

Many patients suffering from undiagnosed mycotoxin induced Multiple Sclerosis thought they were simply coming to Florida Detox for addiction treatment. Had they gone another rehab center for help with their addiction, their Multiple Sclerosis symptoms would have been blamed on their drug addiction or alcoholism. The true cause of their physical and mental demise, Multiple Sclerosis, could have gone undiagnosed for years as “alcoholic brain” or “fried brain” from drug addiction. Dr. Sponaugle has not found a brain with drug induced damage that he can not heal with his Brain Wellness Program.

Dr. Sponaugle uses his Brain Wellness Program combined with his Intravenous Toxin Removal Program to reverse brain and nerve damage caused by Multiple Sclerosis. See Multiple Sclerosis page for more information.

Dr. Sponaugle diagnoses many Alzheimer’s and Parkinson’s patients with a combination of Mold Toxicity and stealth brain infections. Infectious organisms like Lyme, Babesia, Bartonella and Mycoplasma are labeled “intracellular” because they live inside our cells, including our brain cells. Recent research has proven the Lyme Spirochete enters brain cells within 12 hours of a Tick or Mosquito bite. See Lyme page for more information.

Exposure

All of us have been exposed to mold or mold spores through the environment in which we live. Simply put, molds are parasitic, microscopic fungi that produce spores that float in the air like pollen and are common triggers for allergies. They can be found in damp areas, such as the basement or bathroom of your house, as well as in the outdoor environment in grass, leaf piles, hay, mulch or under mushrooms.

If you can smell a musty odor or see mold (although not all molds are visible to the naked eye), you have a mold problem. In fact, there are estimated to be over 50,000 different species of mold but only about 200 species may present serious health risks to human beings and animals (like the beloved family pet). These harmful species of mold are referred to as toxic producing molds and are potentially poisonous because they can produce toxins or poisons (known as mycotoxins).

The impact on your health or that of a loved one can be life-threatening. Therefore anyone exposed to mold should consider being tested even if the symptoms have yet to be experienced. Preventive medicine can be a life-saver.

What are the sources of black mold (a generic term because most molds growing on building surfaces are black)? Documented sources of such mold (see testimonials for some examples) may be one’s home (for example, through dampness in basement areas, air conditioning vents or bathrooms), schools and hospitals (but not to the exclusion of other buildings).

Eye and/or nose irritation, wheezing, nasal stuffiness and coughing may be experienced by individuals sensitive to mold. However, more severe documented responses to black mold exposure include respiratory problems (including asthma, shortness of breath, chronic rhinosinusitis and pneumonitis) as well as problems in the central nervous system (headaches, confusion, depression, fatigue, sleep disorders and cancer). In some cases, it may prove fatal (symptoms).

In light of the above, if you believe or suspect the existence of black mold in your everyday environment (such as in your home), what should you do about it? There are two different categories of mold testing, environmental testing and human testing. For example, if you wanted to determine if black mold is found in your home (that is, environmental testing), you have a number of options. These include taking a culture from the open air in the home by opening the plate and letting it remain open for one hour.

Then, closing the plate, taping it shut and sending it to the lab. This may include, as well, taking a swab of the mold if contaminated wall board exists, cut a piece and send it to RTL. For your convenience, kits for your use in the evaluation of the presence of mold in your environment are available from labs. In all cases, kindly telephone us first so we may provide appropriate instructions and assistance where required.

Human testing for mold in usually a non-invasive procedure. This may involve the need for a urine sample, nasal secretion, sputum or tissue biopsy which was taken previously by your doctor. Your specimen can only be evaluated if a doctor has ordered the tests. The doctor must sign RTL request form. Following analysis by RTL, the referring doctor will be informed of the results and if toxic mold or mycotoxins are found to be present, the doctor will be advised.

Allergic Mold Symptoms

Mild Reactions to Mold:

• Nasal Stuffiness
• Cough
• Eye irritation
• Wheezing
• Skin irritation

Severe Reactions to mold may include, but are not limited to:

• Fever
• Chills
• Muscular Aches
• Respiratory Problems:
• Asthma
• Shortness of breath
• Chronic Rhinosinusitis
• Pneumonitis
• Central Nervous System Problems:
• Headache
• Confusion
• Depression
• Fatigue
• Irritability
• Sleep Disorders
• Cancer
• Death

Mycotoxins

Mycotoxins are toxins produced by molds or fungi. The mycotoxins discussed here are the Tricothecenes, (which include T-2, macrocyclic tricothecenes, Zearalenone, Fumonosins, Aflatoxins, and Ochratoxins. Where conditions are right, fungi proliferate into colonies and mycotoxin levels become high. Toxins vary greatly in their severity.

Some fungi produce severe toxins only at specific levels of moisture, temperature or oxygen in the air. Some toxins are lethal, some cause identifiable diseases or health problems, some weaken the immune system without producing symptoms specific to that toxin, some act as allergens or irritants, and some have no known effect on humans. Some mycotoxins generally have more negative impacts on farm animal populations than on humans. Some mycotoxins are harmful to other micro-organisms such as other fungi or even bacteria (penicillin is one example).

Mycotoxins can appear in the food chain as a result of fungal infection of crops, either by being eaten directly by humans, or by being used as livestock feed. Mycotoxins don’t decompose easily so they remain in the food chain in meat and dairy products. Even temperature treatments, such as cooking and freezing, do not destroy mycotoxins.

Buildings are another source of mycotoxins. Public concern over mycotoxins increased following multi-million dollar toxic mold settlements in the 1990s. The negative health effects of mycotoxins are a function of the concentration, the duration of exposure and the individual’s sensitivities. The concentrations experienced in a normal home, office or school are often too low to trigger a health response in occupants. However, concentrations experienced in a home or building which has experienced water leaks are often high enough to trigger health responses in the occupants. Such health responses are noted in the symptoms section.

Trichothecenes:

Trichothecenes are the most dangerous mycotoxins. They are produced by a number of different molds such as Stachybotrys and Fusarium. Their dangerous mechanism of action is the inhibition of protein synthesis. Trichothecenes shut down RNA-DNA synthesis in cells and are known to cause apoptosis – killing of cells.

It is known that when Stachybotrys grows in a mold infested building, the organism produces dangerous tricothecene mycotoxins. These dangerous toxins go airborne and when inhaled move throughout the body.

However, because of the extreme toxicity of these compounds, this is felt to be a potentially dangerous situation. The tricothecene mycotoxins produced by Stachybotrys are macrocyclic tricothecene mycotoxins. Other tricothecenes are called simple tricothecene mycotoxins. These include most prominently T-2 toxin, HT-2 toxin, neosolaniol and fusarenon-X. These are stongly toxic compounds. Like the macrocyclic tricothecenes mentioned above, their primary toxic methancism is the inhibition of protein synthesis at the level of the ribosome. For the most part, their effects are known from instances in which humans or animals ate contaminated grain, or from laboratory animal or in vitro (in lab) studies. The major effects (of symptoms) observed in humans exposed to these mycotoxins include “vomiting; inflammation; diarrhea; cellular damage of the bone marrow, thymus, spleen and mucous membranes of the intestines; and depression of circulating white blood cells.” Humans who have eaten contaminated grain develop “alimentary toxic aleukia,” which begins with burning sensations of the mouth, throat, esophagus and stomach, continues with vomiting, diarrhea and gastric cramps, and finally progresses to severe leucopenia (drop in white blood cell count), which renders the patient susceptible to infections.

Death may then be a result. Skin contact with material contaminated with these trichothecenes induces contact dermatitis, and in stronger exposures, lesions may be necrotizing (that is, may contain dead tissue, a significant risk factor for the development of bacterial infections). Effects on immune system components apart from the above-mentioned killing of thymus and spleen cells include inhibition of lymphocyte (white cells in the blood) responses and disruption and killing of alveolar (lung) macrophages (clean up cells).

Clotting factors in the blood are also significantly affected and the patient could bleed excessively if cut. Trichothecenes in general seem to have little effect on producing cancer, but when consumed or administered in pregnancy some scientist believe that they may have some teratogenicity (inducing deformed offspring) or abortifacient (abortion producing) properties.

When a person is exposed to Tricothecenes, the first symptoms exhibited are general discomfort, dry eyes, and drowsiness. A red skin rash appears shortly, starting in blotches and swiftly covering the entire body. Symptoms of a classic hemorrhagic fever set in, which include blood-red eyes, vomiting/urinating of blood, nosebleed, and patches of skin ranging in size from a quarter- to a silver dollar begin to bleed without reason. Brain function is also impaired, with the victim progressing from slurred speech to classic ‘fever dreams’ to various psychological conditions from Multiple Personality Disorder to Paranoia. The victim succumbs because of loss of blood, fever, or an infection brought on by the weakened immune system, whichever comes first.

If the patient survives, he will recover from most of the symptoms, although patches of skin will still bleed spontaneously for short periods of time. His immune system remains weakened, and his mental faculties will be severely damaged.

Zearalenone: A few isolates of Fusarium. sporotrichoides have been verified as producing this toxin. This compound is an estrogen mimic, most commonly causing vulvovaginitis (swelling and reddening of the vulva) in gilts (young female pigs) and sows which have consumed contaminated feed. This condition sometimes leads to vaginal or rectal prolapse which commonly results in reduced litter size, loss of pregnancy, and poor milk production in affected swine. Males may be feminized to some extent. Similar syndromes occur in cattle and sheep fed zearalenone-contaminated feed.

Fumonosins: These toxins were first described in 1984 after a thorough search for the cause of equine leukoencephalomalacia, a disease of horses in which brain tissue is damaged and horses show ataxia (inability to coordinate walking), facial and other paralysis, partial blindness, lethargy or excitement, and in later stages lameness, inability to stand, seizures and death. After the purification of fumonisins, the disease was induced in horses with purified material, confirming the etiologic role of the mycotoxin. Liquefactive necrosis of white matter areas of brain tissue is the main pathological sign observed. Hepatotoxicity (liver damage) is also seen. Experimental animals often experience hepatotoxicity, nephrotoxicity (kidney damage) or both; rats have also been shown to experience necrosis (destruction) of stomach lining and heart muscle (myocardium). Liver cancers can be caused by Fumonisins . Fumonisins are also among the chief suspects for the agent(s) of elevated levels of esophageal cancer in certain parts of the world.

Aflatoxins are naturally occurring mycotoxins that are produced by many species of Aspergillus.The organisms that usually produce aflatoxins are Aspergillus flavus and Aspergillus parasiticus. Aflatoxins are toxic and can be cancer producing. . After entering the body, aflatoxins are metabolized by the liver to a reactive intermediate, aflatoxin M1.

High-level aflatoxin exposure produces an acute damage and cirrhosis of the liver as well as cancer of the liver. It appears that no animal species is immune to the acute toxic effects of aflatoxins including humans; however, humans appear to have an extraordinarily high tolerance for aflatoxin exposure and rarely die to acute aflatoxicosis.

Chronic, of long term exposure does not lead to as dramatic of symptoms as seen in acute aflatoxicosis. Children, however, are particularly affected by aflatoxin exposure which leads to stunted growth and delayed development. Chronic exposure also leads to a high risk of developing liver cancer due to the metabolite aflatoxin M1.

Chronic, of long term exposure does not lead to as dramatic of symptoms as seen in acute aflatoxicosis. Children, however, are particularly affected by aflatoxin exposure which leads to stunted growth and delayed development. Chronic exposure also leads to a high risk of developing liver cancer due to the metabolite aflatoxin M1.There are two techniques that have been used most often to detect levels of aflatoxin in humans.

The first method is measuring the AFM1-guanine adduct in the urine of subjects. Many believe that the presence of this breakdown product indicates exposure to aflatoxin in the past 24 hours. However, this technique has a significant flaw in that it only produces a positive result in approximately one-third of positive test subjects. Additionally, due to the half life of this metabolite, the level of AFM1-guanine measured can vary significantly from day to day, based on diet, and thus is not useful for assessing long term exposure.

Another technique that has been used is a measurement of the AFB1-albumin adduct level in the blood serum. This approach is significantly more accurate, as positive results are generated in 90% of positive test subjects. This test is also useful for measuring long-term exposure, as it remains positive for two to three months.

Many patients and physicians are concerned about infestation of the sinuses with Aspergillus in patients who have sinusitis. Thus, there is also a concern of whether or not the organism present produces the toxin aflatoxin. RTL measures the presence of toxins and organisms in sinus fluids, nasal washes, urine, and tissues (especially respiratory biopsies, ie. Bronchoscopy specimens).

RTL has isolated aflatoxins from tissues from lung biopsies (See Seth K. testimonial), tissues from animals, and also from urines and sinus washes. RTL uses immuno-affinity columns for isolation of the aflatoxins from body fluids and tissues.

Ochratoxin A, a mycotoxin produced by Aspergillus ochraceus and Penicillium verrucosum and is one of the most abundant food-contaminating mycotoxins in the world. Human exposure occurs mainly through consumption of improperly stored food products, particularly contaminated grain and pork products, as well as coffee, wine grapes, and dried grapes. The toxin has been found in the tissues and organs of animals, including human blood and breast milk.

Ochratoxin A is potentially carcinogenic (cancer producing) to humans. There is sufficient evidence in experimental animals for the carcinogenicity of ochratoxin A. Ochratoxin A was tested for production of cancer by oral administration in mice and rats. It increased the incidence of liver tumors in mice of each sex and produced renal-cell (kidney) tumors and cancers in male mice and in rats of each sex. Ochratoxin A can cause suppression of white cells and immunity (immunosuppression) in animals.

Little is documented concerning the actual presence of Ochratoxin A in the air or dust of samples taken from the environment. This mycotoxin, however, has been found in food samples and in storage areas where foods known to have these toxins are stored. The organisms that produce these toxins have also been documented to be isolated in the respiratory tract of patients. Thus, it would not be surprising to find Ochratoxin A in the body fluids of some patients. RTL uses immunoaffinity columns to as screening procedures to isolate this toxin from urine and other body fluids and/or tissues.

Methods are available to examine urine for determination of ocratoxin A. The level of detection used at RTL is 2.0 ppb. At present, the test used at RTL is a qualitative test only. In other words, RTL can determine whether the toxin is present or not present. New methods for the determination of ocratoxin A in human urine samples have been reported in 2007 in medical literature. Thus, it is not surprising to find Ochratoxin A in some fluids from the human body.

courtesy of Real Time Laboratories

http://www.realtimelab.com/patients-mold-and-mycotoxin-information/mold-symptoms?t

Health Inspector Dies From Mold Exposure in Work Office

watch the ABC news video below for the full story

]]> http://floridadetox.com/mold-toxicity-blog-post/feed 0 http://floridadetox.com/we-are-proud-to-announce-that-dr-rick-sponaugle-was-featured-in-the-october-2011-edition-of-life-extension-magazine http://floridadetox.com/we-are-proud-to-announce-that-dr-rick-sponaugle-was-featured-in-the-october-2011-edition-of-life-extension-magazine#comments Mon, 12 Sep 2011 21:58:05 +0000 audrac http://floridadetox.com/?p=6201

We are proud to announce that Dr. Rick Sponaugle was featured in the October 2011 edition of Life Extension Magazine.

This is a great honor as Life Extension is one of the most prestigious Anti-aging and Wellness Institutions in America. They are the nation’s leader in research for Anti-aging and Longevity Medicine.

Click HERE to read Dr. Sponaugle’s featured article in Life Extension Magazine!

Jennifer is a 54-year old nurse who relapsed to alcohol just four days after leaving an Arizona rehab center where she spent 28 days and $46,000.

Before age 50, Jennifer never had a problem with alcohol nor did she ever suffer a drug addiction. Jennifer drank one glass of wine with dinner until she entered menopause and suddenly found she needed alcohol to “quiet her anxious brain.”

Most rehab doctors remain unaware that the female hormone, Estradiol, modulates the “receptivity” of serotonin in the female brain. When Estradiol levels fall below 60-80 pg/ml, serotonin receptors in the female brain partially close and are unavailable for activation by serotonin, thus, reduced receptivity.

For this reason, when women like Jenifer enter menopause, they suddenly develop symptoms of severe serotonin deficiency – even when they produce healthy levels of serotonin. This serotonin deficiency syndrome causes two brain regions to become overactive leaving the patient with a new onset of psychological symptoms – anxiety and depression.

Women finding themselves in this strange new world of “menopausal anxiety and depression” often survive by using alcohol to “quiet” their anxious brains. Jennifer is a classic example of the professional female who succumbs to alcoholism because of menopausal effects on Brain Chemistry. Dr. Sponaugle has successfully treated many of these professional women, as he did Jennifer,  on an outpatient basis.

Jennifer’s 4 years of drinking 2-3 bottles of wine a night exacerbated her problems with anxiety.

Alcoholism disrupts the normal function of gastrointestinal serotonin production. Most of our serotonin precursor [5-HTP] is made in the small intestine. Chronic alcoholism actually causes deficiency of two “relaxing” brain chemicals, serotonin and taurine, and excessive production of histamine, one of the brain ‘s electrifying brain chemicals. By the time Dr. Sponaugle first evaluated Jennifer, she had acquired alcohol induced changes in her Brain Chemistry that were causing excessive electrical activity throughout her brain. See Below.

Jennifer’s brain chemistry analysis reveals a classic pattern Dr. Sponaugle observes in all of his alcoholic patients.

Dr Sponaugle’s research in alcoholic patients like Jennifer has proven they develop severe deficiencies of serotonin and taurine, two calming brain chemicals and, excessive levels of histamine, an excitatory brain chemical.

Jennifer’s Arizona rehab doctors remain unaware that their alcoholic patients develop significant changes in their brain Chemistry and furthermore, that their attempt to treat her with medication alone would not stop her biochemical craving.

The Arizona rehab center had just incorporated SPECT brain imaging into their addiction treatment.

Dr. Sponaugle has used SPECT imaging in addiction treatment since 2005. Jennifer was advised that she should bring her SPECT scan to her first appointment at Florida Detox & Wellness Institute as Dr. Sponaugle would go over the findings with her.

Jennifer’s Brain Scan (surface)

The holes seen at the top of Jennifer’s surface scan represent a localized dopamine deficiency in her brain’s prefrontal cortex, the brain region above the eyes and behind the  forehead.

Jennifer’s localized dopamine deficiency is derived from inheriting a gene that produces a super COMT enzyme, an enzyme that metabolizes or breaks down dopamine four times faster than normal.

Patients who inherit a “super COMT enzyme” metabolize Dopamine before it can activate sequential brain cells in the prefrontal cortex. The holes represent “a string of light bulbs” that have failed to activate.

Jennifer’s SPECT scan as seen below on the right is called a deep scan. Notice Jennifer’s scan as compared to the healthy scan of the left, has a white and red oval in the middle, this  finding on Jennifer’s scan represents her severely overactive deep limbic system. The deep limbic system is about the size of a walnut and resides in the mid-brain. It is larger and more active in women than men, this makes women more sensitive and better at discerning social cues than men.

Dr. Sponaugle’s research has proven that excessive activity in the deep limbic system is caused by alcohol induced serotonin and taurine deficiency.

Jennifer also has an overactive basal ganglion [dopamine factory] just above and to the right of her deep limbic system. This can be a normal presentation, if abnormal, it can be derived from excessive dopamine activity.

In Jennifer’s case, her dopamine levels were normal. Her basal ganglia was overactive due to excessive histamine activation derived from alcohol induced leaky gut syndrome. Histamine activates dopamine receptors throughout the brain. This causes generalized anxiety and insomnia.

Deep Limbic System – Emotional Center

When the deep limbic system is quiet, we are much more relaxed and much happier. When the deep limbic system becomes overactive, we develop symptoms of depression, moodiness and irritability. If you have recently developed an overactive emotional center, you are experiencing feelings of hopelessness and excessive guilt. You no longer enjoy things that you once considered fun and you generally feel more depressed. You have developed a more negative personality and your desire to socialize is less that before.

During Jennifer’s initial consultation, Dr. Sponaugle noticed considerable tension between Jennifer and her husband. Jennifer’s Arizona rehab doctors had suggested to Jennifer’s husband that her relapse just four days after leaving their rehab center was her fault, that she was not serious about her sobriety. Jennifer insisted that she needed the alcohol to calm her anxious brain and lift her depression.

Jennifer did not know why, but, she insisted alcohol made her “feel more normal and that without it, she felt miserable.

Dr. Sponaugle explained to Jennifer’s husband, a hospital administrator from Atlanta, that Jennifer was most likely being truthful. Dr. Sponaugle explained that Jennifer was suffering “dry drunk” syndrome. Dry drunk syndrome is the miserable state alcoholics experience when they stop drinking. Alcohol induced changes in brain chemistry make them miserable unless they are properly diagnosed and corrected. The misery associated with “dry drunk syndrome” is the primary reason alcoholics relapse.

Florida Detox Relapse Rate for Alcoholics – only 9 percent

At Florida Detox & Wellness Institute, Dr. Sponaugle corrects these alcohol induced imbalances of Brain Chemistry in the patient’s first week of alcohol treatment, and thus, stops alcohol craving in days – for this reason, our alcohol relapse rate is only 9 percent verses a national average of 90 percent.

Dr. Sponaugle’s addiction research has matched SPECT brain imaging with specific brain chemistry profiles, female hormonal deficiencies and alcohol craving patterns. Alcohol craving is truly biochemical in nature – craving for the biochemical effect alcohol has on the brain.

Menopause Brain Physiology

The pertinent brain physiology regarding menopause is that serotonin receptors in the female brain close and are unavailable for serotonin activation when estradiol levels fall below 60-80 pg/dl. Dr. Sponaugle recently taught this concept to Dr. Daniel Amen and 200 psychiatrists at an Amen brain conference in Washington D.C.

Women with normal serotonin production, but, post menopausal estradiol levels suffer serotonin deficiency symptoms! Post menopausal women get less benefit from a serotonergic medication like Lexapro because their serotonin receptors are closed and cannot receive serotonin molecules.

When Jennifer turned 50, she reached full menopause and her estradiol production ceased. She began suffering classic symptoms of serotonin deficiency depression with the inability to enjoy things that used to be fun, increased moodiness, irritability, negativity, less desire to socialize, feelings of hopelessness, excessive guilt, and she became more easily offended.

Serotonin is a calming brain chemical – serotonin deficiency causes excessive electrical activity in the brain’s emotional center – the deep limbic system. Jennifer’s brain scan below demonstrates a severely overactive emotional center [deep limbic system].

Jennifer began drinking more alcohol for it’s calming GABA effect. Alcohol activates the Xanax receptor – the GABA receptor. Activation of the GABA brain receptors reduces electrical current in the brain. Alcohol produced a calming effect Jennifer badly needed once she reached menopause – her menopausal estradiol levels fell too low for her serotonin receptors to accept serotonin.

Once Jennifer began using wine as a medication to calm her overactive brain, she developed a myriad of alcohol induced brain chemistry imbalances. Dr. Sponaugle’s research has proven that Alcoholic patients develop a toxic gut – an intestine that suffers excessive overgrowth of Candida yeast and Klebsiella bacteria. Toxins from these foreign invaders shut down Serotonin production in the small intestine causing a deficiency of this important calming brain chemical.

Alcohol Induced Candidiasis

Enzymatic breakdown of Candida Yeast in the alcoholic gut produces excessive production of Beta-alanine, a protein that competes with Taurine for re-absorption in the kidneys. Taurine is a calming brain chemical. Dr. Sponaugle’s research in alcoholic patients has proven that all alcoholics suffer Serotonin and Taurine deficiencies. Dr. Sponaugle has designed an intravenous protocol to quickly correct deficiencies of these and other brain chemicals to prevent the alcoholic patient from relapsing.

Alcohol Induced Leaky Gut Syndrome

The toxins from pathogenic yeast and bacteria destroy the intestinal lining allowing abnormal “leakage” of undigested food particles, parasites and toxins. This phenomenon is known as LGS or “leaky gut syndrome.” The alcoholic intestinal wall ”leaks” larger than normal proteins from the gut into the bloodstream. Antibodies naturally attack these ”foreign bodies” like they would a bacteria or virus as they have no business floating around the bloodstream.

Alcohol Induced Inflammation

The constant antibody attack up-regulates the immune system producing excessive levels of inflammatory cytokines and excessive levels of circulating histamine. The classic “red flush” on the alcoholic’s face is derived from excessive histamine levels. Most psychiatrists are unaware that Histamine is an excitatory or “electrifying” brain chemical. Histamine has a similar chemical structure to dopamine and it can activate the brain’s dopamine receptors causing excessive electrical current throughout the brain – this is a common cause of anxiety and insomnia in Americans.

With knowledge of the Gut – Brain connection, especially the classic alcohol induced changes in brain chemistry revealed through Dr. Sponaugle’s research, we can better explain why – the more an alcoholic drinks – the more “over electrified” their brain becomes – the more they must drink – to quiet their brain!!

Jennifer’s Relapse

Jennifer relapsed to alcohol just four days after leaving alcohol rehab because her Arizona rehab doctors failed to correct multiple biochemical issues that made her crave alcohol so badly that she was planning her next drink in rehab. Even with the assistance of a SPECT scan, they failed to properly diagnose multiple biochemical imbalances that must be corrected immediately to stop alcohol craving.

They had learned from my colleague, Daniel Amen of the Amen Clinic, that increasing serotonin activity would most likely calm Jennifer’s overactive deep limbic system, the brain region that was most significant in causing Jennifer to self-medicate with the GABA effect of alcohol.

Placing Jennifer on Lexapro, an SSRI, serotonin enhancing anti-depressant, failed to calm her anxious brain leaving her with alcohol craving because:

Jennifer’s menopausal estradiol levels were too low for her serotonin receptors to remain open, they were not available for increased serotonin activation from Lexapro.

Alcoholic patients like Jennifer produce no serotonin in their intestinal factories, therefore her brain’s serotonin storage units were empty. Drugs like Lexapro do not assist patients in making one molecule of serotonin, they work with available serotonin in the brain, in Jennifer’s case, there was very little serotonin availability for Lexapro to work with.

In alcoholic patients, Candida mycotoxins and Klebsiella endotoxins block the first step, the gut step, of serotonin production, the gut conversion of tryptophan into 5-Hydroxytryptophan. 5-HTP undergoes conversion to serotonin inside the brain’s serotonin factories. Normally, the brain’s serotonin factories receive a healthy supply of 5-HTP from the gut, however, in the alcoholic gut, tryptophan is converted into a toxic chemical called kinurenic acid.

Jennifer’s rehab doctors failed to treat the localized dopamine deficiency in Jennifer’s pre-frontal cortex. The estradiol dropout Jennifer suffered with menopause exacerbated her inherited dopamine deficiency – Estradiol enhances dopamine production and prevents the breakdown of dopamine.

Estradiol enhances tyrosine hydroxylase, the enzyme that converts tyrosine into dopamine and estradiol inhibits monoamine oxidase, the enzyme that metabolizes dopamine.

Furthermore, Jennifer, like all alcoholics, suffered severe Vitamin D deficiency and iron deficiency. Both Vitamin D and iron are necessary co-factors for tyrosine conversion to dopamine.

Alcohol stimulates a temporary dopamine surge from brain storage units, with decreased dopamine activity, Jennifer would have craved the dopamine effect of alcohol more than she would have in her premenopausal life.

Jennifer’s rehab doctors failed to diagnose her severe testosterone deficiency and her alcohol induced hypothyroidism. Testosterone in both sexes and Thyroid T3 hormone are necessary for dopamine receptivity in the dopamine driven pleasure [reward center]. The combination of alcohol induced hypothyroidism and menopausal dropout of testosterone and estradiol caused diminished Dopamine D2 activity and subsequent depression that responds to a temporary dopamine hit from alcohol.

Jennifer’s rehab doctors failed to perform extensive hormonal testing and therefore failed to diagnose her alcohol induced adrenal insufficiency. The alcoholic gut toxins are neurotoxins, they readily travel from the gut to the brain and shut down pituitary function.

The reduced production of pituitary hormones TSH [thyroid stimulating hormone] and ACTH [adrenocorticotropic hormone] cause subsequent deficiencies of thyroid hormone, Cortisol, DHEA and Adrenaline. This produces physical fatigue, Jennifer felt like she had a 20 pound cement block attached to each leg. The “dopamine hit” derived from drinking alcohol gave her fake energy.

At Florida Detox & Wellness Institute, we give our addicted patients a comprehensive Brain Wellness Program that provides evaluation of 250 biochemicals. We optimize and balance all brain chemistry and hormonal issues immediately, this stops alcohol and drug craving.

As of this writing, Jennifer is doing amazing well. She has chosen to continue follow up for through our anti-aging/wellness program. She has now been alcohol free for 2 years and denies any craving for alcohol! She is back on the tennis court and her husband is a happy man!

Read Jennifer’s full story here, and visit our blog to read more patient stories.

Our Safe and Painless Alcohol Detox Protects the Brain

We do not allow our patients to suffer any of the typical alcohol withdrawal symptoms associated with alcohol detox. No tremors, no twitching, no spasms, no mini seizures. These alcohol withdrawal symptoms are forbidden in our detox unit because they are indicative of excessive electricity that causes damage to the brain.

You have lost enough brain cells from chronic alcoholism, you can’t afford to lose more going through a dangerous alcohol detox. The loss of brain cells you have sustained from alcohol abuse already increases your risk of getting earlier Alzheimer’s Disease.

Fortunately, our Brain Wellness program has recently reversed Alzheimer’s Disease and is provided to our alcoholic patients at no additional cost. See our Alzheimer’s page under Wellness programs. We can heal brain damage derived from your alcoholism.

Our painless alcohol detox protects your brain from detox induced loss of brain cells.

Recent PET scan studies performed at the University of Toronto have revealed that the old fashioned “shake and bake” alcohol detox performed at most detox centers destroys more brain cells than continuous alcoholism. The University doctors found that the brain of patients who drank alcohol without once stopping in a ten year period sustained better brain volume than the patients who went through alcohol detox once a year.

During your alcohol detoxification, we begin rejuvenation therapy with my intravenous treatment protocol for healing the brain. We replace vitamins, minerals, amino acids and other nutrients that are commonly deficient in alcoholic patients. This aggressive restoration treatment facilitates a much faster recovery and enhances our ability to prevent relapse to alcohol.

Alcohol patients who simply undergo detox, have so many hormonal and biochemical deficiencies, they feel terrible unless they start drinking again. This is called the “dry drunk” syndrome. They might not be drinking, but they feel miserable.

Our three-month alcohol treatment program is not mandatory, it is provided at no extra cost to our alcoholic patients. Most of our patients come back for several outpatient appointments, even if they live in California, because they benefit so much from our advanced anti-aging and wellness treatment. Most of our patients look ten to fifteen years younger after just four to six weeks of this program

Below is a list of just a few biochemical causes of alcohol craving:

• Attention Deficit Disorder
• Anxiety Disorders
• Depression
• Insomnia
• Nutritional Deficiencies
• Hormonal Imbalance
• Hidden Food Allergies
• Allergies to the wheat or corn in the alcohol itself
• Hypoglycemia
• Systemic Yeast and Fungal Overgrowth
• Mold Toxicity
• Lyme’s Disease
• Bartonella
• Babesia
• Epstein Barr
• etc.

If you have already been to a rehab center for alcoholism, you know they did not even look for most of these.

We do not discount the fact that patients use alcohol to anesthetize emotional pain, however, we have never treated an alcoholic patient who did not also have many treatable biochemical issues that also caused alcohol craving. We refer those alcohol patients who are suffering severe emotional pain to some of the best counselors in America.

Isn’t it time you chose scientific alcohol treatment that stops your alcohol craving?

(888) 775-2770

Jennifer’s history of alcohol abuse tells the real story.

http://www.canlyme.com/alz.html

Judit Miklossy

University Institute of Pathology, Division of Neuropathology,
University of Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland

The aetiology of Alzheimer’s disease (AD), which affects a large proportion of the aged population is unknown and the treatment unresolved. The role of beta amyloid protein (ßA4), derived from a larger amyloid precursor protein (APP) in AD is the subject of intense research. Here I report observations that in 14 autopsy cases, with histopathologically confirmed AD, spirochetes were found in blood and cerebrospinal fluid and, moreover, could be isolated from brain tissue. Thirteen age-matched control cases were without spirochetes. Reference strains of spirochetes and those isolated from brains of AD patients, showed positive immunoreaction with monoclonal antibody against the ß amyloid precursor protein. These observations suggest that spirochetes may be one of the causes of AD and that they may be the source of the ß amyloid deposited in the AD brain.

EMPHASIS ADDED

Dr. Sponaugle has developed a protocol for Alzheimer’s Treatment that has completely reversed the the Alzheimer’s changes on the PET SCAN of his most recent Alzheimer’s patient, Douglas.

Doug had his first PET scan February 2010 which confirmed his neurologist’s clinical diagnosis of Alzheimer’s Disease. Dr. Sponaugle began treating Doug in February of 2011.

Doug’s repeat PET scan reveals complete reversal of the Alzheimer’s pattern seen on his first PET scan. This radiological report correlates with Doug’s remarkable clinical improvement. Doug no longer has any Alzheimer’s symptoms. See the Radiologist’s reports, both before and after Dr. Sponaugle’s Alzheimer’s treatment before you watch the video testimonies of Doug and his wife Dottie.

Doug’s PET Scan reports, before and after Dr. Sponaugle’s Alzheimer’s Treatment

Complete Reversal of ALZHEIMER’S PATTERN

click for larger view

Watch the three video testimomies below. They demonstrate Doug’s progressive reversal of Alzheimer’s Disease!

Part 1 – February 2011

Part 2 – March 2011

Part 3 – May 2011

Dr. Sponaugle acquired the expertise needed to promote healing of Alzheimer’s brains from 13 years of treating brain damage in 6,000 addicted and non addicted patients. Those 6,000 patients suffered from various causes of brain damage including Drug Abuse, Alcohol Abuse, Industrial Solvent Toxicity, Mold Toxicity, Lyme Disease and Traumatic Brain Injury. Dr. Sponaugle’s protocol for healing Alzheimer’s consists of oral and intravenous treatment and is based on thousands of hours of his personal research. has proven he can promote healing of the Alheimer’s brain if we;

The brain’s electrical function can be measured via QEEG, qualitative EEG studies, via SPECT scans which measure brain blood flow that correlates directly with the brain’s electrical activity and via PET scans that measure glucose metabolism in the brain. The hallmark of Alzheimer’s Disease is slowing of electrical activity on EEG, marked reduction of brain blood flow on SPECT imaging and markedly reduced metabolism on PET imaging.

Dr. Sponaugle has noticed that SPECT scans of his Alzheimer’s patients have similarities to SPECT scan changes derived from OxyContin abuse and Methadone addiction. See comparison of SPECT scans below. In comparison, Doug’s Alzheimer’s scan and the Methadone Addiction scan both demonstrate severe reduction of blood flow throughout the brain. Remember, reduced blood flow in the brain means deprivation of oxygen and nutrients and less washout of brain toxins.

Notice the Methadone brain suffers from more severe loss of blood flow than Doug’s Alzheimer’s brain. Doug’s brain scan reveals an additional “localized” reduction of blood flow in the front of his brain, this is where he was hit with a large pipe from a job site accident.

Doug and his wife Dottie, came to Florida Detox & Wellness Institute in February 2011 seeking Dr. Sponaugle’s help with Alzheimer’s. Doug was not officially diagnosed with Alzheimer’s Disease until February of 2010, however, he had ten years of frightening progression of Alzheimer’s symptoms; memory loss, cognitive decline, depression and confusion.

Doug’s neurologist made a clinical diagnosis of Alzheimer’s and confirmed it with PET imaging in February 2010. The PET scan confirmed moderate diffuse hypometabolism in the parietal lobes and the temporal lobes, this pattern on PET scan is consistent with classic Alzheimer’s Disease. A moderate reduction of metabolism as seen on Doug’s PET scan means severe loss of brain function!!

Doug enrolled in Dr. Sponaugle’s program for Alzheimer’s Treatment program and within three weeks, Doug regained most of his memory and his cognitive function. Prior to Dr. Sponaugle’s Alzheimer’s treatment, Doug could no longer safely drive his car, after just three weeks of treatment, Doug could not only drive his car again, he took his boat out in the Gulf of Mexico for the first time in years.

After just three weeks of Dr. Sponaugle’s Alzheimer’s treatment, Doug, a man who couln’t safely drive around his hometown of Port Charlotte, Florida, drove 16 hours to Washington, DC for the SPECT scan Dr. Sponaugle ordered from the AMEN clinic. We will never know how much worse his scan would have looked before undergoing the three weeks of Dr. Sponaugle’s treatment.

After just six weeks, Dottie felt Doug had regained the brain function and physical energy [ability] he had in his thirties. See the three videos of Doug and Dottie that demonstrate his progression over several weeks.

ALZHEIMER’S DISEASE

The hallmark of Alzheimer’s disease is memory loss, confusion and decreased cognitive skills. Patients who suffer years of Oxycontin abuse, Heroin abuse and Methadone addiction suffer many of the same symptoms, in fact, patients suffering opiate addiction often have worse looking brains as seen on SPECT brain imaging than Alzheimer’s patients!

When Dr. Sponaugle attempts to heal the brain of an Alzheimer’s patient, his goal is to increase blood flow in their brain in a similar fashion as he does for the OxyContin abuse and alcohol abuse patient. The markedly reduced cerebral [brain] blood flow is demonstrated on SPECT brain imaging as the holes seen below. When the blood flow in any brain region is less than 50 percent of normal, it is represented as a hole on the scans seen below.

Below you can study the SPECT brain images of a healthy brain as compared to the Methadone addiction brain and that of Dr. Sponaugle’s Alzheimer’s patient, Doug.

Methadone Brain vs Healthy Brain

Doug's Alzheimer Brain with Additional Frontal Lobe Head Trauma - During First week of Dr. Sponaugle's Treatment

Methadone Damaged Brain Compared to Deborah's Brain with Improved Bloodflow after only 6 Weeks of Treatment with Dr. Sponaugle!

Dr. Sponaugle’s clinical research has proven that the brains of Alzheimer’s patients suffer from many of the same biochemical deficiencies [brain chemicals, hormones and amino acids] as do the brains of patients suffering from Methadone Addiction and Oxycontin abuse. Dr. Sponaugle’s analysis of brain neurotransmitters in Alzheimer’s patients proves they suffer from multiple brain chemical deficiencies, yet, American neurology is focused on just one, acetylcholine.

Acetylcholine is a “memory” chemical, however, there are many other important brain chemicals that affect memory, cognition and the overall electrical activity and performance of the brain. Aricept is a medication that enhances acetylcholine activity in the brain, however, Dr. Sponaugle’s Alzheimer’s patients have all been prescribed Aricept by their neurologist, yet, they received little if any benefit from the medication.

The majority of the brain’s neurotransmitters [chemical messengers] can not activate their respective brain receptors without optimal levels of specific hormones that control their receptivity.. Dr. Sponaugle’s research has proven that Alzheimer’s patients suffer from numerous hormonal deficiencies that disallow neurotransmitter – receptor activation.

The brains of Alzheimer’s patients suffer from excessive inflammation and often from neuron demyelination both of which are derived from decades of accumulating neurotoxins. Dr. Sponaugle’s Alzheimer’s research suggests that those patients who suffer Alzheimer’s symptoms earlier in life are usually those suffering from toxic overload, excessive accumulation of fatty toxins in their fatty brain, the brain is 60 percent fat. Harmful lipophillic or fatty neurotoxins displace good fats like Omega-3 from brain tissue.

Doug’s Story – Parkinson’s / Alzheimer’s

Dr. Sponaugle diagnosed my husband with chronic, but active Lyme disease, mold toxicity and Benzene toxicity. As it turns out my husband has special genetics that prevent him from fighting these things like other people, Dr. Sponaugle suspected these things and numerous other problems when he first met Doug, none of our other doctors had ever tested for or discovered these problems.

After Dr. Sponaugle’s first IV treatment, my husband felt that he could focus better. After the second treatment, he was no longer shuffling his feet. His driving skills improved immediately and within 3 weeks, our boat left the driveway and was put in the water for the first time in three years. My husband no longer wants to spend his days sleeping; hes too busy socializing. He now thinks nothing of driving three or four hours to visit one of our children.

Dottie and Doug

My husband’s other doctors are amazed at his progress. He no longer has a flat affect. His eyes are bright and hes eager to learn or relearn things that hes been unable to understand for years.This week, we bought him an IPAD so he can learn email, facebook and how to navigate the internet.

Dr. Sponaugle’s staff is very friendly and caring. Additionally, we’ve met many wonderful people fellow patients and their families from all over the country. While we’re all together in the IV drip room, we get talking and sharing our stories. These people are as grateful as we are for the wonderful work being done there. While we sometimes have to wait to see Dr. Sponaugle, we understand that he is spending time with other patients. When we do get to see him, we never feel shortchanged. He gives us all the time we need.

Without the care my husband has received from Dr. Sponaugle, we would still be living life in the difficult Alzheimer’s world. Instead, we have a wonderful, active life and a bright future. Thank you, Dr. Sponaugle, for your caring and the miracles you are performing in peoples lives.”

ED’S STORY: Stroke – Alzheimer’s – Cognitive Coma

Dr. Sponaugle recently treated a 94-year-old gentleman from Clearwater, Florida. Ed lost all his mental cognition lapsing into a cognitive coma following his second stroke at age 92. His family had heard about Dr. Sponaugle’s work with brain disorders and asked if he could possibly help Ed regain his cognition.

After just 11 days of Dr. Sponaugle’s Alzheimer’s treatment, Ed woke up from his cognitive coma of two years. This occurred in Dr. Sponaugle’s office in the presence of his nurse, Dennis, and Ed’s family. Ed immediately recognized his wife and his 58 year old son. He began singing beautiful Italian songs.

In his two year state of a cognitive coma, Ed had required three caretakers, each taking 8 hour shifts to cover a 24 hour day. They had to to dress Ed and feed him, Ed’s night caretaker of two years had no idea he even spoke Italian, she was overtaken with joy. It was a Hallmark moment.

Dr. Sponaugle’s treatment not only brought Ed out of a cognitive coma, it increased the pumping function of Ed’s heart by 50 percent. This was enough to bring Ed out of severe heart failure which was subsequently causing kidney failure. The improvement in Ed’s cardiac output was documented by Ed’s cardiologist, Dr. Kalani, with ultrasound of the heart [Echo-cardiogram]. The test proved that Ed’s “ejection fraction” had increased from 20 percent to 30 percent, a 50 percent improvement.

Before Dr. Sponaugle treated Ed, his urinary creatinine was elevated indicating renal failure, after 11 days of Dr. Sponaugle’s treatment, his creatinine went down from 2.0 to 1.1. This occurred because his kidneys were receiving much better delivery of oxygen via increased blood flow derived from his stronger heart.

Ed went into a cognitive coma after he suffered a second stroke at age 92. Ed could no longer speak, he became confused, disoriented, angry and frustrated. He could no longer communicate with his wife and he required 24-hour professional caretakers. He could not perform mundane tasks like dressing or going to the bathroom without his caretakers.

Ed’s neurologist and cardiologist had previously informed his family that Ed was only going to get worse and eventually would be totally bed ridden. After Dr. Sponaugle’s treatment, they were astonished with his transformation. Ed no longer had leg swelling, pedal edema and foot pain from all the swelling in his feet.have disappeared. Ed no longer had to sleep sitting upright nor did he fear drowning when he went to bed.

Even though Ed had three physicians, an internist, a cardiologist and a neurologist, they failed to provide the comprehensive wellness treatment needed to strengthen his heart or “wake up” his brain. Their medical training was the same as Dr. Sponaugle’s, American medicine does not teach optimization of brain and body biochemicals to improve function, Dr. Sponaugle has taught himself how to integrate natural and western medicine with modern brain science, this turns back the hands of time and restores physical and mental health.

Rick Sponaugle MD

Founder, Florida Detox & Wellness Institute

Stroke and Cerebrovascular Disease

Stroke Prevention

Cerebrovascular disease, including stroke, is the third-leading cause of death in the United States and a leading cause of disability among older Americans. Cerebrovascular disease occurs when the blood vessels supplying the brain with oxygenated blood are damaged or their function is compromised. If the blood flow is severely restricted, depriving the brain of adequate oxygen even briefly, a stroke can occur. It has been estimated that every 45 seconds, another American suffers from a stroke, often with debilitating consequences or even death. One in four men and one in five women over the age of 45 will suffer a stroke.

There are two main kinds of stroke. The most common, an ischemic stroke, occurs when an artery in the brain is blocked by a blood clot, usually because of atherosclerosis (the deposition of plaque on the inside of artery walls). Alternatively, a hemorrhagic stroke can occur when a portion of the arterial wall weakens and bursts. A stroke is a serious medical emergency that requires immediate medical attention. Time is a critical factor in stroke management: some experts now refer to strokes as “brain attacks” to stress the need for emergency treatment.

Researchers have conducted thousands of clinical trials searching for better ways to prevent and treat stroke victims. As a result, we have a robust knowledge of cerebrovascular disease, and we are learning more every day. As with atherosclerosis in the coronary arteries (coronary artery disease), the underlying cause of ischemic stroke can often be traced back decades, to early insults to the inner lining (endothelium) of the arteries that set a deadly chain reaction into motion. Now that they have identified endothelial dysfunction as a fundamental process of cardiovascular and cerebrovascular disease, along with the prime risk factors for endothelial dysfunction, such as high blood pressure and smoking, researchers are pursuing new therapies aimed at stroke prevention by improving the health of our arteries.

Stroke is primarily a condition of the elderly, mostly because of the cumulative effects of endothelial dysfunction, which can take decades to reach a crisis point. Nearly three quarters of all strokes occur in people who are over the age of 65, and the risk of stroke more than doubles every decade beyond the age of 55 (NINDS 2005).

Stroke is an insidious condition because of the nature of the anatomy of the brain. Heart disease is often preceded by a characteristic pain in the chest or arm (angina) or shortness of breath. These symptoms occur when the blood supply to the heart is temporarily reduced. The brain, however, lacks pain receptors, so temporary episodes of ischemia don’t cause pain. Although there may be warning signs, the first signal of atherosclerosis in the brain is often a stroke.

When blood flow to the brain is briefly disrupted, causing what is called a ministroke, the symptoms are similar to those of a stroke (vision and speech difficulty, limited paralysis) but not as severe, and they usually subside within 24 hours. In the past, physicians viewed ministrokes as relatively benign events, or “near misses.” Today, we understand that not only are they damaging in their own right because of the deprivation of blood to the brain, but the presence of ministrokes is a major warning signal. Any person suffering from suspected cerebrovascular disease should seek immediate medical supervision and comprehensive diagnostic testing to assess the likelihood of a stroke and take active steps to reduce the risk.

Kinds of Stroke

Strokes are caused either by an arterial blockage that reduces blood flow to the brain (ischemic stroke) or by a rupture in an artery that allows blood to spill into the surrounding area (hemorrhagic stroke). It is extremely important that the kind of stroke be identified as quickly as possible because each is treated differently. For example, if the stroke is caused by a blood clot (an ischemic stroke), drugs should be administered to help dissolve the clot. If, however, these drugs were administered to a person suffering from a bleeding stroke, the damage could be intensified because of increased bleeding (NINDS 2005).

Ischemic stroke. Ischemic stroke is responsible for 80 percent of all strokes (NINDS 2005). There are two kinds of ischemic stroke. The first, a thrombotic stroke, results from a blood clot (thrombus) forming in a vessel inside the brain and cutting off the blood supply to the tissues served by that vessel.

The second, an embolic stroke, occurs when a clot forms somewhere else in the body, breaks off, and travels to the brain. The clot can originate in a peripheral artery, in the heart itself, or in the arteries in the neck or brain. Among people with an abnormal heart rhythm called atrial fibrillation, clots can arise in the left atrium and travel through the left side of the heart and the aorta and into the brain. When the clot becomes lodged in the artery, the tissue beyond the blockage is starved of oxygen and begins to die.

Hemorrhagic stroke. The second category of stroke, hemorrhagic stroke, occurs when a vessel in or near the brain ruptures and leaks blood into the brain or surrounding tissues. In this case, the blood pushes against otherwise healthy brain tissue and compresses it. The increased pressure reduces blood flow into the area, and if the pressure becomes high enough, it can cause damage to brain cells. There are two primary kinds of hemorrhagic strokes, named according to the location of the bleeding (Stanford Stroke Center 2005):

• Subarachnoid hemorrhage occurs when blood floods the space between the brain and the skull.
• Intracerebral hemorrhage happens when an artery inside the brain ruptures, spilling blood into the surrounding brain tissue.

Hemorrhagic strokes are often caused by aneurysms, or weakened portions of the artery wall. An aneurysm may have no symptoms and go unnoticed for years. In many cases, the first sign of an aneurysm is a stroke.

Effects of Stroke

Strokes are so feared because of their debilitating effects. Even ministrokes have been shown to reduce cognitive function (Mosley TH Jr. et al 2005), and large strokes can have serious, life-altering and life-threatening consequences. Common effects from stroke include the following:

• Paralysis or weakness. Paralysis, weakness, and tiredness are the most common effects from stroke. These effects may involve one side of the body or just the face or an arm or leg. A survivor also may lose the ability to recognize the need to urinate or to control bladder or bowel muscles, which can result in not getting to the toilet in time. Constipation can also occur. Incontinence problems are usually temporary, but they can be emotionally distressing.
• Aphasia. At least 25 percent of all stroke survivors lose the ability to speak, write, or understand spoken or written language. This condition can improve with therapy.
• Spatial perception, thinking, and memory. Stroke can damage areas of the brain that control memory, spatial relationships, learning, and awareness. Survivors may have significantly shortened attention spans or find short-term memory problematic. They may lose the ability to learn new tasks, follow a set of instructions, make plans, or carry out actions in sequential steps.
• Mental health changes. Depression, personality changes, and trouble controlling emotions are common after stroke because of the debilitating emotional effect of the trauma. Strokes can also damage the frontal cortex and other parts of the brain involved with emotion. Poststroke depression usually responds well to antidepressant medications and psychological counseling (NINDS 2005).

Endothelial Dysfunction and Stroke Risk

Most strokes are caused by blood clots that form as a result of atherosclerosis (Gorelick PB 2002). Once known as “hardening of the arteries,” atherosclerosis occurs when the arteries become clogged with plaque deposits and the structure and function of the inner arterial wall (the endothelium) are compromised. If atherosclerotic plaque deposits become brittle and rupture, blood clots can form that lead to stroke. Scientists have spent decades unraveling the complicated biological processes that lead to atherosclerosis. We now understand atherosclerosis as a long-term disease, one that accelerates as we age, raising the risk of heart attack and stroke.

For many years, conventional science has depicted the arteries as pipes, often using plumbing analogies to describe procedures such as balloon angioplasty or endarterectomy, an operation in which plaque is stripped away from the linings of arteries. The problem with the plumbing analogy, however, is that the arteries are actually muscular, complex organs that play an active role in regulating blood pressure and other biological functions.

Arteries are composed of three layers. The outer layer is mostly connective tissue and provides structure to the layers beneath. The middle layer is smooth muscle and contracts and dilates to help blood flow and maintain blood pressure. And the inner layer is a thin layer of endothelial cells and provides a smooth, protective surface. Endothelial cells prevent toxic, blood-borne substances from penetrating the smooth muscle of the artery. They also respond to changes in blood pressure and release substances into the cells of the smooth muscle that help change the tone of the artery. Furthermore, endothelial cells secrete chemicals that provoke a protective response in the artery after an injury.

In the event an artery is injured, the endothelium signals smooth muscle cells to gather at the site of the injury. Endothelial cells also signal white blood cells to congregate on the injured vessel wall, provoking an immune response. As we age, however, the endothelium becomes leaky, allowing lipids and toxins to penetrate the endothelial layer into the smooth muscle cells. As a result, smooth muscle cells gather at the site of the injury, and the artery in turn loses some flexibility. In response, the endothelium signals white blood cells to congregate along the cell wall. The endothelium is further weakened by the pro-inflammatory immune response, in which leukotrienes and prostaglandins contribute to inflammation, which aggravates the abnormal smooth muscle tone of the arterial wall (Touyz RM 2005). Toxins soon begin to penetrate into the arterial wall. Inside the artery, lipids such as low-density lipoprotein (LDL) cholesterol and triglycerides accumulate and gradually become oxidized.

At this point, the atherosclerotic process has begun in earnest. In response to the oxidized lipids, the body mounts an immune response that causes more white blood cells to attack the fats, producing more inflammation within the arterial wall. In an attempt to heal the injury, smooth muscle cells begin to produce collagen to form a cap over the injury site. The mixture of oxidized lipids, white blood cells, and smooth muscle cells forms a plaque deposit. Over time, calcium accumulates on the deposit and forms a brittle cap. If this calcified plaque ruptures, a blood clot can form.

All the processes described above, in which the arterial wall is damaged and normal endothelial function is compromised, are collectively referred to as endothelial dysfunction. Risk factors that aggravate endothelial dysfunction include high blood pressure, smoking, elevated LDL and triglycerides, low levels of high-density lipoprotein (HDL) cholesterol, diabetes, elevated insulin levels, obesity, lack of exercise, and several recently identified risk factors, such as elevated levels of homocysteine and C-reactive protein. Each of these contributes to endothelial dysfunction of cerebral arteries and the subsequent increased risk of stroke.

High blood pressure, for example, is very strongly associated with stroke; in fact, high blood pressure is associated with about half of ischemic strokes. It is known that high blood pressure contributes to endothelial dysfunction. Cigarette smoke is another major risk factor because the smoke contains many toxins that contribute to endothelial injury, while homocysteine has been shown to cause the initial injury to the endothelium that begins the atherosclerotic process (Sainani GS et al 2002). Similarly, a Physician’s Health Study found that men in the highest quartile of levels of C-reactive protein (an inflammatory marker that signals inflammation somewhere in the body) had twice the risk of ischemic stroke of those in the bottom quartile (Ridker PM et al 1997). Other studies have found that C-reactive protein is a strong independent predictor of a reduced survival rate after ischemic stroke (Di Napoli M et al 2001).

If researchers can identify drugs or supplements that support healthy endothelial function, it may be possible to slow the relentless advance of atherosclerosis and reduce the risk of the most common kind of stroke. One common therapeutic focus is nitric oxide, which causes arteries to dilate and improves blood flow. A nutrient or drug that improves the production of nitric oxide may have the potential to reduce the risk of stroke or other atherosclerotic insults.

It also makes sense to modify as many other risk factors as possible, including high blood pressure, cholesterol, and even infection. Studies have linked certain common infections to increased stroke risk, including Chlamydia pneumonia, Helicobacter pylori, cytomegalovirus, and C Pneumonia (Winkelstein JA et al 2001; Meier CR et al 1999; Nieto FJ et al 1999). The first National Health and Nutrition Examination Survey (NHANES) found that periodontal disease, though treatable, is a risk factor (Wu T et al 2000). Other studies indicate that patients hospitalized with bacterial and viral infections had increased risk of stroke within one week of the infection, highlighting the importance of infection, even in younger people (Grau AJ et al 1995, 1998, 1999).

Stroke Screening: Advances in Technology

Although transient ischemic attacks are the most obvious warning signs of stroke, the risk of having a stroke can be gauged before an ischemic attack occurs. All that is required is diagnostic testing. Clearly, it is preferable to avoid a stroke through early intervention and preventive measures than to treat strokes that have already occurred.

In the past, the most accurate test to measure atherosclerosis was angiography. During this procedure, a catheter is threaded into the arteries and a special dye sensitive to x-ray is injected into the catheter. While this is an important test, it has some powerful limitations. First, it is invasive and therefore not practical as a widespread screening tool. Second, it can show the physician only the shadowy outlines of plaque inside arteries. It cannot measure the stability of the plaque or determine the health of the arterial wall.

Today, noninvasive imaging techniques are available to measure the health of the arterial wall and even determine the stability of the plaque deposits on the inside of the artery. Although these tests are most often used to diagnose existing strokes, they are also highly effective screening tools.

Advanced CT scanners, including a newly introduced 64-slice machine, are able to provide an unprecedented view of the arteries. No studies have yet been conducted on the value of this new technology in screening people for stroke risk. Older, 16-slice CT scanning is often recommended to evaluate the damage of ongoing strokes because of its specificity (Kirchhoff K et al 2002). CT scans, however, expose people to very high levels of radiation. For example, an average CT head scan exposes the body to as much radiation as 100 chest x-rays, or 243 days of natural background radiation, according to the European Commission’s Radiation Protection Report, conducted in 2000.

Perhaps the most widely used screening tool for stroke is the carotid ultrasound, which provides physicians with valuable information on the health of carotid arteries. Using widely available and relatively inexpensive ultrasound technology, physicians can detect the degree of blockage in the carotid arteries and measure the thickness of the intima-media. The well-known Rotterdam study showed that if carotid intima-media thickness is greater than 1 mm, the risk of stroke is increased even if no arterial plaque is present (Hollander M et al 2003). The information obtained from ultrasound screening can be used to identify people at high risk of atherosclerosis.

A number of blood tests also measure vascular health and may help identify people at high risk of stroke. Life Extension believes that people should have at least annual blood tests for homocysteine, C-reactive protein, and fibrinogen, in addition to the more well-known tests, such as those for cholesterol and triglycerides. Homocysteine, C-reactive protein, and fibrinogen each have been shown to be elevated among people at risk of stroke.

Reducing Homocysteine to Lower Stroke Risk

At the 2001 meeting of the American Stroke Association, researchers reported studies showing that increasing levels of homocysteine are associated with elevated stroke risk. One of these presentations was a meta-analysis of 15 published studies and showed that mild to moderate elevations in homocysteine were independently associated with an astounding 86 percent increase in the risk of stroke (Kelly PJ et al 2000).

Folic acid and other B vitamins help decrease homocysteine concentrations. The metabolism of homocysteine has been linked to several vitamins, but particularly folic acid (folate), B6, and B12 (Schwammenthal Y et al 2004). The Vitamin Intervention for Stroke Prevention trial, among many studies, showed that homocysteine levels decreased and risk of stroke, death, and other coronary events fell by 21 percent in patients who received high doses of vitamin B12 (Spence JD et al 2005).

Another well-designed study found that giving B vitamins within 12 hours of an ischemic stroke reduced oxidative damage and the tissue inflammation marker C-reactive protein, regardless of homocysteine levels (Ullegaddi R et al 2004). Studies have also found that vitamin B6 alone is strongly associated with lower risk of cerebrovascular disease (Kelly PJ et al 2003).

Other studies show that individuals with homocysteine levels elevated by 25 percent have increased risk of stroke of 11 percent. A meta-analysis of 20 studies reported that elevated homocysteine levels increased risk of ischemic heart disease by 32 percent and risk of stroke by 59 percent (Wald DS et al 2002). Multiple studies have shown folate to prevent endothelial dysfunction even in people with normal levels of homocysteine, high cholesterol, diabetes, and heart disease (Moat SJ et al 2004), which emphasizes the importance of the B vitamins (He K et al 2004, Bazzano LA et al 2002)

C-Reactive Protein and Fibrinogen

There is a clear association between elevated levels of C-reactive protein and fibrinogen and the incidence and severity of stroke. Also at the 2001 American Stroke Association meeting, researchers presented evidence that elevated C-reactive protein doubled or tripled the risk of stroke (Kelly PJ et al 2000). Another presentation showed that in those who have a major stroke, higher levels of C-reactive protein portended a high likelihood of having another vascular event, such as a heart attack or stroke, or of dying within the following year. Stroke patients with the highest C-reactive protein levels were nearly 2.4 times more likely to experience death or a vascular event within the next year than were patients with the lowest levels (Di Napoli N et al 2001).

Similarly, the Physician’s Health Study found that apparently healthy men with the highest C-reactive protein levels had twice the risk of stroke, three times the risk of future heart attack, and four times the risk of future peripheral vascular disease (Ridker PM et al 1997). The Women’s Health Study reported that C-reactive protein was the single strongest predictor of future vascular risk (Ridker PM et al 1998).

Elevated levels of fibrinogen are also associated with increased risk of stroke. Fibrinogen is a protein produced by the liver. It circulates in the blood and helps stop bleeding by helping blood clots form. Today’s standard laboratory reference range for fibrinogen is between 193 and 423 mg/dL. That means according to conventional standards, fibrinogen levels as high as 423 mg/dL are acceptable.

However, a study reported in the Journal of the American Medical Association found that no matter what a patient’s level was within the range tested (between 250 mg/dL and 562 mg/dL), an increase of 100 mg/dL was associated with a significantly increased risk of heart disease and stroke (Danesh J et al 2005). Another study found that those with high fibrinogen levels, above 343 mg/dL, had a twofold increase in the risk of heart attack (Ma J et al 1999). Fibrinogen levels can be reduced by taking dietary supplements such as fish oil and vitamin C and by lowering homocysteine.

Responding to a Stroke: Speed Matters

Most of the damage from a stroke occurs within 24 hours following the event, so it is crucial that people get adequate treatment as fast as possible to reestablish blood flow and limit the damage. If stroke-like symptoms last for more than 10 to 15 minutes or worsen, call 911 without delay even if it is unclear whether a stroke has occurred (NINDS 2005).

Once a patient has arrived at the hospital, physicians will quickly seek to determine what kind of stroke (ischemic or hemorrhagic) occurred, then take steps to treat it. Diagnostic imaging tests are usually performed as soon as possible to determine the kind of stroke.

Treatment of ischemic stroke. The goal of acute therapy in ischemic stroke is to dissolve the blood clot as rapidly as possible (a process called lysis). Studies show that when thrombolytic (clot-busting) agents are administered within three hours of symptom onset, they can dramatically decrease damage (Burger KM et al 2005). These drugs are still effective if given within 4.5 hours of the stroke (Davalos A 2005). Unfortunately, however, most stroke patients do not receive the appropriate thrombolytic agent quickly enough (Burger KM et al 2005; Davalos A 2005).

The most common thrombolytic agent used is tissue plasminogen activator. It is typically administered intravenously, and newer methods using ultrasound-enhanced delivery promise to make this drug even more effective (Davalos A 2005).

After stroke, there is a significant risk of a repeat stroke. To help prevent secondary strokes, people may be prescribed anticoagulant therapy, including low-dose aspirin or long-term warfarin (Coumadin®) therapy, or antiplatelet therapy (such as Plavix®).

• Anticoagulants. These drugs work by preventing clot growth or preventing new clots from forming. Warfarin is the most common example. It is often used when a patient’s doctor suspects that a blood clot has originated in the heart and traveled to the brain and lodged in a vessel, blocking blood flow and causing an embolic stroke. Anticoagulants are not indicated when there is increased risk of bleeding or in patients with uncontrolled high blood pressure (NINDS 2005).
• Antiplatelet agents. Antiplatelet agents work by preventing blood platelets from sticking to each other and forming a clot. Common examples are aspirin, dipyridamole, and clopidogrel. They are also often used to reduce the risk of stroke in individuals who have had a transient ischemic attack or to decrease the risk of a second ischemic stroke.

For more information on preventing blood clots, see the chapter titled Blood Clot Prevention.

Treatment of hemorrhagic stroke. Acute treatment of hemorrhagic stroke focuses on surgery and medications. Surgical procedures can help alleviate the damage (hematoma), but the condition of the patient before surgery is critical to the recovery rate. People who are conscious and have small blood clots often improve without surgery. But people in comas, who have large clots, do very poorly, regardless of treatment approach (National Stroke Association 2005)

After the acute treatment, medications may be prescribed to control blood pressure, which is a major risk factor for hemorrhagic stroke (Clarke CRA 1998). Prescription medications for lowering blood pressure include diuretics, calcium channel blockers, beta blockers, ACE inhibitors, and others. For more information on natural ways to lower blood pressure, see the chapter titled High Blood Pressure.

Stroke Prevention

Stroke prevention is a subject of much debate. Approximately 25 percent of people who recover from a first stroke will have a second within five years. While the chance of death and disability increases with each stroke, risk of another stroke appears to be greatest within the first year (National Stroke Association 2005).

Using measurements such as the degree of artery occlusion (how much of the carotid artery is blocked by atherosclerotic plaques), medical experts have sought to establish firm guidelines to help physicians choose between the various options, including medication, angioplasty, and surgery. Common prescription drugs used to help prevent stroke include antihypertensive agents (Gorelick PB et al 1999; Goldstein LB et al 2001), cholesterol lowering agents (statins), and antiarrhythmics to help control irregular heartbeats that might contribute to stroke risk. Angioplasty is a procedure in which a balloon is threaded into the artery and inflated rapidly, crushing the plaque against the arterial wall and opening the artery. The most common surgery used to prevent stroke is called carotid endarterectomy, in which the surgeon opens the arteries in the neck and strips away the inner lining of the artery.

While these strategies have been shown to work in specific circumstances, a common flaw also unites them: they are often used only after stroke risk has reached an unacceptable level. Life Extension prefers a much more proactive approach. By using advanced early screening tests to determine risk, then taking action to improve endothelial function and reduce blood risk factors (such as homocysteine and fibrinogen) and blood pressure, Life Extension seeks to maintain the lowest possible risk profile.

Diet. Multiple studies have found that a diet high in fruits and vegetables lowers risk of cerebrovascular disease and both ischemic and hemorrhagic stroke (Gariballa SE 2000; Sauvaget C et al 2003). Two major reviews recommended that public health policy promote increased dietary intake of antioxidant vitamin C, beta-carotene, vitamin E, B vitamins (including folate), potassium, calcium, magnesium, vitamin D, fiber, and omega-3 fatty acids to reduce risk of stroke (Gariballa SE 2000; Johnsen SP 2004). These vital nutrients can also be obtained through dietary supplements in conjunction with a healthy diet.

Nutritional Support for Healthy Arteries

Nutritional therapy in cerebrovascular disease associated with atherosclerosis has several interrelated goals. These include reversing endothelial dysfunction with nutrients that stimulate endothelial nitric oxide production, reducing inflammation, enhancing and restoring cerebral blood flow, and providing antioxidant support to reduce the level of damaging free radicals. A number of nutrients have been studied that often accomplish several of these goals.

The following nutrients protect the endothelium:

• L-arginine. L-arginine is a basic amino acid found in many proteins and is essential to growth and maintenance in all vertebrates. There is evidence that L-arginine plays a major role in maintaining blood vessel dilation and reducing blood pressure, a major risk factor for stroke. L-arginine helps lower blood pressure by serving as a precursor to nitric oxide, which helps keep blood vessels dilated and blood flowing easily (Chionglo BM et al 2006; Boger RH et al 2005).In an animal model of stroke, L-arginine was shown to induce an endothelium-dependent increase in cerebral blood flow (Willmot M et al 2005). Among humans, intravenous L-arginine has been shown to alleviate all stroke-like symptoms if administered within 30 minutes of their onset (Koga Y et al 2005). Another study showed that intravenous L-arginine given to patients undergoing carotid endarterectomy surgery was able to reduce the number of embolic signals (restrictions in blood flow) for up to 24 hours after the surgery (Kaposzta Z et al 2001). Although these results are encouraging, oral L-arginine has not been studied in human stroke patients—although human studies have been conducted in heart attack patients and patients with cardiovascular disease.While the association between L-arginine and nitric oxide is clear, a few newer studies have suggested that supplemental L-arginine alone may not boost nitric oxide among patients who recently had a heart attack. One study from Johns Hopkins Medical Institutions in Baltimore was stopped after researchers found an increased risk of death in heart attack patients taking L-arginine. There are several possible reasons for this, including the important point that nitric oxide can generate free radicals. By generating production of nitric oxide, L-arginine can raise free radical levels. Life Extension, however, notes that studies questioning L-arginine’s effectiveness failed to provide the necessary antioxidants to counteract any elevation in free radicals caused by the supplement. Thus, Life Extension believes that any person taking L-arginine to lower blood pressure and improve blood flow should also take antioxidants, such as vitamin C and vitamin E.
• Acetyl-L-carnitine. Acetyl-L-carnitine is a derivative of carnitine. It is involved in the transport of fatty acid across the cell membrane, and it is used as energy in the mitochondria of the cell (Rebouche CJ 2006). It also provides the acetyl component for the synthesis of acetylcholine, an important neurotransmitter. One study has shown evidence that among stroke patients, acetyl-L-carnitine has a beneficial effect on abstract and concrete thinking and memory. The study concluded that acetyl-L-carnitine possesses antioxidant activity that offers protection against lipid peroxidation (Suslina ZA et al 2003). Two other studies reported that large doses of intravenous acetyl-L-carnitine significantly improved cerebral blood flow in patients with chronic cerebrovascular disease who had experienced ischemic stroke (Postiglione A et al 1991, 1990).
• Propionyl-L-carnitine. Like acetyl-L-carnitine, propionyl-L-carnitine plays an important role is fatty acid oxidation. Research has shown that propionyl-L-carnitine can help protect against endothelial dysfunction. One study in human endothelial cells showed that the carnitine derivatives stimulate the production of nitric oxide in the endothelium, which has an antioxidant, antiproliferative, and anti-inflammatory effect (Calo LA et al 2006). Another study found that propionyl-L-carnitine stimulated nitric oxide’s ability to relax hypertensive arteries in rats (Bueno R et al 2005).

The following nutrients enhance cerebral blood flow, reduce blood pressure, and reduce the size of stroke lesions:

• Vinpocetine. Vinpocetine has been widely studied for its ability to restore blood flow to the brains of stroke victims. It appears to have multiple effects that interfere with the ischemic cascade. Studies have shown that it reduces the depletion of adenosine triphosphate, which is the main cellular energy source, and functions as an antioxidant (Hadjiev D 2003; Vas A et al 2002). Recently, researchers have found that high-dose, intravenous vinpocetine (at doses up to 70 mg daily) is able to restore blood flow to the brain and reduce the size of ischemic stroke lesions, leading several researchers to identify vinpocetine as a potential therapy for the acute treatment of ischemic stroke (Szilagyi G et al 2005; Szapary L et al 2003; Dezsi L et al 2002). The protective effects are most pronounced in areas of the brain with the highest uptake (Szilagyi G et al 2005). These studies build on previous work showing that oral vinpocetine is also effective in enhancing cerebral blood flow (Dezsi L et al 2002).
• CDP-choline. CDP-choline is a chemical compound present in a wide array of foods. It plays a life-sustaining role in the normal function of all cells and the structural integrity and signaling capacity of cell membranes, and it moves fats in and out of cells throughout the body (Zeisel SH et al 2006). More than 70 countries, including Japan, use CDP-choline as a prescription drug to treat stroke (Adibhatla RM et al 2005). It appears to have a neuroprotective and reparative effect on cerebral ischemic lesions, reducing the size of lesions during 12 weeks of treatment (Warach S et al 2000). Several additional studies indicate that CDP-choline leads to significant decreases in lesion size and can be used safely in acute stroke treatment (Clark WM et al 1997; Tazaki Y et al 1988). Regrettably, some U.S. studies failed to demonstrate efficacy, and the Food and Drug Administration did not approve it as a drug.
• Potassium, calcium, and magnesium. Potassium can help lower blood pressure, decreasing risk of cerebrovascular disease and stroke (Sacks FM et al 2001; Suter PM 1999). Evidence has emerged that a balance of potassium, calcium, and magnesium may reduce platelet aggregation and improve insulin resistance. Other studies have shown that combining magnesium and calcium with potassium is more effective than any one of these supplements alone in reducing blood pressure, atherosclerosis, and risk of stroke (Ahsan SK 1998; Sacks FM et al 2001; Broadhurst CL 1997; Ravnskov U 1998; Gillman MW et al 1997; Ascherio A et al 1997; Tavani A et al 1997; Appel LK et al 1997).
• Vitamin D. There is evidence from clinical trials that vitamin D may play a modest role in blood pressure control and insulin metabolism, both important in slowing the progression of atherosclerosis and reducing risk of stroke (Dakshinamurti K et al 1996; Lind L et al 1995; Boucher BJ 1998). A recent study also showed that deficiencies in vitamin D and flavonoids may predict heart attack and stroke (Marniemi J et al 2005). This new finding is relevant because the NHANES III study, funded by the National Institutes of Health, estimated that 42 percent of African American women between 15 and 49 years of age and 32 percent of white men and women are vitamin D deficient. The overall average increases to 50 percent in the over-fifty population, and vitamin D deficiency is much higher than that in older people, who have decreased capacity to produce vitamin D from exposure to sunlight (Holick MF 2006).

Omega-3 fatty acids are another important nutrient for stroke victims and those at risk of stroke because of their ability to reduce inflammation. They are found in the oil of cold-water fish and in flaxseed oil. Most people get too much pro-inflammatory omega-6 fatty acids in their diet but not enough omega-3 fatty acids to balance the omega-6. The balance is essential in regulating blood pressure and also in reducing inappropriate platelet aggregation, inflammation, LDL, and other atherosclerosis risk factors (Knapp HR et al 1989; DeBusk RM 2000).

Randomized clinical trials have found that patients with high omega-3 fatty acid intake experienced decreased incidence of stroke (He K et al 2002; Jeerakathil TJ et al 2001). Omega-3 intake may also slow the progression of atherosclerosis (Kris-Etherton PM et al 2005). One study found that eating coldwater fish as little as once per month reduced risk of ischemic stroke (He K et al 2002). American Stroke Association data indicate that individuals may not get enough omega-3 fatty acids through diet alone; the association suggests that individuals who don’t should consider taking a supplement. Those who have high levels of triglyceride (blood fat) may need larger doses of fish oil supplements (more than 4 g daily) than normally recommended for general prevention purposes (Kris-Etherton PM et al 2005).

The following nutrients are antioxidants:

• Coenzyme Q10. Coenzyme Q10 (CoQ10) is a powerful antioxidant found in the energy-producing center of the body’s cells. It is involved in making the molecule known as adenosine triphosphate, which is the cell’s major energy source. CoQ10 provides several weapons against atherosclerosis and stroke; it prevents oxidation of LDL, reduces total cholesterol and triglyceride levels, improves insulin sensitivity, decreases glucose levels, and lowers blood pressure, among other things (Ernster L et al 1995; Digiesi V et al 1994, 1990; Langsjoen PH et al 1999; Morisco C et al 1993; Kontush A 1997). The primary food sources of CoQ10 are meat and seafood.
• Green tea. Green tea catechins, which are rich in flavonoids, possess powerful antioxidant properties that have been studied in the context of limiting damage due to ischemic stroke. Animal studies have shown that green tea extract limits the size of stroke lesions in a dose-dependent manner when administered immediately after an ischemic episode, leading researchers to suggest that green tea may have promise in the acute treatment of ischemic stroke (Suzuki M et al 2004; Lee SY et al 2003). Another study found that animals that had a high intake of green tea experienced less cerebral damage after a stroke than did their counterparts who weren’t consuming green tea (Hong JT et al 2001).
• Beta-carotene. Beta-carotene is an antioxidant. Large long-term studies have found that daily dietary intake of beta-carotene plays a protective role against atherosclerosis and decreases risk of ischemic stroke (Hak AE et al 2004; Hirvonen T et al 2000). Rich sources of beta-carotene include carrots, squash, green leafy vegetables, milk, lean meat, fish, and poultry.
• Vitamin C. Vitamin C, also known as ascorbic acid, is a water-soluble antioxidant that protects other compounds from oxidation by being oxidized itself. While it has been shown to lower blood pressure (Duffy SJ et al 1999), other long-term follow-up studies in human beings have found that vitamin C also reduces risk of cardiovascular and heart disease and stroke (Simon JA 1992; Enstrom JE et al 1992; Gale CR et al 1995). A small, well-designed study also found that giving antioxidant vitamins, particularly vitamin C, within 12 hours of an ischemic stroke increased antioxidant capacity, reduced inflammation, and reduced the oxidation of dangerous lipids (Ullegaddi R et al 2005). An earlier, 20-year follow-up study reported that higher vitamin C concentrations reduced incidence of both ischemic and hemorrhagic stroke (Yokoyama T et al 2000). Another study examined the benefit of vitamin C in overweight men with high blood pressure and found that low plasma levels of vitamin C were associated with increased risk of stroke (Kurl S et al 2002).Although vitamin C provides cerebrovascular benefits when taken alone (Hirvonen T et al 2000), studies have shown that it may be more powerful when combined with other nutrients, vitamins, minerals, and antioxidants (Galley HF et al 1997; Sacks FM et al 2001; Fotherby MD et al 2000; Toivanen JL 1987; Hajjar IM et al 2001).
• Vitamin E. Vitamin E is an antioxidant. It regulates oxidation reactions and protects polyunsaturated fatty acids and vitamin A. A large study supplying people with foods that have high levels of vitamin E (plant oils, green leafy vegetables, whole grains, butter, liver, egg yolk, milk, nuts, and seeds) found that higher intake of vitamin E helped reduce risk of death from stroke (Yochum LA et al 2000). Another study reported that eating foods high in antioxidant vitamins C and E helped lower the incidence of stroke, especially notable in smokers (Voko Z et al 2003).A study from Helsinki looked at vitamin E supplementation in high-risk individuals with high blood pressure and concluded that although vitamin E supplementation may increase the risk of hemorrhagic stroke, this small risk was outweighed by its protective effect against ischemic stroke (Leppala JM et al 2000). Studies have also shown benefits of vitamin E in improving insulin sensitivity and glucose metabolism, thereby lowering risk of atherosclerosis and stroke (Barbagallo M et al 1999).

Nutrients That Increase Glutathione

Glutathione is the major cellular antioxidant and has a central role in the antioxidant systems that help the body respond to oxidative insults. When glutathione levels are low, oxidative stress is more likely to occur (Thomas JA 2006). Deficiency in glutathione has been associated with atherosclerosis (Morrison JA et al 1999), and evidence indicates that increasing glutathione levels through diet or supplementation may reverse endothelial damage by enhancing nitric oxide production (Prasad A et al 1999). A number of nutrients have been shown to improve glutathione levels:

• N-acetylcysteine. N-acetylcysteine (NAC) is an antioxidant that helps overcome oxidative stress and enhance glutathione levels (Jiang B et al 1999; Vasdev S et al 1997, 1996; Meister A et al 1986; Lu Q et al 2001). Moreover, NAC lowers homocysteine and lipoprotein that can lead to atherosclerotic changes and helps reverse platelet aggregation that can result in blood clots (Gavish D et al 1991; Wiklund O et al 1996; Bostom AG et al 1996; Hultberg B et al 1997; Horowitz JD 1991).
• Garlic. Garlic has a long history of medicinal use. It supplies a component of glutathione metabolism, and it is an antioxidant that helps reduce damage from free radicals. Studies have demonstrated that garlic also slightly lowers cholesterol and has antiplatelet effects that help prevent blood clots (Barrett S 2006; Chang HS et al 2005).
• Selenium. Selenium is a metallic and essential trace element required for glutathione peroxidase. Deficiencies in selenium can produce oxidative stress as well as other stresses that make people vulnerable to infection or disease. It has also been shown to protect against the effects of cerebral ischemia (Ansari MA et al 2004; Schweizer U et al 2004).

DHEA and Stroke

Dihydroepiandrosterone (DHEA) is the most abundant adrenal androgen in the body. It can be converted into both testosterone and estrogen, and many studies have shown that DHEA levels decline as people age. In recent years, researchers have investigated the relationship between DHEA levels and cerebrovascular disease, found compelling evidence that low levels of DHEA are associated with cerebrovascular disease, and even identified DHEA as a possible therapy for the treatment of ischemic stroke.

In one study, researchers hypothesized that DHEA functions as a neuroprotective agent that protects the central nervous system and brain against a variety of insults. After performing the study on rabbits, they found that DHEA, at a daily dose of 50 mg/kg, was able to significantly reduce the damaging effects of ischemia. Perhaps better yet, the protective effect of DHEA was durable, meaning that it lasted more than four days.

Dr Rick Sponaugle, Medical Director of Florida Detox & Wellness Institute, applauds Governor Rick Scott, Attorney General Pam Bondi and our own local State Senator Mike Fasano for their efforts in passing the “pill mill” legislation.

Doctors throughout America, including Dr. Phil, have referred patients suffering from OxyContin addiction to Florida Detox for Dr. Sponaugle’s scientific addiction treatment that stops drug and alcohol craving by balancing brain chemistry. Traditional rehab centers use “talk therapy” in their attempt to coach patients through each day of drug craving.

As a Florida physician, it has been embarrassing for Dr. Sponaugle to learn that his patients from Chicago, Dallas, Atlanta and even Toronto had been riding the “Oxy Express” all the way to Florida just so they could buy their “Oxys and Roxys” from unscrupulous drug dealing doctors in Tampa Bay.

Parents throughout America will applaud the crackdown on drug dealing doctors in Florida. Out of state parents often rush their sons/daughters into Dr. Sponaugle’s rehab center stating, “my nephew back in Philly overdosed Saturday night, he and my son were snorting OxyContin they bought right here in Tampa, they were supposedly coming down for the beaches.”

The Prescription Drug Monitoring Program is not perfect, but it will enable Attorney General Pam Bondi to focus on illegitimate “pain specialists“ and the pain clinics whose doctors routinely prescribe opiate pain pills to out of state residents. Common sense dictates that patients with legitimate pain do not need to travel out of state, bypassing several other states to procure opioid pain medicine in Florida.

Furthermore, the exponential increase in physician prescribing of opiate pain medicines since 1990 is not warranted. True pain specialists, not simply the doctor who hangs a pain shingle outside of his office, but, those who actually matriculate in specialty training for pain management as Dr. Sponaugle did at the University of Florida, are taught to use every means possible to avoid prescribing addicting opiate medications.

Medical doctors have known for ten years that patients who take opiate pain medication on a chronic [daily] basis, will within a couple of years, suffer more physical pain from their injury than they experienced immediately following their accident. This well documented phenomenon is called hyperalgesia.

University pain professors suggest we know little regarding the mechanism of hyperalgesia, this void in knowledge is derived from the fact that America’s rehab centers have failed to perform any sophisticated testing on patients with OxyContin addiction.

Dr. Sponaugle’s research at Florida Detox has proven that daily consumption of Oxycontin changes the addicted brain in a manner that up regulates electrifying brain chemicals and down regulates relaxing brain chemicals, thus, Oxycontin induced up regulated brian “voltage” amplifies incoming electrical pain signals after they reach the brain.  The 3/10  sciatica pain is amplified to a 7/10.

For this reason, chronic pain patients must constantly raise their dose of Oxycontin, Dr. Sponaugle treats many patients who suffer an OxyContin addictions of 3,000 mgs a day, they were initially prescribed only 30 mgs a day.

Furthermore, SPECT brain research on Dr. Sponaugle’s addicted patients in addition to research from university medical centers has proven that patients suffering high dose Methadone and OxyContin addiction can have much worse looking brain scans than patients abusing street drugs.

Associated Press

FORT LAUDERDALE, Fla.—Florida Gov. Rick Scott signed a bill into law Friday aimed at controlling the state’s “pill mills” and ending Florida’s reputation as the “oxy express” by penalizing doctors who overprescribe painkillers, tightening rules for operating pharmacies and authorizing a prescription-drug monitoring database.

Scott signed the legislation in Fort Lauderdale and was to have other signing ceremonies in Tampa and Orlando later in the day.

Florida is considered the epicenter of prescription drug abuse, with pain-management clinics supplying drug dealers and addicts with illicit prescription painkillers. The federal government says 85% of the powerful painkiller oxycodone is sold in Florida, much of it to people from out of state who then illegally resell the pills, primarily along the East Coast and Appalachia.

“I am proud to sign this bill which cracks down on the criminal abuse of prescription drugs,” Scott said. “This legislation will save lives in our state and it marks the beginning of the end of Florida’s infamous role as the nation’s Pill Mill Capital.”

The Republican governor originally opposed the prescription-drug monitoring database, calling it a waste of money and an invasion of privacy. But Republican Attorney General Pam Bondi and several GOP legislators pushed for the database and Scott eventually agreed.

“Not a day goes by that I don’t hear a story of someone who has lost a family member or friend to prescription drug abuse,” Bondi said in a statement. “This legislation will make significant strides in ridding Florida of unscrupulous doctors and pill mills, making our state a safer place to live and raise our families.

Soon after the bill signing Friday, federal authorities executed two search warrants in Orlando as part of a pill mill investigation. One doctor allegedly prescribed more pills than the entire state of California, according to the Orlando Police Department. The State of California dispensed 303,000 oxycodone pills in one year, a spokeswoman said in a statement.

The Obama administration last month announced that the federal government will aim to cut the abuse of oxycodone and other opioids by 15% in five years through education, stepped-up law enforcement and pill-tracking databases.

When used properly, OxyContin—oxycodone’s trade name—and similar medications help people deal with chronic pain, slowly releasing key ingredients over many hours. Abusers crush the pills and sniff or inject them, resulting in a euphoric heroin-like high.

According to the state, more than 2,500 people—seven a day—die in Florida from painkiller abuse. According to the federal Centers for Disease Control and Prevention, overdose deaths from painkillers have risen from less than 4,000 in 2000 to more than 11,000 in 2007, the most recent statistics available.

Florida’s new law:

—Creates a prescription-drug monitoring database but bars pharmaceutical companies from funding it, to avoid a conflict of interest. Bondi said a group of local law enforcement agencies agreed to pay for the database out of their forfeiture funds. It should be operating by Aug. 28.

—Makes clinics keep track of patients who get drug prescriptions and if any of them develop drug-abuse problems.

—Penalizes doctors who overprescribe painkillers with minimum fines of $10,000 and 6-month suspensions.

—Makes it a first-degree misdemeanor if a pharmacist “knowingly fails” to tell local police if someone tried to fraudulently get drugs.

—Tells drug wholesalers to police themselves and alert state police if clinics appear to buy more than they need.

—Tightens rules for prescription writing, medical records and pain-treatment plans.

—Tightens rules on getting a permit to open and run a pharmacy and on pharmacy record-keeping.

—Requires certain pain-management clinics to register with the state and orders doctors to tell the state when they begin and stop working at such a clinic.

—Creates signage rules and other requirements. Clinics must have restrooms and waiting areas, be “structurally sound” and have at least one employee on duty trained in basic life support.

—Allows law enforcement to look at or copy clinic records without a search warrant.