ACAM, Medical Conference Report, October 2000, Salt Lake City 

by Ivy Greenwell 

Introduction

Several years ago I heard a holistic practitioner say, “If we prevent inflammation, we can prevent Alzheimer's disease.” I was stunned. The mainstream view was, “If you live long enough, you will develop Alzheimer's.” The same went for cataracts and cardiovascular disease. Then last June Paul Ridker, MD, a Harvard cardiologist, publicly stated, “We have to think of heart disease as an inflammatory disease, just as we think of rheumatoid arthritis as an inflammatory disease.” He asserted that it's inflammation that leads to pieces of arterial plaque breaking off and causing heart attacks, even in people with normal or low cholesterol. Recently headlines announced that men regularly taking non-steroidal anti-inflammatories (NSAIDs) such as ibuprofen lowered their risk of prostate cancer by 66%; some risk reduction with NSAID use has also been reported for breast cancer and colon cancer. On a minor but important note, Dr. Nicholas Perricone, an innovative dermatologist, is now saying (or at least implying) that if we prevent inflammation, we can prevent a lot of skin aging.

Because of our new awareness of the importance of inflammation, it is not surprising that the most recent conference of the Academy for the Advancement of Medicine (ACAM) had inflammation and infection as its main theme. Only by understanding the mechanisms involved in the pathogenesis of diseases such as AIDS, cancer or Alzheimer's disease can we develop effective therapies. The growing understanding of the major role that oxidative stress and inflammation play in the development and progression of various pathologies has brought progress in devising more effective treatment protocols. In addition, the conference also included lectures and workshops dealing with updates in hormone replacement. Here are some of the highlights. 

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“The brain on fire”—Inflammation as the key to neurodegenerative diseases 

The brain in a state of chronic inflammation is, in Perlmutter's colorful phrase, "the brain on fire." Current therapies "treat the smoke, but not the fire."

David Perlmutter, a neurologist and director of the Perlmutter Health Center in Naples, Florida, and the author of BrainRecovery.com — Powerful Therapy for Challenging Brain Disorders, delivered an exciting lecture on the nature, prevention and treatment of neurodegenerative diseases such as Alzheimer's and Parkinson's. He concentrated on two factors: inflammation and glutathione depletion. Once we understand the critical importance of inflammation and glutathione depletion in brain diseases, we can take steps to prevent or even reverse the damage. 

First, Dr. Perlmutter presented evidence that the current mainstream drugs such as Aricept are “essentially useless” in actually treating Alzheimer's disease. Their effectiveness is minimal at best, while their side effects include vomiting, dizziness and insomnia. These drugs do not correct the underlying inflammation. The brain in a state of chronic inflammation is, in Perlmutter's colorful phrase, “the brain on fire.” Current therapies “treat the smoke, but not the fire.” 

The first real breakthrough in the understanding and treatment of Alzheimer's disease has been the discovery that the use of aspirin and NSAIDs such as ibuprofen (Advil) has a very significant protective effect. In one large study of those who used aspirin, NSAIDs or acetaminophen, NSAIDs reduced the risk of Alzheimer's disease to only 40% that of nonusers. Aspirin reduced the risk to 74%. Acetaminophen, however, raised the risk by 35% (this may have something to do with a toxic metabolite of acetaminophen, which depletes glutathione). 

This finding is of tremendous importance to arthritis sufferers—they must become aware that their choice of a pain reliever is crucial in determining their risk of developing Alzheimer's disease. The effectiveness of ibuprofen is likely to stem from its superior ability to inhibit Nuclear Factor kappa B (NFkB), a transcription factor that switches on the production of inflammatory cytokines that initiate the process of cell death. It also supports Dr. Perlmutter's thesis that inflammation (“fire”) is at the core of Alzheimer's disease, and may turn out to be far more important than the beta-amyloid plaque. 

We need to put out the fire in the brain—that is, reduce inflammation. Fortunately, we have some knowledge about how to accomplish this goal. For instance, we know that simply by taking nonsteroidal anti-inflammatories on a preventive basis, we can cut the risk of developing the disease by as much as 60%.

Can anti-inflammatories be used not only for prevention of neurodegenerative diseases, but also as treatment? Indomethacin, a well-known nonsteroidal anti-inflammatory, has been found to produce improvement in Alzheimer's patients, Perlmutter pointed out. The improvement was modest, but dramatic in the light of the fact that over the six-month course of the study the placebo group continued to deteriorate. Currently there is also great interest in the effect of selective COX-2 inhibitors (Celebrex, Vioxx) on the prevention of Alzheimer's disease, Perlmutter said. A few participants were concerned that “we may discover the price later on,” but for now we simply have to wait for more research findings. The main point is there has been a revolution in medical thinking. The gloomy dogma that nothing can be done to prevent Alzheimer's is giving way to an increasing awareness that reducing inflammation is powerful prevention. And now that we have those expensive COX-2 inhibitors, with more underway, the drug companies are certainly interested. 

Pharmacological NSAIDs are not the only way to reduce inflammation. Fish oil has been shown to be an effective natural anti-inflammatory. The consumption of fish oil results in a different composition of cell membranes, with less arachidonic fatty acid available for the production of pro-inflammatory cytokines. Animal studies showed that diets containing fish oil profoundly reduce the levels of pro-inflammatory chemicals such as tumor necrosis factor alpha (TNF alpha) and various interleukins. Flax oil, a rich source of short-chain omega-3 fatty acids, also appears to be anti-inflammatory, though to a lesser degree. Epidemiological studies have amply demonstrated that frequent fish-eaters enjoy much better health, including less cognitive impairment and lower incidence of Alzheimer's disease, than those who eat little or no fish.

In addition, all antioxidants are also anti-inflammatory. Alpha lipoic acid and various flavonoids (such as those found in green tea and blueberries) may be particularly effective. A diet that emphasizes fish and seafood rather than meat, along with antioxidant-rich fruits and vegetables, can be useful in preventing degenerative brain disorders. This type of anti-inflammatory diet can make all the more difference with the right supplementation. 

Perlmutter, however, placed special emphasis not on reducing inflammation once it has already started, but on trying to prevent it in the first place. “It's best to prevent inflammation from starting, rather than use drugs to dampen it,” he said. He emphasized that inflammation in the brain is particularly difficult to control. Cerebral inflammation tends to be self-perpetuating. We know that head injury and strokes (including mini-strokes), as well as various toxins and infections, produce inflammation and increase the risk of neurodegenerative disease. But few people know about the role of excess blood sugar in producing inflammation and thus contributing to the death of neurons. Perlmutter observed that Ronald Reagan's notorious sweet tooth might have contributed to the pathogenesis of his Alzheimer's disease.

A diet that emphasizes fish and seafood rather than meat, along with antioxidant-rich fruits and vegetables, can be useful in preventing degenerative brain disorders.

Perlmutter cited a Dutch study that found a more than quadruple risk of dementia in type II diabetics who use insulin. On the other hand, calorie restriction, which profoundly reduces blood sugar and insulin, is perhaps the best dietary protection against age-related brain damage. Consuming fewer calories translates into lesser production of free radicals. In addition, glucose can damage proteins, modifying them to pro-inflammatory compounds called AGEs (Advanced Glycosylation End Products). AGE -modulated beta-amyloid is extremely pro-inflammatory. One way or another, Perlmutter kept returning to the theme of reducing inflammation as a means of preventing, and possibly even treating, Alzheimer's disease. 

Apart from anti-inflammatory supplements, magnesium may also prove a useful neuroprotector. One cause of neuron death is excess influx of calcium ions. If magnesium is present in sufficient concentration, the resulting “magnesium block” (magnesium is a natural calcium channel blocker) can save the neurons.

People who have suffered head trauma, small strokes or infections affecting the brain are especially likely to have the kind of low-grade cerebral inflammation that makes them more susceptible to developing Alzheimer's disease. These high-risk individuals should be made aware that they can reduce their risk with fish oil, NSAIDs, lipoic acid, flavonoids and through calorie restriction.

Those protective measures should be practiced by all of us. The dismal prediction is that by the year 2030 there will be nine million Alzheimer's victims in the United States. Some even predict that the economic burden of Alzheimer's disease alone will be enough to bankrupt the medical system. Such disaster can be averted through relatively simple means. It is time to educate the public about the prevention of brain diseases.

Parkinson's disease and “The glutathione miracle”

Perlmutter went on to discuss his approach to Parkinson's disease. It is more than a brain disease, he said. Parkinson's is a systemic disease as well, with the whole body involved. More specifically, Parkinson's patients tend to be poor detoxifiers. They show low levels of glutathione not only in the brain (especially in the dopamine-producing region of substantia nigra), but also in the liver. This may be why exposure to pesticides and herbicides can be so damaging to individuals with a genetic vulnerability to Parkinson's. We all have to deal with a tremendous toxic burden, but those who happen to be poor detoxifiers are at a special risk. 

The central feature of Parkinson's is the progressive destruction of substantia nigra, resulting in a profound deficiency of the neurotransmitter dopamine. Mainstream treatment centers on the use of l-dopa, a precursor of dopamine. This approach to increasing dopamine works for a limited time, though not without severe side effects, including further brain damage. “The very drug that's used to treat the smoke increases the fire,” Perlmutter stated. It turns out that l-dopa reduces detoxification. L-dopa also increases the conversion of S-adenosyl-methionine (SAMe) to homocysteine, and thus promotes vascular disease. At the same time, it's sometimes not possible to take patients with advanced Parkinson's off l-dopa. It may be possible, however, to counteract the drug's side effects and increase the patient's motor ability through a relatively simple alternative treatment.

Within less than an hour of the injection, Parkinson's patients experienced an almost complete restoration of the ability to walk, turn around and move their arms.

Perlmutter's holistic approach is based chiefly on the need to increase detoxification, and thus enhance glutathione levels. The most dramatic part of Perlmutter's presentation consisted of slides showing a profound improvement in Parkinson's symptoms after intravenous glutathione. Within less than an hour of the injection, Parkinson's patients experienced an almost complete restoration of the ability to walk, turn around and move their arms. Perlmutter calls this “the glutathione miracle.” He uses 1200 mg of injectable glutathione at first, then lowers the dose to 600 mg per injection. The injections are given two days apart. The effectiveness of the treatment has been validated in a controlled study. Many holistic physicians already use intravenous glutathione as part of their treatment for Parkinson's disease.

If the treatment is discontinued, its benefits last for up to four months after the end of the treatment. Besides acting as a detoxifier and lowering oxidative stress, glutathione may also enhance the sensitivity of dopamine receptors in Parkinson's patients, Perlmutter speculated. He also mentioned that intravenous glutathione is immediately effective against irritable bowel syndrome and diarrhea.

Is there a more convenient way to increase glutathione levels, for longevity in general and as part of a preventive neuroprotective protocol? It turns out that lipoic acid is the most effective supplement for raising glutathione—especially if it is taken together with N-acetyl-cysteine (NAC) and vitamins C and E. In addition, the amino acid glutamine is, like NAC, an important precursor of glutathione. Silymarin (milk thistle extract) has also been shown to increase glutathione in the liver. 

In addition, lipoic acid is known to chelate iron. The elevated levels of free iron in Parkinson's patients increase free-radical damage and the destruction of neurons. And, like ibuprofen, lipoic acid inhibits NFkB and thus the production of inflammatory cytokines.

Perlmutter mentioned other helpful supplements, including CoQ10, which enhances mitochondrial function and is known to be low in the cerebral mitochondria of Parkinson's patients (and, interestingly, also of their spouses). Ginkgo biloba was also discussed. Ginkgo has been shown to have many neuroprotective properties, including the protection of brain mitochondrial glutathione against oxidation. Ginkgo also inhibits the enzyme monoamine oxidase B (MAO-B), and thus helps protect dopamine against quick degradation. The drug seleginine (Deprenyl) also acts as a MAO-B inhibitor. 

Predictably, there also arose some controversy over coffee, recently shown to be protective against the development of Parkinson's disease. Raising cyclic adenosine monophosphate (cyclic AMP—a “second messenger” that amplifies the hormonal message) has been shown to protect against Parkinson's. 

“Caffeine dramatically increases cyclic AMP and decreases the risk of Parkinson's,” Perlmutter said. Caffeine also competes for receptors with adenosine, an inhibitory compound. By displacing adenosine, caffeine indirectly increases the action of dopamine. 

Perlmutter condemned the use of long-term antibiotics. Certain antibiotics are mitochondrial inhibitors. “If you increase antioxidants, you don't need long-term antibiotics,” he stated. He also suggested that if a patient is put on statins, s/he ought to take supplemental CoQ10 to try to compensate for the CoQ10 deficiency induced by the drug. (Incidentally, a recent British study has found that statins appear to reduce the risk of dementia. As in the case of heart disease and stroke, this may be due to the anti-inflammatory properties of statins.)

One conference participant, an MD from England, suggested that supplementing with Vitamin B12 can be of enormous importance in treating dementia. He described a patient of his whose dementia virtually disappeared after treatment with B12. Many elderly are deficient in this vitamin, crucial for brain function. B12 also increases the oxygen-carrying capacity of red blood cells, and helps lower homocysteine. Dr. Perlmutter agreed that B12 should be an important part of the treatment. He also discussed magnesium as protective against excess calcium ion influx. 

In summary, current research findings suggest the following: take lipoic acid and other antioxidants, eat fish and/or take fish oil, drink coffee (unless you can't tolerate it) and be happy. And forget about dessert. Calorie restriction still appears to be the most potent brain saver.

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Another speaker, Christian Renna, DO, presented an interesting thesis that without sufficient serotonin and antioxidant defenses, the brain decides that it's not safe to produce dopamine and norepinephrine—hence chronic fatigue and related neurosomatic disorders. A central feature of chronic fatigue-like disorders is a deficiency of norepinephrine. But simply increasing norepinephrine through pharmacological means is not appropriate, since the brain is already overwhelmed with stress, and thus with free radicals. In Renna's view, both stress reduction and antioxidant supplements are absolutely necessary to help the brain produce and maintain inhibitory and excitatory neurotransmitters in proper ratios. This applies not only to those diagnosed with chronic fatigue, but to all of us, especially as we age. 

In the presence of excess free radicals, the brain seeks to protect itself by lowering its activity. This means lower production of excitatory neurotransmitters such as dopamine, and less energy production in the mitochondria. Every neuron has an excitatory threshold beyond which it will not fire, Renna explained. Instead, the overstimulated neuron shifts to an “escape pathway,” preventing the synthesis of dopamine and norepinephrine. In chronic fatigue, the neuroexcitatory threshold is set too low. Raising it requires increasing the brain's safety mechanisms: serotonin and antioxidants. “If the cell doesn't need to fear oxidative stress, the mitochondria light up like Las Vegas,” Renna said. 

He also pointed out that many chronic fatigue patients responded well to fen/phen, which was a combination of a serotonin-raising drug and an amphetamine analogue. “Overcoming serotonin deficiency allows the brain to tolerate more norepinephrine,” Renna said. He didn't favor long-term use of antidepressants, however. He felt such use prevented the patient from achieving a more complete recovery. The point is to help the brain produce more of its own serotonin. Thus, we need to address the necessity of lowering stress—not only emotional stress, but also stress coming from chronic low-grade infections, toxins (including endotoxins [toxins produced within the body] originating in the gut under conditions of dysbiosis, meaning an overgrowth of harmful intestinal flora), excess calories, insufficient sleep or any other source. “The more gentle the stimulation, the better,” Renna said. “So don't rush.”

In addition, we must make sure the patient's antioxidant defenses are adequate before we use any kind of stimulant. “If a person is not energetic, maybe it's not safe for them to be energetic,” Renna said, again reinforcing the point about low serotonin and depleted antioxidant defenses. Both need to be corrected through stress reduction, diet, the right exercise and supplements. The brain will produce more dopamine when it becomes safe to do so.

Dopamine is a very energizing, feel-good neurotransmitter; in addition, dopamine stimulates the release of nerve growth factors. But dopamine has its dark side. “Dopamine is the most dangerous of all neurotransmitters because the brain needs to defend itself against overstimulation,” Renna explained. When serotonin is low, the threshold for what constitutes overstimulation is also set low. Low serotonin, low dopamine, and low energy production in cerebral mitochondria all lead to a cascade of harmful consequences. Since the brain is in constant chemical communication with the rest of the body, including the endocrine system and the immune system (in fact Renna calls the immune system “morcelized brain”), the whole body suffers. We see this not only in the chronic fatigue syndrome, but above all in aging. 
 

• Tofu has recently come under suspicion as deleterious to the brain. In an ironic reversal of our previous beliefs, coffee and tea are now seen as neuroprotective, while tofu is increasingly under attack.

Renna also discussed neuroprotective supplements. His special emphasis was on flavonoids as particularly effective antioxidants and neuroprotectants. Flavonoids (such as those present in blueberries and bilberries, green tea, grape seed extract, and various fruits and vegetables) not only raise glutathione levels, but also help prevent inflammation by inhibiting the enzymes in the lipoxygenase family (LOX), which NSAIDs and COX-2 inhibitors cannot do. Renna added folic acid, SAMe and acetyl-l-carnitine to the list of essential neuroprotective supplements. As for the so-called smart drugs, such as deprenyl and piracetam, these too are worth looking into, according to Renna. They increase energy production while reducing oxidative stress (acetyl-l-carnitine works the same way). 

Tofu has recently come under suspicion as deleterious to the brain. In an ironic reversal of our previous beliefs, coffee and tea are now seen as neuroprotective, while tofu is increasingly under attack. Renna takes his patients off tofu, at least until there is some solid new evidence of its safety.

Both Perlmutter and Renna covered a huge territory, at times overwhelming the audience. Permutter focused on the “anti-inflammatory breakthrough”: preventing and fighting inflammation in the prevention and treatment of Alzheimer's disease, as well as on the use of intravenous glutathione, the body's chief detoxifying compound, as a new and potentially revolutionary treatment for Parkinson's disease. Perlmutter also touched on the production of energy in the cerebral mitochondria, a subject developed more fully by Renna. The main message was clear: we already know a great deal about preventing and treating brain diseases and age-related cognitive and motor dysfunction. Relatively simple measures such as reducing caloric intake and taking fish oil, NSAIDs, lipoic acid and CoQ10 could save millions from terrible brain diseases. It is high time to start implementing this knowledge on a much broader scale. 

Antioxidants against vitamins: lipoic acid and selenium improve the survival of AIDS patients

The excitement over the new anti-retroviral drugs designed to fight the AIDS virus is yielding to a sober assessment of their limitations. By now it has been shown that these drugs do not fully restore immune function. They are not the long-awaited cure. Their side effects are so severe that many AIDS patients drop out of treatment. In addition, the majority of the virus is in the latent stage in the nuclei of T cells, and antiviral drugs cannot affect latent viruses. 

Are there effective alternative treatments? An affirmative answer was compellingly presented by two speakers: Raxit Jariwalla, PhD, a research scientist at California Institute for Medical Research in San Jose, and Lynn Patrick, ND, medical director of HIV Wellness Program in Tucson, Arizona. The speakers cited study after study showing improved survival rate for AIDS patients who used certain critical supplements known to reduce oxidative stress (a major factor in the progression of the disease) and, in some cases, to significantly suppress viral reproduction.

Both presenters singled out lipoic acid as particularly important. All antioxidants are also anti-inflammatory agents, but lipoic acid is regarded as an especially effective anti-inflammatory.

It has been known for almost a decade that lipoic acid effectively inhibits the replication of the AIDS virus in vitro. This is not surprising in view of our knowledge that lipoic acid inhibits the activation of Nuclear Factor kappa B (NFkB), which is believed to play an important role in the activation of the HIV virus. Essentially, the latent virus is activated by certain inflammatory cytokines that result from the activation of NFkB. These cytokines include Tumor Necrosis Factor alpha (TNF alpha)—hence the goal of reducing TNF alpha, and the similarity between alternative treatments against AIDS and hepatitis, Dr. Patrick pointed out. Both protocols emphasize lipoic acid, selenium and a combination of various other antioxidants. In addition, many AIDS patients are co-infected with Hepatitis C. “All AIDS patients need liver support,” Patrick said. In addition to 500 mg of lipoic acid/day, she also uses silymarin, shown to be remarkably effective in restoring liver health.

Lyn Patrick largely confirmed Dr. Jariwalla's primary emphasis on lipoic acid, stating that “lipoic acid is of extreme importance for HIV patients.” She reinforced this with some added details. Studies have found that lipoic acid inhibits reverse transcriptase (a viral enzyme needed for replication), and makes AZT significantly more effective. 

Another obvious reason for the importance of lipoic acid for HIV patients is its ability to raise glutathione, our chief detoxifier and a crucial endogenous antioxidant. Glutathione is low in all serious illnesses. When the levels of glutathione rise, the result is reduced oxidative stress. The role of oxidative stress has been neglected in the discussion of AIDS, with the public getting the impression that the sole factor in the progression of this disease is the presence of AIDS virus, commonly referred to as HIV. Yet oxidative stress and consequent inflammation play a major role in whether symptoms of AIDS will appear at all, and in the rate of progression. Some people who are HIV positive do not show any symptoms of AIDS. Interestingly, this group tends to have a higher intake of antioxidants, from diet or supplements or both. Even merely taking a multivitamin turned out to reduce the risk of developing the symptoms of AIDS by 33% in HIV-positive individuals.

While lipoic acid plays a starring role in the alternative treatment for HIV patients, another thiol (i.e. sulfur-containing) antioxidant, the acetylated form of cysteine known as NAC, appears to be somewhat helpful as well. NAC too helps raise the levels of glutathione, but by itself it is not likely to have enough effect in AIDS patients; lipoic acid is far more efficient at raising glutathione and blocking NFkB. The special effectiveness of lipoic acid may derive from the fact that it's a dithiol (it has two sulfur groups), while NAC is a monothiol.

NAC is more effective when used with other antioxidants. In particular, it synergizes with high-dose ascorbate. High-dose ascorbate, Dr. Jariwalla stated, is unique in that it recycles itself to the reduced state. It also produces “dramatic dose-dependent suppression of viral reproduction.” It is believed that high-dose ascorbate suppresses viral replication through a different mechanism than thiol antioxidants (lipoic acid and NAC) and selenium. Some participants suggested that intravenous delivery of ascorbate would be most effective, due to the large dose required (6 to 12 grams if taken orally).

Selenium also plays a starring role in anti-viral regimens. It too inhibits NFkB. But the main reason that selenium is known as “birth control for viruses” derives from the fact that many viruses, including HIV, need selenium to replicate. Interestingly, in a selenium-rich milieu the viral genes that control replication stay turned off. In addition, selenium is required by T cells, and potentiates the action of interleukin-2. An AIDS patient is ten times more likely to die if s/he is selenium-deficient, according to Dr. Patrick. She uses the dose of 400 mcg per day.

Vitamin E is known to play an important part in bolstering immunity and reducing inflammation. Like lipoic acid, vitamin E also inhibits NFkB, essential for viral replication. Dr. Patrick stressed that only the succinate form of vitamin E inhibits both the activation of NFkB and the binding of activated NFkB to DNA, as shown by the research of Dr. Lester Packer in the early nineties. Vitamin E has also been shown to enhance the action of AZT. Thus, the form of vitamin E known as alpha-tocopheryl-succinate (“dry E” in popular parlance) is of crucial importance for HIV patients. It is possible, however, that gamma-tocopherol, being a COX-2 inhibitor, is also of value. 

Vitamin A and beta carotene have been found helpful, as has zinc—but only in small doses. Zinc supplements in excess of 10 to 15 mg appear to increase disease progression. We don't know very much about zinc and HIV, but we do know that zinc is important for the immune system. Zinc activates the thymus hormone thymulin, which plays a part in the differentiation of T cells. Zinc is also involved in protease and integrase enzymes. It seems that supplementing with 12 mg of elemental zinc works best, according to Patrick.

HIV infection has also been linked to deficiencies in B6, B12 and folate—the methylating factors. There is a “rampant deficiency” of B12 among AIDS patients, according to Dr. Patrick. Such nutritional deficiencies in patients with full-blown AIDS result mainly from their poor absorption of nutrients due to gut problems, Patrick explained. Thus doses need to be especially large. 

Most HIV patients are also glutamine-deficient, Patrick said. This is true of anyone under chronic severe stress, even though glutamine is abundant in any protein-rich diet (interestingly, the immune dysfunction seen in AIDS resembles the symptoms of protein-calorie malnutrition). Glutamine helps stop diarrhea and prevents muscle wasting. Large doses are needed (Patrick uses 40 g/day in four divided doses), but the cost is only $31 per week versus $1000 a week it would take for growth hormone treatment, another therapy aimed at preventing wasting.

Patrick mentioned yet another supplement: acetyl-l-carnitine. AZT is a mitochondrial toxin. It turns out that the combination of acetyl-l-carnitine and lipoic acid can reverse this toxicity.

After learning about the effectiveness of lipoic acid, NAC, Vitamin E, high-dose ascorbate and other supplements in fighting the HIV virus and improving the survival rate of AIDS patients, it was sad to hear that AIDS activists have largely lost interest in alternative therapies and are mostly waiting for the next “miracle drug.” So far, the drugs have proven highly toxic and not effective in many patients. We need to seriously consider the preventive and therapeutic use of supplements such as lipoic acid. In Dr. Jariwalla's words, “nutrients are compelling candidates for treatment of immune dysfunction underlying AIDS.”

A dramatic moment in the conference happened to underscore the effectiveness of alternative therapies for AIDS. One of the presenters, Victor Marcial-Vega, MD, publicly stated that back in the eighties he was diagnosed as HIV-positive. After undergoing various alternative treatments, Dr. Marcial-Vega took another blood test. This time, “nothing showed.” The virus could no longer be found. 

Much is to be gained from paying attention to the developments in the alternative treatment for AIDS. Cellular immunity decreases not only in the course of AIDS, but also during aging. It is of utmost importance that we learn how to sustain a healthy immune system that can fight viruses and bacteria. Thus, the results presented in the lectures on AIDS are of special interest for anti-aging medicine. Antioxidants, with special emphasis on lipoic acid and selenium, once again show their amazing potential.
 

While it all sounds very good, please understand that scientifically there is no actual independent proof of these claims, be a skeptic, your life depends on it, and check at quackwatch.com

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• My doctor told me my BP was too volatile for beta blockers, sound like you are similar.  I do drink coffee when my BP is low and green tea when it shoots up (also help to take your mind of high BP by doing something as lovely as having tea).  Caffeinated drinks do have a diuretic effect, but if you have problems with retention and edema, that would certainly not be a problem.  Pop has a lot of caffeine (almost all flavours) and huge amounts of sodium and sugar, I'd think that unsweetened coffee or tea is a far better idea.  My heart rate is much higher than it ever was before (and I am fit), but it is a healthy heart, for me the anxiety it makes me feel is hard to deal with (HR does not differentiate between being active and resting, steadily between 80 and 110) and is entirely independent of what my BP is.

It is my theory that with all these neuro-degenerative illnesses we do ourselves the greates favour by keeping ourselves in survival mode, eating the minimum, moving around to the maximum, breathing deeply, stretching, and keeping our bodies just a little cooler.  Comfort makes us complacent and the body stops working in our interest, give it less and it will do more.  Works for me, some days I only consume 600 calories, my energy is fine on those days, if I eat more I grind to a halt.  I've not lost any muscle (all the fat is gone - so what) my iron and vitamin levels are fine, the cholesterol which was always sky high is now optimal, so screw the x servings of this and that, this works really well.  On the very low calorie days I will sometimes take a children's vitamin but that's it.  There was a published story that people with Alzheimers lost less memory when kept on a calorie restricted diet (so see, I was onto something all along).  Buy yourself some fruit if that is what you want, and when you suddenly crave something else do it.  Why is it women are only smart enough to listen to their bodies when they are pregnant, and men from what I can see rarely listen  to their bodies?

Nothing I could do had any effect on my weight, not gaining it and not losing it.  By the time my body ground to a halt and I was fired for appearing drunk on a new job (no recourse if you've just been hired), I weighted 150 lbs. and looked ok, had no need to lose more.

I became more and more restricted activity wise I ate more thinking it would help my energy level, but nothing, within months I was down to 120 (size 16 to size 7), currently I am a size five, just as in the 1993 before picture. So I ate more exercised less and kept on shrinking.  My size is stable (for the past two years), largely due to eating no more than I can reasonably process and because the meds I take and the laxatives I take have me up and about.

At no point did it seem I had any control over my weight.  I miss the soft butt I used to be able to sit on, having cheeks was nice and the insulation was a good thing.  The body needs to have a bit of fat, structural fat, insulation, something to burn during a famine, a soft body for little kids to lean up against.

I can't explain it except to say, when the autonomic stuff is screwy, normal has ceased to exist.

More to come, very soon...

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when I have impactions (about once ever two months), it is caused by several things, and can be helped along: 

• do not eat more than my stomach and digestive tract can process 
• without proper saliva nothing is predigested slowing the process down and making for more solid feces than someone with normal saliva which breaks food down before getting to the stomach, this is why raw vegetables and fruit are not a good idea, nor amounts over a few ounces 
• my anal sphincter cannot open to allow the solids to pass out (damaged nerves), so only liquids or very soft feces are able to pass 
• being stationary does nothing to promote moving intestinal contents through the bowels and collects up in corners and loops to form impactions, must keep moving especially stretching out and walking to help it along 
• if you start to have edema (swelling of belly, ankles or around the eyes - stop taking in fluids, we cannot sweat it out, cry it out or manufacture saliva, so without proper bladder strength we retain 'all' of it - just sip to keep mouth moist, nothing else 
• when it comes to fluids people with PAF and SDS have little in common with PD+, most doctors don't seem to realize that 
• raising oil/fat content in foods (on a regular basis) does help to make feces slip more easily through the tract - again this is not the same in PD+ - I like olive oil and greasy french fries (patat), greasier the better 
• our body temp is lower (more often than not) than normal people and docs often think we don't run a fever when in fact we actually do, my usual body temp is 35.5, by the time our skin is clammy we are seriously life threateningly ill 
• the digestive tract is regulated by the autonomic nervous system, without extra help (meds and the stuff I've listed) it will not function well enough to sustain us
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Description of Enterra Therapy or gastic pacemaker 

Anne (AU) has one and has benefitted greatly.

• Enterra Therapy may reduce symptoms of nausea and vomiting for many people suffering from              gastroparesis when drugs are ineffective. The therapy is reversible and can be turned off at anytime.

           Will the Enterra Therapy cure my stomach problems?

• This therapy is not a cure, but may be a beneficial treatment for your symptoms. How well it relieves symptoms varies from person to person. 

           What is an Enterra Therapy (Gastric Electrical Stimulation) System?
             Enterra Therapy is prescribed by a physician. The Enterra Therapy system components include: 
 

• An implanted neurostimulator that is usually surgically placed in the lower abdomen                  region. 
• Two intramuscular leads (wires) with electrodes implanted in the muscle wall of your stomach. 
• A programmer that the physician uses to control and adjust the settings of your implantedneurostimulator. 

           Risks and Probable Benefits of Enterra Therapy 

             Enterra Therapy may reduce symptoms of nausea and vomiting for certain people suffering from
             gastroparesis when drugs are ineffective. The therapy is reversible and can be turned off at any
             time.

             Results of clinical studies done on Enterra Therapy.
             Enterra Therapy has been used successfully in people over several years. Enterra Stimulation is
             approved for the treatment of nausea and vomiting from gastroparesis when drug treatments are
             not effective.

             A worldwide clinical trial was conducted with people who had severe symptoms of nausea and
             vomiting associated with gastroparesis. Clinical trials are controlled studies carried out to
             evaluate how well a therapy treats a condition and how safe it is. The study results help
             government agencies (such as the FDA) decide whether to approve a device or therapy for
             commercial use. 

             The interim results of the clinical trial (Medtronic FDA Application H990014) show that the
             therapy successfully reduces symptoms of nausea and vomiting in patients for whom drug
             treatments did not work. The average number of vomiting episodes before implant and at 6 and
             12 months after surgery are shown in the chart.
 
 

            Weekly Vomiting Frequency

•  100% of patients experienced a reduction of vomiting at 12 months following implant versus baseline. 
• 93% of patients experienced a reduction of vomiting episodes greater than 50% at 12 months following implant vesus baseline. 
• 53% of patients experienced a reduction of vomiting episodes greater than 80% at 12  months following implant versus baseline. 
• 66% of patients experienced a reduction of vomiting to less than 7 episodes per week at 12 months following implant. 

             NOTE: (Medtronic FDA Application H990014)

             The interim results of clinical studies indicate that Enterra Therapy may be a beneficial treatment
             alternative for patients suffering from drug refractory gastroparesis of idiopathic or diabetic
             etiology. Patients treated with Enterra Therapy had a significant reduction in vomiting frequency
             at 6 and 12 months. Patients also experienced improvements in other upper gastrointestinal
             symptoms, solid food intake, and a reduction in hypoglycemic attacks (diabetics), as well as
             significant improvements in health related quality of life.
 

             What problems did patients experience in this study?
             The adverse events observed during the clinical evaluation of the Enterra Therapy system
             include: lead impedance out of range, device infections, device erosion, device migration,
             stomach wall perforation, upper gastro-intestinal (GI) symptoms, extra-abdominal pain, feeding
             tube complications, lower GI symptoms, dehydration, bone- and joint-related pain, acute
             diabetic complications, dysphagia, cardiovascular/renal related events, urinary tract infections,
             stress incontinence, fever, and infections (sinus, pink eye, herpes zoster). These effects were
             related to the device, implant, underlying disease, other therapies, or other.

             Other potential complications which were not seen during clinical evaluation include: undesirable
             change in stimulation, possibly related to cellular charges around the electrodes, shifts in
             electrode position, loose electrical connections, or lead fractures; hemorrhage, hematoma, and
             possible GI complications resulting from the surgical procedure to implant the neurostimulator
             and leads; migration of lead or stimulator, which may necessitate surgical revision; persistent pain
             at the neurostimulator site; seroma at the neurostimulator site; allergenic or immune system
             response to implanted materials; and loss of therapeutic effect.

             Enterra Therapy Surgery

             Implantation of the Enterra Therapy system is a surgical procedure done under general
             anesthesia. During this operation, your surgeon will implant two small electrodes in the muscle
             wall of the stomach. The lead will then be connected to the implantable neurostimulator that is
             placed beneath the skin, and usually positioned below the rib cage and above the belt line in your
             abdomen. This operation may last from one to three hours. You should speak with your doctor
             and/or surgeon beforehand so that you understand how the operation will be performed, what
             the risks of surgery are, and what you should expect during your post-operative recovery.

             NOTE: Cardiac pacemakers may be affected by the Enterra Therapy if the two systems are
             too close to each other. Tell your doctor if you have a cardiac pacemaker so he or she can
             assess any possible electrical interference problems and decide if you can also have Enterra
             Therapy. 

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