Parkinson’s disease Archives

Nov

2023

Help to Walk for Parkinson’s Disease Patients

By Ray Schilling | neurological disease, Parkinson’s disease

A new study describes how a spinal cord implant provides help to walk for Parkinson’s disease patients. The original study was published in Nature: . CNN published a simplified article that describes how a Parkinson’s patient with gait problems could walk again, when a spinal cord implant was inserted. This patient’s name is Marc Gauthier from a town near Bordeaux, France. He was 36 years old when he was diagnosed with Parkinson’s disease. For many years he could control his Parkinson’s disease symptoms with Dopamine replacement therapy.

Insertion of deep brain stimulator

But by 2004 the medication did not control his gait anymore. His doctors inserted a deep brain stimulator, which helped with tremors and muscle stiffness. But as the disease progressed, he developed a severe walking disorder. The drugs and the deep brain stimulator no longer helped his walking problem. His muscles stiffened up, and often he fell 4-times per day. He had to give up his work as an architect. Finally, in 2021 his doctors inserted a nerve stimulator with electrodes connecting to the lower spinal cord.

Spinal cord stimulation

Researchers from France, Switzerland and other parts of the world determined which part of the spinal cord were in need of electrical stimulation to improve his gait and balance problems. Dr. Eduardo Moraud is an author of the study and researcher at Lausanne University Hospital. He said: “The stimulation here is focused on the spinal cord. We target the region of the spinal cord that will control all the leg movements.” The team managed to develop an electric stimulator for implantation under the skin over the abdomen with electrodes going to the lower spinal cord. This way his physicians stimulated muscle groups and also relaxed them in sequence so that his gait improved and steadied. His balance stabilized as well and he could walk stairs again.

Future routine surgery to implant spinal stimulator

Marc Gauthier’s case is a first in approaching Parkinson’s disease with a spinal stimulator. The researchers stressed that they will improve the technology and learn from other patients how to individualize this technique. But eventually the spinal cord stimulator could become a routine approach for end stage Parkinson’s disease. Dr. Moraud said: “Addressing deficits of gait and balance in Parkinson’s disease is extremely challenging. These deficits can be very heterogenous. They can be variable across patients. They can affect walking but also symmetry, balance, posture. The neuroprosthetic approach that we have developed here allows for the first time to target and address these problems individually in a highly specific manner for each patient. It operates in real time, and importantly, it is complementary to other existing therapies.”

Marc Gauthier’s progress since his spinal cord stimulator

The researchers identified hotspots in the lower spinal cord with connection to the gait and balance problem of the patient. The surgeon connected the neuroprosthesis to these hotspots to stabilize gait, balance and muscle strength. Following the surgical procedure Mr. Gauthier had to undergo a few months of rehabilitation with the neurostimulator to practice walking, develop strength and coordination between the right and left leg. His body was no longer stiffening or freezing in place. He could now take a 3-mile lakeside stroll without stopping. He can now manage stairs going up or coming down smoothly. In the past his gait would suddenly freeze or he lost hist balance. None of this

Is happening now. He simply is walking normally.

The final word of Dr. Moraud

“The stimulation here is focused on the spinal cord. We target the region of the spinal cord that will control all the leg movements.” Inserting a neurostimulator is not a cure, simply a procedure to help the patient lead a normal life.

Help to Walk for Parkinson’s Disease Patients

Conclusion

A new surgical procedure, namely inserting a neurostimulator under the abdominal wall, is the latest approach to treat Parkinson’s disease. This is help to walk for Parkinson’s disease patients. The case, which I described here is the first case where doctors performed this new procedure. They identified hot spots in the lower spinal cord and connected them to the neurostimulator with electrodes. After a lengthy rehabilitation period the patient learned how to use the stimulator for optimal walking, balancing, and going stairs up and down. There are no more falls or gait problems and no freezing. At the end the patient can walk normally and even manage a walk of 3 miles. Researchers anticipate that this method will become an accepted treatment modality for gait problems of Parkinson’s disease patients.

Sep

2023

How the Immune System affects Parkinson’s Disease

By Ray Schilling | autoimmune disease, diet, Fitness, immune system, Inflammation, Parkinson’s disease

This article explains how the immune system affects Parkinson’s disease (PD). Notably, in the past physicians thought that Parkinson’s disease was due to a degenerative change of the substantia nigra. This explained why balancing was a problem, why shaking of the hands occurred and why falls happened often. It it important to realize that nobody thought about the immune system. And no-one knew that an autoimmune process could be behind Parkinson’s disease.

T cells that react to a damaged protein called alpha-synuclein

There are specific changes in the immune system approximately 10 years before Parkinson’s disease symptoms occur in patients who come down with the disease. Researchers from the La Jolla Institute for Immunology showed that T cells play a key role in causing PD. They react to a damaged protein called alpha-synuclein build up in the dopamine-producing brain cells. Laboratory physicians can assay this through a simple blood test, which becomes a screening tool for early Parkinson’s disease. The reactive T cells stay around for about 10 years, then fade away. There seem to be other immune factors that weaken the initial aggressive phase of the T cells.

The role of inflammation in Parkinson’s

When the immune system malfunctions chronic inflammation can develop. In farmers exposed to pesticides the later development of Parkinson’s disease was observed. The researchers thought that the pesticides caused an irritation of the immune system leading to chronic inflammation. There is evidence that the gut bacteria are different in Parkinson’s disease patients when compared to normal controls. The gut absorbs the metabolites of the abnormal gut bacteria and causes chronic inflammation. In an attempt to stop the inflammatory process, the immune system can develop autoimmune antibodies, which can cross react with cells of the substantia nigra. This in turn can cause Parkinson’s disease.

Lifestyle factors that people can change to prevent PD

Dr. Rebecca Gilbert, vice-president and chief scientific officer for the American Parkinson Disease Association (APDA) commented on the importance of lifestyle changes. She said: “It makes intuitive sense that instituting lifestyle modifications that potentially decrease inflammation may decrease the risk of Parkinson’s disease. Exercise, for example, has been shown to reduce inflammation and is probably one of the many reasons that exercise reduces the risk of Parkinson’s disease and also improves established Parkinson’s disease.” She commented further: “Also, we should avoid things like excessive alcohol and nicotine that we know have negative effects on the immune system,” she added. “And managing our stress as best as possible can slow and help maximize outcomes of many diseases.”

Changing diet can help postpone Parkinson’s disease

With regard to the best diet that will help Parkinson’s disease patients she said: “The MIND diet emphasizes whole grains, vegetables, nuts, legumes, and berries. Fish is the preferred protein and olive oil is the preferred fat. Recently a study showed that adherence to the MIND diet and the Mediterranean diet had an association with later onset of Parkinson’s disease.”

The gut connection to Parkinson’s disease

According to the WHO the global prevalence of Parkinson’s disease has doubled in the last 25 years. At this point we do not know why this is so. But many investigations have shown that there is a significant difference in the gut bacteria composition of healthy controls and Parkinson’s disease patients. There is a 30% difference between the bacterial composition of healthy controls and patients with Parkinson’s disease. This has led to Braak’s Hypothesis of Parkinson’s Disease. This hypothesis says that an unknown pathogen enters through the nose, the person swallows it and it ends up in the gut. Absorption gets it into the gut wall and it migrates through the vagus nerve into the central nervous system where it leads to accumulation off alpha-synuclein in the substantia nigra. This destroys the dopamine producing cells in that region causing the symptoms of PD.

Can any diet fight gut dysbiosis?

In 2022 study they found that flavonoids, the pigments of fruit were associated with a lower mortality of patients with Parkinson’s disease.
In an earlier study of 2018 researchers determined that a protein from fish with the name parvalbumin helped Parkinson’s patients to stop producing alpha-synuclein. PD patients suffer from clumping of alpha-synuclein, which causes their symptoms.
Restriction of refined carbohydrates “especially diets with a low glycemic index, rich of vitamins and polyphenols, a Mediterranean diet for example, can be recommended”.

Regular exercise to prevent Parkinson’s disease

Regular physical exercise maintains body function and muscle strength. Dr. Emer MacSweeney said: “Being physically active is one of the best things you can do for your body. Exercise helps protect against many diseases and keeps the heart, muscles, bones, and brain in optimum condition. Exercise promotes the oxygenation of the brain and stimulation of multiple neurochemicals.”

Several studies showed that patients with PD deteriorate slower, if they exercise regularly. Part of that response is due to the release of endorphins and serotonin, but we do not know all of the positive mechanisms of exercise at this time.

How the Immune System affects Parkinson’s Disease

Conclusion

Recent research changed what we know about Parkinson’s disease (PD). Braak’s Hypothesis of Parkinson’s Disease states that an unknown pathogen enters through the nose, gets swallowed and ends up in the gut. From there it gets taken up into the gut wall and migrates through the vagus nerve into the central nervous system. There it leads to accumulation of alpha-synuclein in the substantia nigra. This destroys the dopamine producing cells in that region causing the symptoms of PD. But we also know that chronic inflammation can aggravate the symptoms of PD patients. When the composition of the gut bacteria deteriorates, this too will make PD patients worse.

Lifestyle changes help to postpone Parkinson’s disease

A healthy diet, like the MIND diet, DASH diet or the Mediterranean diet have beneficial effects on PD patients. Many studies also found that regular physical exercise is a stabilizing factor in PD patients. There are still many gaps in what we know about the causation of PD. But the above summarized factors are a good start.

Jan

2021

Melatonin Is More Than a Sleeping Aid

By Ray Schilling | Alzheimer’s disease, Anti-aging medicine, Autism, autoimmune disease, Cancer, Cardiovascular disease, Circadian rhythm, Dementia, Diabetes, Health, heart attack, Heart Disease, Hormones, immune system, Inflammation, Insomnia, melatonin, Menopause, mitochondria, Multiple sclerosis, neurological disease, Osteoporosis, Parkinson’s disease, sleep, Stroke

Notably, the January 2021 issue of the Life Extension magazine informs you that melatonin is more than a sleeping aid. It contains an interview between Dr. Roman Rozencwaig and a Life Extension (LE) magazine reporter. It must be remembered that Dr. Rozencwaig dedicated much of his career to the healing effects of melatonin. Another keypoint is that in 1987 Dr. Rozencwaig published a paper together with two other researchers. Specifically, it showed that melatonin production by the pineal gland declines in older age. Markedly, they stated that this is the reason why people age and why diseases of aging develop. Another key point is that Dr. Rozencwaig also stated that taking oral melatonin can promote a healthier life.

Melatonin deficiency causing aging and various illnesses

With the aging process the pineal gland calcifies and melatonin production is steadily declining. Surely, along with this is a deterioration of the circadian hormone rhythm. Meanwhile, the neuroendocrine system in the brain gets disorganized. Accordingly, this causes various diseases to occur. To emphasize, Dr. Rozencwaig says that a proper balance between melatonin and neurotransmitters is what we need to maintain health and longevity. As a result, a daily intake of melatonin supports healthy aging and longevity.

The many clinical effects of melatonin

Oral melatonin tablets help you to fall asleep easier, particularly the population that is older than 60 years.

But besides that, melatonin has many other clinical effects.

Melatonin improves immunity, which improves resistance against infections. It helps also in cancer prevention
Melatonin maintains the circadian hormone rhythm by synchronizing pituitary and hypothalamic hormone production
It protects the brain and may prevent Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, autism, and others
Melatonin modulates anti-inflammatory cytokinins in different diseases

Dr. Rozencwaig mentioned that melatonin slows down the aging process. There are multiple intertwining reasons for this.

Melatonin’s actions against the aging process

Melatonin regulates gene expression. This means that some signs and symptoms of aging can be reversed through genetic switches
Because melatonin regulates the immune response, the body is more protected against viral, bacterial and parasitic infections
Melatonin helps to overcome chronic inflammation that produces cytokines
Melatonin is also liver-protective through stimulation of an enzyme (AMPK). This enzyme regulates cellular metabolism.
There are other processes that melatonin is involved in: energy metabolism by protection and restoration of mitochondria.
Melatonin protects against osteoporosis by balancing and regulating bone formation versus bone loss.

More actions of melatonin

An important function of melatonin is the stimulation of antioxidant enzymes like glutathione peroxidase and superoxide dismutase (SOD)
Melatonin regulates sirtuins, which are proteins that maintain cellular health. They protect you from obesity, type 2 diabetes, cancer, heart attacks and strokes, dementia and more
As already mentioned, melatonin is a neuroprotective agent and may prevent Alzheimer’s and dementia
Melatonin stimulates apoptosis of cancer cells.
Oral health and melatonin are related. Melatonin suppresses herpes infections and periodontal disease. Melatonin prevents oral cancers to a certain degree. In addition, dental implants survive better when melatonin is present in saliva.

Prevention of cognitive decline

Dr. Rozencwaig mentioned that melatonin stops much of the cognitive decline of aging. To achieve this the following processes take place.

Melatonin improves the sleeping pattern and increases the amount of REM sleep.
During sleep melatonin removes toxic amyloid and tau proteins. We know that with Alzheimer’s disease these are the proteins that accumulate in the brain.
Melatonin improves myelination of white matter in the brain. This prevents brain atrophy of old age.
The brain is metabolically very active and produces toxic free radicals. But melatonin is a strong antioxidant dealing with free radicals. Melatonin can cross the blood brain barrier and stimulates enzyme production to eliminate toxic reactive oxygen species.
Chronic inflammation also increases with age, but melatonin deals with this condition in the brain.
Here are 3 subtypes of melatonin receptors. The body integrates the multitude of actions of melatonin with the help of these receptors.

Melatonin Is More Than a Sleeping Aid

Conclusion

Melatonin is a powerful antioxidant that has many other useful protective qualities as explained. The body integrates various functions like anti-aging, anti-free radical activity, neuroprotection in the brain and more. Melatonin even synchronizes pituitary and hypothalamic hormone production. This helps to integrate the effect of melatonin, which benefits the body in many ways. Melatonin prevents Parkinson’s and Alzheimer’s disease, multiple sclerosis, autism, obesity, type 2 diabetes, cancer, heart attacks, strokes and dementia. Melatonin production deteriorates from the age of about 60 onwards. It is important to supplement with melatonin at nighttime from that age on. Usually, you only need small amounts of melatonin, between 1mg and 3 mg at bedtime. This prevents most of the serious diseases of old age, stimulates your immune system and lets you age gracefully.

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Aug

2019

Connection Between Parkinson’s Disease And The Removal Of The Appendix

By Ray Schilling | Parkinson’s disease

In the first place, a large study from Cleveland Medical Center found a connection between Parkinson’s disease and the removal of the appendix. It is important to realize that Dr. Mohammed Z. Sheriff who was the main investigator assembled 62.2 million patients’ records. Of these 488,190 (0.78%) patients had an appendectomy done. 4,470 (0.92%) among these patients went on with a diagnosis of Parkinson’s disease. Of the remaining 61.7 million patients physicians eventually diagnosed 177,230 individuals (0.29%) with Parkinson’s disease. This means that the patients with a prior appendectomy had a 3.17-fold higher risk to develop Parkinson’s disease. Whoever did not have their appendix removed had a lower risk to develop Parkinson’s disease.

Older, smaller studies in the past were ambiguous

A 2016 Movements Disorders study with 1.5 million people in Denmark found that patients who had an appendectomy were a slightly higher risk of developing Parkinson’s disease later in life.

In contrast, a 2018 Science Translational Medicine study found the opposite among 1.6 million Swedes. Patients who had an appendectomy had a lower risk of developing Parkinson’s disease and there was a delay in the onset of it.

It was this discrepancy what motivated Dr. Mohammed Z. Sheriff to design the much larger study that he carried out. He presented the findings at the 2019 Digestive Disease Week meeting that took place May 18–21 in San Diego, CA.

Alpha-synuclein associated with Parkinson’s disease

At the same time other investigators found that alpha-synuclein, an abnormal protein in nerve cells, is important for the development of Parkinson’s disease. It plays a role in patients with appendicitis who need surgery. But it also is present in the substantia nigra in the brain of patients with Parkinson’s disease. Notably, patients with Parkinson’s disease often have problems with their balance, muscle rigidly, tremor and slowness of movements.

Indeed, alpha-synuclein has become an important marker for the development of Parkinson’s disease. This publication indicates that monocytes that are activated by the presence of alpha-synuclein can cause significantly more inflammation in the nerve cells of the substantia nigra in the brain. Other authors postulate that oxidative stress in vagal neurons may lead to alpha-synuclein, which can be transported from foci such as in the appendix to the substantia nigra in the brain. More recent studies have shown alpha-synuclein in the gut of patients with Parkinson’ disease according to Dr. Sheriff. In particular, it clearly shows that our gut biome plays a role in the development of disease.

Older people affected by Parkinson’s disease

Certainly, it is mostly people above the age of 60 that come down with Parkinson’s disease. Another key point is that there is no known effective treatment for Parkinson’s disease. However, the new information that alpha-synuclein is a factor in the early stages of Parkinson’s disease is most compelling evidence. By and large, this process leads to toxic clumps of Lewy bodies in nerve cells of the brain and in the gut wall including the appendix. Nobody knows exactly the meaning of Lewy bodies and alpha-synuclein. But if they are playing a part in the initiation of Parkinson’s disease, medications that fight oxidative stress in the nervous system may be a new approach to treating Parkinson’s disease. There is a need for more research.

New approaches to treat Parkinson’s disease

Here is a publication that points out that existing treatment for Parkinson’s disease does not include targeting alpha-synuclein. In the future, these authors state, this will change, as immunotherapy directed at alpha-synuclein will interrupt the development of Parkinson’s disease. Here is another publication that stresses the importance of alpha-synuclein in the development of Parkinson’s disease. It points to testing new therapies in animal experiments and in clinical trials.

Connection Between Parkinson’s Disease And The Removal Of The Appendix

Conclusion

The observation that people who had an appendectomy have a 3.17-fold higher risk to develop Parkinson’s disease led to more investigations. It became obvious that an alpha-synuclein accumulation in the nerve cells of the gut wall was playing a role in the disease and formed Lewy bodies. It confirms the concept that disease processes can start with our gut biome. These cells can travel via the vagal nerve into the part of the central nervous system, called substantia nigra. It is there that the dopamine producing nerve cells reside. Destruction of these dopaminergic nerve cells leads to the symptoms of Parkinson’s disease. One of the new approaches to treat Parkinson’s disease is by immunotherapy where antibodies destroy the alpha-synuclein protein. However, clinical trials will have to follow that are testing this new treatment possibility.

Jul

2019

Common Drugs Have A Connection To Dementia Risk

By Ray Schilling | Cancer, Dementia, Drugs, epilepsy, Parkinson’s disease, seizure disorder

A recent publication stated that common drugs have a connection to dementia risk. The study had an observation time of 12 years (from 2004 to 2016) and involved 284,343 patients in the United Kingdom. There is a group of drugs, namely anticholinergic drugs, that were particularly strong with regard to causing side effects of dementia. A variety of anticholinergic drugs exist, such as antidepressants like paroxetine or amitriptyline. But there are other anticholinergic drugs like bladder antispasmodics (they also go by the name bladder antimuscarinics, such as oxybutynin or tolterodine). Other anticholinergic medications are antipsychotics that are in use for psychotic diseases. Examples are chlorpromazine or olanzapine. Anti-epileptic drugs also belong into the anticholinergic drug group. Common anti-epileptic drugs are oxcarbazepine or carbamazepine.

The researchers found that 58,769 of the patients that took strong long-term anticholinergic medication developed a dementia diagnosis.

More about the study

The researchers found that the risk of developing dementia for those who consumed only a few anticholinergic drugs was low. It amounted to only 6%. In contrast, patients who took a lot of anticholinergic drugs at least for 3 years or more developed dementia in 49% of all cases, which is quite a significant amount.

Dr. Douglas Scharre, director of the division of cognitive neurology at the Ohio State University Wexner Medical Center in Columbus was not involved in the study. He said: ”I spend a lot of my time in the memory disorder clinic seeing geriatric patients and taking people off medications, mostly those medications that have anticholinergic properties. Many times there can be another drug out there that has less anticholinergic impact or is non-anticholinergic that may work.”

Risk-benefit discussion

He went on to say that some drugs are really necessary to control a psychosis or seizures, so it is a matter of discussing with the physician whether it is worth taking a risk of possible dementia versus a risk of a flare-up of psychosis or of a seizure.

More statistics

Patients who received treatment for depression with anticholinergic antidepressants had a risk of 29% of developing dementia. Anticholinergic anti-Parkinson drugs had an association of a rate of 52% of dementia. Anti-psychotic drugs led to dementia in 70% of the treated cases. Bladder relaxing medications (medically called antimuscarinic drugs) had a risk of 65% to cause dementia. Finally, anti-epileptic drugs had a risk of causing dementia in 39%.

The researchers noted that these findings highlight how important it is reducing exposure to anticholinergic drugs in middle-aged and older people.

Serious side effects from other medication

Unfortunately there is a history of serious side effects regarding several medications.

Tardive dyskinesia with antipsychotics

Long-term treatment of schizophrenia with antipsychotic drugs can cause severe side effects. One of the more severe side effects is tardive dyskinesia, which occurs in 5% per year of antipsychotic medication use, and in about 1%-2% of these it is severely disfiguring the face. Tardive dyskinesia can lead to permanent involuntary movements of the muscles around the mouth and the eyes. The jaw and the tongue may also show involuntary movements, and in time this leads to a disfigured look of the face, often with asymmetries between the right and left side of the face. Unfortunately, withdrawal of the antipsychotic medications will not improve the tardive dyskinesia. Often expensive lifelong Botox injection therapy every 6 to 8 weeks is necessary to alleviate some of the effects of this devastating dyskinesia.

Side effects from antacid pills

Lansoprazole (Prevacid) belongs to the proton pump inhibitors and is a very strong acid production inhibitor. Because it is so reliable in suppressing stomach acid, it is popular with the public. What is not so well known are the side effects of this drug. The most common side effects are about bone fractures, severe diarrhea, kidney damage, systemic lupus erythematosus and fundic gland polyps. These polyps can later turn into stomach cancer. Unfortunately, drug companies do not always report about the less frequent side effects.

A rare side effect: muscle tremor

One of these side effects is a muscle tremor (jerking movements or shaking). It is listed under the side effects way down the list where you may overlook this. To the patient it can be devastating as the symptoms are very similar to Parkinson’s disease. Imagine a 40-year old man taking this medicine for stomach acid and coming down with these muscle tremor symptoms! Fortunately, when you recognize the connection, you can stop the medication and the symptoms frequently go away or at least diminish.

Rhabdomyolysis from statins

When a patient is receiving statins because of high cholesterol, one of the possible side effects can be rhabdomyolysis. This typically presents with muscle weakness, fatigue, and lower urine output. The urine may be of a dark color. Confusion, vomiting and agitation can also set in. It is necessary to immediately recognize these type of side effects, and the statin drugs should be stopped. The patient requires a kidney specialist to watch the kidney function. Often these patients need treatment in hospital.

Cancer and heart attacks from synthetic hormones

The “Women’s Health Initiative” with a study on 16,000 postmenopausal women had to be stopped prematurely in 2002. This was a study that examined the effects of two synthetic hormones, the estrogen Premarin and the progesterone-like substance Provera. The purpose of the study was to show whether heart attacks, osteoporosis and strokes would be reduced on hormone replacement compared to controls. But the results were shocking: the opposite was true! The risk in the treatment group for strokes was 41% higher than for the controls and for heart attacks it was 29% higher! But this was not all. The treatment group had twice as many blood clots in their legs and 26% more breast cancer. Colorectal cancer was 37% higher and Alzheimer was a whopping 76% higher than in the controls.

Synthetic hormones caused estrogen dominance

The synthetic hormones functioned like xenoestrogens, meaning that there was a partial resemblance of the synthetic hormones to estrogen and progesterone, blocking their hormone receptors, but not stimulating them. The end result was an estrogen dominance state in the blood, which caused all of the problems. When bioidentical hormone replacement is done with bioidentical estrogen and progesterone, the opposite is the case. Women live longer because they get less heart attacks and strokes; they also get less cancer. In Europe bioidentical hormone replacement has been in use for over 50 years, and in the US physicians who use bioidentical hormone replacement have experience for almost 30 years.

Discussion

We started this article describing side effects of anticholinergic drugs and how this can bring on dementia. Other researchers have noted that dementia and strokes can be brought on by diet drinks. We then got into side effects of other drugs like tardive dyskinesia with antipsychotic drugs. We discussed the possibility of tremors from antacid drugs. A rare side effect of statins is rhabdomyolysis. And we talked about cancer and heart attacks from synthetic hormones in postmenopausal women. We need to be aware that any chemical brought into our system can cause undesirable side effects. Chemicals like drugs can interfere with biochemical reactions in the body that ultimately result in side effects including cancer and heart attacks.

Common Drugs Have A Connection To Dementia Risk

Conclusion

In a recent publication we learnt that patients who took a lot of anticholinergic drugs at least for 3 years or more developed dementia in 49% of all cases, which is quite a significant amount. But there are other drugs that have serious side effects. For instance, there is tardive dyskinesia, a disfiguring condition in the face that can develop with antipsychotic medicine for schizophrenia. Statins can cause a painful muscle condition, rhabdomyolysis. The “Women’s Health Initiative” showed a study that examined the effects of two synthetic hormones, the estrogen Premarin and the progesterone-like substance Provera.

Synthetic hormones causing problems

The purpose of the study was to show whether heart attacks, osteoporosis and strokes would be less on hormone replacement compared to controls. Unfortunately quite the opposite happened. The risk in the treatment group for strokes was 41% higher than for the controls and for heart attacks it was 29% higher! But this was not all. The treatment group had twice as many blood clots in their legs and 26% more breast cancer. Colorectal cancer was 37% higher and Alzheimer was a whopping 76% higher than in the controls. Only bioidentical hormones are tolerated without any side effects. We need to treat our bodies with respect and stay away from noxious substances.

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Jan

2019

Alzheimer’s disease is treatable with hormones

By Ray Schilling | Alzheimer’s disease, Hormones, neurological disease, Nutrition, Parkinson’s disease, Prevention, testosterone

Dr. Thierry Hertoghe, an endocrinologist from Belgium, stated that Alzheimer’s disease is treatable with hormones. This talk was part the 26^th Anti-Aging Conference of the American Academy of Anti-Aging Medicine in Las Vegas (from December 13 to 15, 2018).

First of all, Dr. Hertoghe treated many Alzheimer’s patients himself and noted that they often have multiple hormone deficiencies. Secondly, common deficiencies affect thyroid hormones, human growth hormone, estradiol for women and testosterone for men. But even vasopressin and oxytocin are hormones that may be lacking. Third, after doing thorough blood tests to assess hormone levels, Dr. Hertoghe replaced what hormones were missing. Finally, many Alzheimer’s patients got their energy, muscle strength and memory back.

In the following I am summarizing what Dr. Hertoghe told the audience about the various hormones. Alzheimer’s disease is treatable with hormones. Later I provide the hormone doses that Dr. Hertoghe uses for replacement.

Progressive memory loss

Generally, patients who develop Alzheimer’s disease start losing short-term memory first, but in time they will also lose long-term memory. Often this disease process starts in the 60’s as age-associated cognitive impairment. In the 70’s it may progress further to mild cognitive impairment, only to take off in the 80’s as Alzheimer’s disease. The astute clinician may order some screening blood tests in the 60’s and 70’s. In a male low testosterone, low DHEAS and low thyroid hormones may be present. Certainly, blood tests will show this readily. Frequently, in women low estradiol, low thyroid and low DHEAS may also be present. The reason this is important is that simple hormone replacement can return a person back to normal. Yes, this is right: hormone replacement can bring a person with age-associated cognitive impairment or mild cognitive impairment back to normal! In other words, Alzheimer’s disease is treatable with hormones.

Hormones important to monitor with Alzheimer’s disease

There are 6 hormones that are important for memory restoration in Alzheimer’s patients: IGF-1 (and growth hormone), thyroid hormones, estrogen and testosterone, vasopressin (and oxytocin) and pregnenolone. However, as Alzheimer’s patients often have sleep problems, another important hormone is melatonin.

Oxytocin to calm down aggressive Alzheimer’s patients

Notably, Dr. Hertoghe found that Alzheimer’s patients often are restless and can be aggressive. This makes it difficult to care for them in a home. Oxytocin is the hormone of trust, affection, sociability and concerns about others. It calms down aggressiveness. But with oxytocin treatment the Alzheimer’s patient feels better, becomes friendly, cooperative and warm-hearted.

As an illustration Dr. Hertoghe gave an example of one of his 80-year old patients with aggressive Alzheimer’s disease. She became unmanageable for her non-married son and other contacts. 5 IU of oxytocin sublingually changed this woman into a friendly, compassionate, warm-hearted woman, and the aggressiveness disappeared completely.

Insomnia in Alzheimer’s patients

About 45% of Alzheimer’s patients develop “sundowning”. When the sun goes down they start getting hyperactive, develop unacceptable behaviors and they become restless. Research papers showed that blood melatonin levels are low in these patients. Indeed, this is why they respond very well to small amounts of melatonin at bedtime. As a conclusion, within only a few days of starting this, their sundowning disappears, and they become easier to look after.

Dr. Hertoghe provided material from several research papers that showed that Alzheimer’s patients are often deficient for melatonin. Replacement with varying doses of melatonin solved even more complicated insomnia problems.

Melatonin is a powerful anti-oxidant. Interesting animal experiments have shown that melatonin has memory-enhancing properties. Researchers believe that melatonin improves the extracellular senile plaques with amyloid-beta peptide accumulation (first of 2 Alzheimer’s lesions). In addition melatonin also decreases the intracellular neurofibrillary degeneration tangles, the second of the two specific Alzheimer’s lesions.

IGF-1 and human growth hormone

Several studies have shown that Alzheimer’s patients have a significant drop in IGF-1 levels and growth hormone levels. This affects their short-term and long-term memory. Serum IGF-1 has an inverse correlation with cognitive impairment. Dr. Hertoghe said that IGF-1 treatment in Alzheimer’s patients increases their brain volume, increases the functional network of neurons in the brain and increases memory.

Brain atrophy in Alzheimer’s patients from chronically depleted IGF-1

Dr. Hertoghe showed a slide of a normal brain with a view from the outside and a cross section view of the brain. The same slide contained the view of an Alzheimer’s patient’s brain. It showed brain atrophy resulting in a much smaller brain and the cross section displayed an increase of the hollow spaces (e.g. the third and forth ventricle). He stressed that in his view the brain shrinkage of Alzheimer’s patients is due to prolonged low levels of IGF-1. This in turn is due to a lack of production of human growth hormone.

With IGF-1 treatment the serum IGF-1 was increasing and the cognitive function in older adults recovered. Dr. Hertoghe provided many literature citations to support this, which I will not repeat here.

Case report of a male patient with Alzheimer’s disease

Dr. Hertoghe presented one of his patients with Alzheimer’s. Lab tests showed that he had deficiencies of thyroid hormones, DHEA and testosterone. But despite replacement of these hormones he remained severely affected with Alzheimer’s. He did not remember his own name, could not go to the toilet on his own, spoke only a few words and suffered from severe fatigue. He received 4 injections around his eyes with IGF-1 and mesotherapy from his doctor (described below) with human growth hormone and IGF-1. Within a few weeks he had a complete reversal of his cognitive decline. He could return to his professional driving career doing halftime work with a delivery van in the city. He could read a newspaper and understood what he was reading. Alzheimer’s disease is treatable with hormones.

Thyroid hormones

According to Dr. Hertoghe thyroid hormones help to establish short-term and long-term memory and treat the apathetic depression in Alzheimer’s patients. Many Alzheimer’s patients are hypothyroid.With this deficiency they have swollen lower eyelids, a puffy face and paleness of the face. In a 1990 study a group of Alzheimer’s patients had 26% lower T3 levels when compared to normal controls. Many patients with hypothyroidism have memory loss, before their deficiency is corrected. Dr. Hertoghe stated that 13% of all dementia cases are reversible by proper thyroid hormone treatment.

Estradiol can improve long-term memory loss

Research showed that estradiol could improve long-term memory in dementia and Alzheimer’s disease cases. Many female Alzheimer’s patients are deficient in estrogens. If they do, they have dry eyes, a pale face and thin, dull hair. In a 2005 study 33 control women were compared to 48 women with Alzheimer’s disease. The estradiol levels in the Alzheimer’s disease group showed significant depletion compared to the normal control group. There was no significant difference found with regard to progesterone, testosterone and LH&HSH levels. Another study showed that in cerebrospinal fluid of women with Alzheimer’s disease the estradiol level was significantly reduced while the beta-amyloid levels were significantly increased.

Dr. Hertoghe reviewed several studies that showed that symptoms of Alzheimer’s disease disappeared with estradiol supplementation. Both memory and mood responded to the treatments.

Men with Alzheimer’s disease are often testosterone deficient

Testosterone is important for long-term memory. Men in andropause report erectile dysfunction, general weakness and memory loss. The physician needs to be aware that the patient may be starting to develop Alzheimer’s disease. Dr. Hertoghe showed a slide based on a publication, which stressed that testosterone enhances memory. It increases brain blood flow and thickens the myelin sheets. Testosterone increases dendrite and synapses and in addition decreases amyloid beta-peptide production. Neurotoxicity is also reduced. The end result is improvement of Alzheimer’s in males with testosterone replacement.

Pregnenolone improves short-term memory

Pregnenolone gets synthesized in the brain, spinal cord and peripheral nerves. Dr. Hertoghe said that pregnenolone is a neurostimulating “neurosteroid”. Pregnenolone concentrations in brain tissue are about 25- to 35-fold higher than in the blood stream. Some cases of Alzheimer’s disease can come from a lack of pregnenolone and pregnenolone sulfate. Patients who have Alzheimer’s because of a lack of pregnenolone have blood levels that are 2.5-fold lower than pregnenolone levels in normal controls. When these patients are treated with pregnenolone, their memory improves. The mechanism of the effect of pregnenolone is by increasing acetylcholine by more than 50% in the hippocampus. It also protects the hippocampus from glutamate and amyloid beta. Pregnenolone improves short-term memory over a period of 3 to 4 months of treatment.

Vasopressin improves short-term and long-term memory loss

Postmortem studies on Alzheimer’s patients showed that there is decreased vasopressin in the brain cortex. In patients with alcoholic dementia (Korsakoff psychosis after recovery) there was decreased vasopressin in the cerebrospinal fluid. Often patients with diabetes insipidus have decreased vasopressin and are in danger of developing dementia. If not treated, they develop short-term and long-term memory loss. When treated with vasopressin or Desmopressin their memory recovers within 4 hours of starting therapy. Younger patients (50 to 73) do better with memory recovery than older patients (74 to 91).

Treatment details of hormone replacement for Alzheimer’s disease

Before hormone treatments are given to a patient it is important to do a battery of blood tests. This will help the physician to identify the missing hormones in a particular patient. Each of the missing hormones are then administered separately.

Oxytocin

This hormone can be given sublingually or intranasally. Sublingually 5-10 IU are given daily. With the sublingual approach 1 or 2 sprays are given daily. Each spray contains 8 IU of oxytocin. Improvement is visible within 2 to 5 days. A full recovery takes 2 to 3 months.

Melatonin

Most patients in the higher age group do no longer produce their own melatonin. With the oral route 1-3 mg are given every night before going to bed. An alternative is to use sublingual tables 0.5mg to 1.0mg at bedtime. The first improvement can be seen 2-5 days after the start of replacing melatonin, the full impact takes about 2-3 months from the start of the treatment.

IGF-1 and human growth hormone

Replacement of IGF-1 can be done by injecting IGF-1 or human growth hormone (HGH). HGH stimulates the liver to produce IGF-1. IGF-1 is somewhat cheaper than HGH. When IGF-1 is used, 0.3mg to 1mg is injected at bedtime. Progress is slow; the first improvement is visible at 2-4 months, it takes up to 24 to 36 months for a full recovery.

For severe memory impairment with Alzheimer’s, the doctor does a double treatment approach with both IGF-1 and HGH: first subcutaneous IGF-1 injections around the eyes 4 times per day (0.01mg each). Secondly, at the doctor’s office the doctor administers mesotherapy injections with 1mg of HGH and 1mg of IGF-1 and vasodilators 3 times per week. Two weeks later the doctor administers another course of mesotherapy. He may repeat this twice in 14-day intervals. Now the interval increases to monthly therapy for 3 months and finally every 3 to 4 months. The patient can use IGF-1 nose drops instead of subcutaneous IGF-1 injections.

Thyroid hormones

Dr. Hertoghe prefers desiccated animal thyroid hormone replacement as the T3/T4 ratio is best matched to what the ratio is in humans. Depending on the severity of thyroid hormone deficiency the patient takes 30-150mg of thyroid hormone every morning. Dr. Hertoghe starts with a low dose and slowly increases the dosage. Clinical progress is very slow. It takes until the second month before the first improvement takes place. Full improvement can take 8-12 months.

Estradiol

Replacement of estradiol in postmenopausal women with Alzheimer’s disease received ether more than 0.1mg per day or 0.625mg of conjugated equine estrogen daily. In both cases there were improvements of their memory and improvement on the Hamilton depression scale.

Dr. Hertoghe’s preferred way to treat postmenopausal women with Alzheimer’s disease is as follows. The first 25 days of each month he gives them 1-2mg of oral estradiol valerate each day and 100mg of micronized progesterone. If they prefer an estrogen cream, he gives them 1-3mg per day transdermal estradiol and 100mg micronized progesterone capsules.

The first improvement is visible after 2-4 months; there is further improvement the next 8-12 months.

Testosterone

There are two methods of how to do hormone replacement with testosterone, either by injection or as transdermal cream. The injection treatment uses 250mg of testosterone enanthate or cypionate every 2 -3 weeks. The patinet can also self-administer testosterone enanthate (50mg twice per week) for a more even blood level of testosterone. The transdermal approach involves 100-250mg transdermal, nanoliposomal testosterone daily.

The memory will improve 2-4 months into replacement therapy. The full improvement takes 8-12 months.

Pregnenolone

The replacement therapy is 100mg per day in the morning for the first 4 months. Then there is a dosage reduction to 50mg daily. Studies have shown that 30mg of pregnenolone is not enough to treat memory loss. Short-term memory improved after 3 to 4 months in about 75% of patients.

Vasopressin

The best vasopressin preparation to use is bio-identical vasopressin. It comes as 1 nasal spray with 10IU of vasopressin. Upon awakening the patient or caregiver applies 1-2 sprays into the nose. The patient receives the second dose 10 minutes before lunch by nasal spray.

Apart from hormones, lifestyle changes are also recommendable.

Alzheimer’s disease is treatable with hormones

Conclusion

Who would have thought that Alzheimer’s disease could have anything to do with hormones? Dr. Hertoghe, the endocrinologist from Belgium did many hormone tests on Alzheimer’s patients and concluded that various degrees of hormone deficiencies can indeed cause Alzheimer’s disease. But what is more is that you can replace the missing hormones and see complete cures in patients with Alzheimer’s disease. Alzheimer’s disease is treatable with hormones. This is something conventional medicine can only dream of. At this point this hormonal approach is not yet mainstream medicine; but it would not be a surprise to me, if in 10 or 20 years interested physicians do this type of therapy routinely in their practice. When hormones are missing, replace them. When the memory is fading, think about testing for missing hormones! It will make a difference in the quality of life for the patient as well as for his family.

Nov

2018

Gut Bacteria Crucial To Healthy Aging

By Ray Schilling | Alzheimer’s disease, Anti-aging medicine, Cancer, lifestyle, Mortality, Parkinson’s disease

New research presented at the London Microbiome Meeting asked the question “are gut bacteria crucial to healthy aging?” Marina Ezcurra, is a Ph.D. is a researcher working at the Queen Mary University of London in the United Kingdom. She uses a nematode (round worm) model to investigate various aspects of aging. Nematodes like C. elegans provide a useful model not only for genetic work, but also for the human gut flora as well. Moreover, it allows making observations about the connection between bacterial genes and aging. Coupled with the fact that the worm has such a short lifespan, the researchers can test bacterial genes, the aging of the worm and get meaningful results in short order.

It seems like one of the research objectives was changing the nematode’s gut flora and observing life expectancy and age-related diseases.

Pathological versus healthy gut bacteria composition

Dr. Ezcurra did a couple of experiments with the nematode C. elegans as a model. She could show that the worm’s gut bacteria composition mattered. First of all, if there was a pathological composition of the gut flora, the worm did not turn as old and there were various age-related diseases that developed. Secondly, they were very comparable to human age-related degenerative diseases like Alzheimer’s disease.

Another senior author researched how genes of gut bacteria influence life expectancy

Meet Dr. Meng Wang, associate professor of molecular and human genetics, Baylor College of Medicine in Houston, TX. He did extensive genetic research on C. elegans. He used this model, because C. elegance lives only 2 to 3 weeks. This animal model is easy to manipulate. For instance, he studied the gut bacteria composition. This link explains that he tested about 4000 E.coli bacteria with various gene defects. 29 E.coli strains when deleted, increased the worms’ lifespan.12 bacterial mutants among those prevented cancer and amyloid-beta, found in Alzheimer’s disease. Some mutant bacteria caused longevity by acting on processes linked to aging.

Colanic acid is an important anti-aging factor in C.elegans

Dr. Wang joined Dr. Christophe Herman, associate professor of molecular and human genetics at Baylor, for further research. It turned out that one of the keys to longevity of the nematodes were the mutant bacteria in the gut over-producing the polysaccharide colanic acid. This allowed the nematodes to live much longer. The researchers could show further that fission and fusion processes with regard to mitochondria are important. Mitochondria are the energy packages in cells and these processes are regulated by the presence of colanic acid. As a result, if your gut has good bacteria you can grow old and escape Alzheimer’s disease and cancer.

Dr. Meng Wang said: “Of the nearly 4,000 bacterial genes we tested, 29, when deleted, increased the worms’ lifespan. Twelve of these bacterial mutants also protected the worms from tumor growth and accumulation of amyloid-beta, a characteristic of Alzheimer’s disease in humans.”

Creating longevity with metformin, a diabetic drug

Physicians have known for some time that metformin stimulates longevity genes. This is the reason why diabetics on metformin live longer than diabetics on insulin. Dr. Ezcurra mentioned on 24 October, 2018 in her talk at the London microbiome Meeting that she had done experiments with C. elegans and metformin. Metformin reduces the risk of cancer and increases longevity in C. elegans as well as in mice (other experiments). Currently there is a clinical trial going on that investigates anti-aging under the influence of metformin in older people.

Effects of metformin on anti-aging

Metformin has the potential to target diabetes, cancer and Alzheimer’s pathologies all at once.

The anti-aging effect in humans with metformin involves the gut bacteria. Dr. Ezcurra says that this is the reason why diabetics on metformin live longer than diabetics on insulin. Metformin influences the folate bacterial metabolism of the gut flora. Other research has shown that the Akkermansia bacteria in the gut, which are good, desirable bacteria, will increase from 3-5% to 12.44% of the gut flora under the influence of metformin. Here is the discussion in detail in the following link.

Effect of gut bacteria on psychiatric diseases, obesity and diabetes

Dr. Ezcurra said that there are many studies showing that dysbiosis of the gut can lead to psychiatric diseases, Parkinson’s disease, obesity and diabetes etc.

We need to know more about whether a healthy gut flora will let us age without causing age-related diseases. Dr. Ezcurra stated: “By better understanding the links between nutrition, microbiome, and health, we can understand how the elderly can maintain their microbiome, and also help them directly by using pre- and probiotic strategies. This would help us age in a better way, maintaining health and quality of life in old age without drugs or surgery.”

Gut Bacteria Crucial To Healthy Aging

Conclusion

The composition of the gut microbiome appears to determine whether we age gracefully or not and whether we get sick as we age or not. Everything depends on the diversity of the gut flora. There are bacteria in the gut that are good for us and also bacteria that are bad for us. Metformin has been shown to stimulate the good gut bacteria to multiply. Dr. Ezcurra is continuing her research into this. She clearly stated that it should be possible for us to age in a better way and maintain health and quality of life in old age without drugs or surgery.

Jan

2018

Bacterial Toxins Threatening The Brain

By Ray Schilling | Alzheimer’s disease, autoimmune disease, depression, Inflammation, mitochondria, Nutrition, omega-3 fatty acids, Parkinson’s disease

Dr. Robert G. Silverman gave a talk about bacterial toxins threatening the brain. He spoke at the 25th Annual World Congress on Anti-Aging Medicine in Las Vegas on Dec. 15, 2017. First of all, he pointed out how changes in the gut flora can affect the integrity of the gut wall. In addition this can eventually this lead to a leaky gut syndrome. But it does not end here. As a result the toxins enter the blood stream and affect the blood/brain barrier. Consequently in the end various neurological diseases can develop from this.

Here I am giving a brief overview of the talk by Dr. Silverman. But he was not the only one speaking to this subject. Several other speakers also brought up this subject throughout the conference. They stressed the importance of rectifying any gut dysbiosis to stop leaky gut syndrome and a leaking blood/brain barrier.

Leaky gut syndrome

When the gut flora changes there are often enteropathogenic E. coli strains, Shigella and Salmonella that invade the lining of the gut causing leaky gut syndrome. When toxins enter the blood stream, the body is starting to form antibodies against various proteins. Antibodies are acting against various targets: bacterial cytotoxins, cytoskeletal proteins, tight junction proteins and food antigens. Lipopolysaccharides (LPS) from toxins of gram-negative gut bacteria can also leak into the blood. This affects key organs like the liver, the heart, lungs, the joints, the immune system and the thyroid. When this process has gone on for some time, the blood/brain barrier is breaking down next. The intestinal inflammation causes the release of inflammatory cytokines that circulate in the blood stream. The cytokines cross the blood/brain barrier and activate the support cells in the brain, called microglia. This in turn causes inflammatory degenerative changes in the brain.

Blood/brain barrier

LPS circulating in the blood from gut bacteria endotoxins increase the permeability of the blood/brain barrier. This is bad news for the brain as it becomes vulnerable to attacks from the antibodies mentioned and from food particles. Dr. Silverman cited papers showing that circulating antibodies that cause inflammation in the brain can be the starting point for early Parkinson’s disease. Autoimmune antibodies can cause even depression.

Intestinal permeability can be assessed by various antibody constellations. For instance IgA antibodies point to an ongoing issue/early leaky gut syndrome. IgM antibodies indicate early onset and IgG antibodies chronic issues of leaky gut syndrome. If you add various antigens like LPS, zonulin and actomyosin you can pinpoint which structure of the gut wall is affected by leaky gut syndrome, and the antibody type adds more information about the timing of the onset of leaky gut syndrome.

Bacterial toxins threatening the brain when BBB damaged

As I already mentioned the blood/brain barrier (BBB) is often simultaneously affected when there has been leaky gut syndrome. There may be a delay, but eventually the BBB breaks down also, and the brain will be in jeopardy. Dr. Silverman gave an example of how depression can develop as result of a breakdown of the BBB. Chronic intestinal inflammation can suppress the sensitive hippocampus cells from regenerating. Physicians call that impairment of hippocampal neurogenesis. Inflammatory cytokines damage the neuronal cell progenitors. As a result patients with inflammatory bowel disease can have mood disorders and cognitive impairment. Sophisticated BBB blood tests can pinpoint whether the BBB is intact or establish whether there is impairment. The important thing to remember: there is a gut brain connection.

Fixing the gut to stop bacterial toxins threatening the brain

In order to fix the BBB, you must first concentrate on fixing leaky gut syndrome.

Avoid gluten, as gluten is causing inflammation of the gut wall.
Start taking probiotics that contain more than 30 Billion lactobacillus plantarum, lactobacillus acidophilus and Bifidobacterium lactis per daily dose.
Do a heavy metal detox involving phytonutrients, hops, turmeric, Andrographis, zinc, polyphenols, omega-3 fatty acids, and watercress plant extract. Andrographis, also known as the “King of Bitters”, is an Ayurvedic medicine used to promote digestion and stimulate appetite.

Nutrients to fix the blood/brain barrier

Dr. Silverman uses the following nutrients to repair the blood brain barrier.

Acetyl L-Carnitine: this helps to protect the mitochondria from oxidative damage
Berberine: reduces inflammation in brain injuries
Alpha-lipoic acid: preserves the integrity of the BBB by controlling oxidative stress
Curcumin: decreases brain swelling, preserves the BBB and increases tight junction protein in brain cells
Vitamin D3 (5000 IU or more): protects the BBB by various mechanisms
Omega-3 fatty acids: they increase cell membrane fluidity and protect the BBB
Resveratrol: reduces inflammation and restores the BBB

Neuroplasticity

In order for the brain to adapt to changes, it must be flexible, which means on a cellular level that nerve cells form new synapses, neurological pathways etc. This is what neuroplasticity means. Here are the factors that Dr. Silverman listed as facilitating neuroplasticity.

Regular exercise
DHA from fish oil capsule supplements
Turmeric
Whole coffee extract
Alpha-lipoic acid
Lactobacillus brevis and Bifidobacterium longum
Bifidobacterium animalis Lactis 420 (B420)
Probiotics: they feed the healthy gut bacteria (e.g. apple cider vinegar)
Elevate magnesium in the brain through L-threonate

Bacterial Toxins Threatening The Brain

Conclusion

In the last few years it has become abundantly clear that leaky gut syndrome is not an isolated matter. It is invariably connected to a breakdown of the blood/brain barrier (BBB). Leaky gut syndrome alone is bad enough as it can lead to a number of autoimmune diseases, like Hashimoto thyroiditis and others. But when the BBB is affected, antibodies can now affect nerve cells, can cause Parkinson’s disease, depression, and even Alzheimer’s disease. There is no reliable database for what can happen to the brain when the BBB breaks down.

Because of these connections it is important to sanitize the gut, re-establish a healthy gut flora and overcome leaky gut syndrome. This will at the same time repair the broken down BBB. It will also prevent further possible damage to the brain in the future. Your gut health is your brain health. Take care of both your gut as well as your brain!

Sep

2017

Parkinson’s Disease May Be Stopped

By Ray Schilling | coffee, depression, Diabetes, Drugs, Parkinson’s disease

Parkinson’s disease is common in the US; new research shows that the use of an old anti-depression medication can stopParkinson’s disease The use of nortriptyline, a 50-year old antidepressant has shown to normalize a nerve cell protein. In rats nortriptyline dissolved toxic alpha-synuclein clusters in brain cells. These toxic protein clusters seem to be happening in the brain of Parkinson’s disease patients also. It is the protein by the name of alpha-synuclein that research first found in rats to cause the toxic protein clusters in nerve cells of the substantia nigra, a part of the brain stem.

But nortriptyline was able to normalize the concentration of the protein. In preliminary studies in humans the investigators found that there was a significant improvement of Parkinson’s disease with the use of nortriptyline.

Placebo controlled trial with nortriptyline

Now a research team from Michigan State University in Grand Rapids conducted a larger clinical placebo-controlled trial. The lead researcher Collier of the study group found that Parkinson’s patients who received treatment for depression with the tricyclic agent nortriptyline needed less dopamine, the main drug used to treat Parkinson’s disease. This indicated to the researchers that nortriptyline was preserving brain cells that were still making their own dopamine. In rat experiments they could show that it was the dissolving of toxic alpha-synuclein proteins by nortriptyline that was the key to therapeutic success.

Lisa Lapidus, a co-worker on the Michigan State University research team summed up their research: “What we’ve essentially shown is that we are dealing with a drug that the FDA approved already 50 years ago. Patients tolerate the medication relatively well. This could be a much simpler approach to treating the disease itself, not just the symptoms.”

Parkinson’s disease may be stopped also by old diabetes drug

Thomas Foltynie found that the diabetes drug exenatide helps patients with Parkinson’s disease. Dr. Foltynie is a professor of neurology at the University College London and co-author of the study.

Exenatide is an injection drug. When preliminary studies showed that this drug was effective in helping Parkinson’s disease patients lose their problems with walking and balance, a formal study followed.

Professor Foltynie designed a study where 60 people with Parkinson’s disease either got injections of exenatide or placebo injections. Patient exams followed regarding their musculoskeletal system and balance at baseline and every 12 weeks. A score system of 132 points assessed their Parkinson’s disease. After 48 weeks those who had been taking exenatide had a gain of 1 point on that scale while the placebo group dropped 3 points. After 48 weeks the drug administration (exenatide) finished. But after another 12 weeks another scoring and assessment of the Parkinson’s disease symptoms took place. The experimental group on exenatide scored 3.5 points higher than the placebo group. This suggests that exenatide is helping to treat the cause of Parkinson’s disease, not just the symptoms.

Parkinson’s disease may also stop through the use of caffeine

Parkinson’s disease was in the news again because of another study that involved breaking up misfolded alpha-synuclein through caffeine.

Misfolded alpha synuclein forms clumps inside dopamine producing cells in the substantia nigra of the brain stem. Misfolded alpha synuclein acts like a toxin to the dopamine producing cells and eventually these cells die off. This is the brain region that is responsible for making muscle movements smooth and stabilizes balance. The cells that have misfolded alpha synuclein clumps in them also go under the name of “Lewy bodies”.

Dr. Jeremy Lee from the University of Saskatchewan (Saskatoon, Saskatchewan, Canada) has isolated two compounds from coffee. They are called C8-6-I and C8-6-N. They can bind to alpha-synuclein and prevent clumping, which stops the toxic effects on dopamine producing nerve cells. Like with nortriptyline the caffeine effect is a curative approach to Parkinson’s disease.

Parkinson’s Disease May Be Stopped

Conclusion

There is a new therapeutic approach to Parkinson’s disease. Researchers have detected a protein called alpha-synuclein to cause toxic protein clusters in nerve cells of the substantia nigra, a part of the brain stem. When these cells die from the accumulation of these misfolded proteins, patients come down with Parkinson’s disease. But three different methods of treatment can improve Parkinson’s disease by dissolving the protein alpha-synuclein.

Nortriptyline was able to normalize the concentration of the protein. In preliminary studies in humans the investigators found that there was a significant improvement of Parkinson’s disease with the use of nortriptyline.
Exenatide, an injection drug for diabetes, has been described to help Parkinson’s patients get better.
Caffeine can also dissolve misfolded alpha synuclein (two compounds from coffee called C8-6-I and C8-6-N). This helps patients with Parkinson’s disease to stabilize.

This is only the beginning of a new approach to Parkinson’s disease and an attempt to cure the disease by dissolving the underlying mechanism. So far the drugs that are in use for Parkinson’s disease are only attempting to stimulate dopamine producing nerve cells to produce more dopamine. But the underlying pathology of accumulating misfolded alpha-synuclein clumps is not yet in the treatment protocol. The new research is different, as it takes this into account in an attempt to prevent the condition.

Incoming search terms:

parkinsons disease

Jan

2017

Gut Bacteria Can Protect Your Brain

By Ray Schilling | Alzheimer’s disease, Autism, autoimmune disease, breast cancer, Cancer, Dementia, immune system, Infectious Disease, Inflammation, Nutrition, Obesity, organic food, Other neurological conditions, Parkinson’s disease, Prevention

The neurologist, Dr. David Perlmutter gave a keynote address where he pointed out that gut bacteria can protect your brain. The topic of his actual talk was “Rewrite your brain’s destiny” and the venue was the 24^th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas. Many of the talks centered around the gut microbiome. Specifically, in this talk Dr. Perlmutter stressed the fact that the right mix of gut bacteria will protect your brain, while the wrong mix can make you sick. There were many slides, but too much information to mention all of details of the talk here. With this in mind, I will summarize the broad outline of Dr. Perlmutter’s presentation and certainly emphasize the practical implications this has for everyday life to prevent degenerative brain diseases.

A few facts

Did you know that the brain uses 25% of the body’s energy, but has only a 3% of the body’s weight?

There are trillions of gut bacteria

The gut flora has trillions of gut bacteria with its own DNA material. 99% of the DNA material in our body comes from the gut bacteria and the bacteria on our skin surface; only 1% of the entire DNA in the body is your own DNA. We are eating for 100 trillion bacteria, but it is important to remember that if they are good bacteria they provide us with important vitamins and they produce molecules that stimulate our immune system.

We need healthy gut bacteria

This means we better have bacteria in our guts that are friendly, not the bad bacteria that can cause us problems. An Italian study determined the gut flora of children in central Africa (Burkina Faso) and compared the gut flora to children from developed countries in Europe. There was a significant difference with the African children having a healthy microbiome in the gut and the children from developed Europe having unhealthy gut bacteria. This is important new information. Many other research papers have established that leaky gut syndrome and autoimmune diseases are linked to dysbiosis, which is the name for the unhealthy microbiome in the gut.

Chronic inflammation

Dr. Perlmutter showed several slides where literature was cited showing that chronic inflammation in the civilized world is increasing. He also showed that dysbiosis (unhealthy gut bacteria taking over) is also increasing. On several slides Dr. Perlmutter showed that in civilized countries like Iceland, Denmark, Germany, the US, Japan and others the bacterial diversity of the gut bacteria in people was vastly reduced compared to the diversity of gut bacteria of people in Kenya, Ethiopia, Nigeria or rural India.

Diminished gut bacterial diversity causes more Alzheimer’s disease

The same countries that have diminished gut bacterial diversity (dysbiosis) also have the highest prevalence of Alzheimer’s disease. On the other hand the same countries with diverse gut bacteria have a low incidence of Alzheimer’s disease. When infestation with parasites was examined there was also a parallel between increased parasitic stress and low Alzheimer’s disease rates, again in countries like Kenya, Ethiopia, Nigeria or rural India. The same countries where gut dysbiosis was present the parasitic infestation was low.

Further research has established that gut dysbiosis leads to an inflammatory condition of the gut where lipopolysaccharides (LPS) from gut bacteria are absorbed causing inflammatory reactions within the body.

Leaky gut syndrome causes neurological diseases

At the same time this leaky gut syndrome can cause obesity and leakage in the gut/brain barrier as indicated in this link. The result is neuroinflammation, cognitive impairment and vulnerability to develop Alzheimer’s disease. Our most dreaded brain diseases come from inflammation: Alzheimer’s, Parkinson’s disease, autism, multiple sclerosis etc. These are degenerative brain disorders due to chronic inflammation. If you eat a lot of red meat, sausages and processed foods your gut microbiome will undergo negative changes. If you eat healthy food with lots of vegetables, fruit and you cut out sugar and too many starches, you have a healthy microbiome, which develops a robust immune system. We have to rethink the gut/brain connection and learn how to prevent these chronic illnesses.

Obesity and gut dysbiosis

The link above showed that obesity has a connection to inflammation. It was also shown with MRI scans that the part in the brain, called hippocampus was shrivelled up (atrophied). This is a typical sign of dementia and Alzheimer’s disease. The investigators also confirmed with mental health functional tests that these patients had cognitive decline.

Another study also noticed that in a group of obese patients the hippocampus part of the brain was shriveled up the more obese people were. Obesity and dysbiosis of the gut flora are part of the same problem.

Practical application: the DASH diet and the Mediterranean diet are both healthy, balanced diets, strikingly different from the Standard American diet. In a study the hypothesis was tested whether the DASH diet and the Mediterranean diet would postpone dementia in a group of elderly patients. The answer was: yes, the hypothesis is true.

What does gut dysbiosis do?

It was shown in mice that chronic inflammation of the gut through ingestion of an irritant (dextran sodium sulfate) led to reduced new nerve growth in the hippocampus compared to control animals. It only took 29 days to show a marked difference between experimental and control animals in terms of reduced growth in the nerve cells of the hippocampus, the center of cognitive control.

The gut wall released inflammatory kinins, which were the negative mediators affecting the brain.

Antibiotic residue and Roundup in food causes gut dysbiosis

Antibiotic treatments and antibiotic residues in milk, milk products, meat, but also in all GMO foods are the irritants of the gut wall in humans. The antibiotics change the gut flora and lead to dysbiosis, which then causes gut wall inflammation and the cascade of events described above. The new finding is that GMO food contains RoundUp (they are “Roundup ready” crops). The herbicide Roundup was originally patented as an antibiotic and still leads to significant dysbiosis. Dr. Perlmutter urged the audience to buy organic food as the only method to reduce our exposure to Roundup. Roundup contributes to causing celiac disease and gluten intolerance in addition to exposure to the modern wheat (Clearfield wheat). The FDA is starting to do testing on foods for Roundup (glyphosate).

Roundup linked to cancer

If things are sounding bad for Roundup, it only gets worse: Roundup has now been linked to causing cancer. In medicine it usually takes some time before the effect becomes obvious is. The agriculture industry has embraced the use of Roundup; I suspect that denial will be the first line of defense. My first line of defense in turn is to stick to organic food.

To sum up: Roundup and the Standard American diet lead to dysbiosis in the gut, which causes leaky gut syndrome. This causes inflammation with the release of cytokines and LPS from the gut wall to the blood. These substances cross the blood/brain barrier and lead to inflammation in the brain. This affects the hippocampus with the classical sign of shrinkage.

Chronic inflammation and neurological disease

But Parkinson’s disease, multiple sclerosis, autism in children and Alzheimer’s disease in older people are all caused by chronic inflammation. There are three more brain-related diseases that are related to gut inflammation: stroke, depression and attention deficit hyperactivity disorder (ADHD). Dr. Perlmutter spent some time explaining that antibiotic overuse even leads to an increase of breast cancer as a Danish study has shown. Antibiotic use showed a linear increase of breast cancer as a result of increased antibiotic amounts used. The highest group had a twofold risk compared to a control group with no antibiotic use. Dr. Perlmutter interpreted this to indicate that chronic gut inflammation can even cause a disease like breast cancer.

What can we do to diversify our gut bacteria?

Exercise: A recent study has shown that regular exercise is associated with a diversified gut flora. The reason seems to be the production of butyrate with exercise, which leads to a diversified gut flora. LPS levels (lipopolysaccharides from gut bacteria) are lower in people with a higher fitness score.
Eat a DASH diet or the Mediterranean diet as indicated above.
Avoid GMO foods because of the presence of Roundup, which functions like an antibiotic and leads to gut bacteria dysbiosis.
Remember “Antibiotics are weapons of mass microbial destruction”. If you need to take them be careful that you rebuild your gut flora with probiotics. Use of antibiotics increases the risk of type-2 diabetes by 1.53-fold. It also causes a quadrupling of Alzheimer’s disease.
A woman should consider natural childbirth whenever possible, as with a vaginal birth the child gets into contact with gut bacteria. Vaginally delivered children remain healthier than children delivered by Cesarean section for several years.
Acid-suppressing medications and NSAIDs (anti-inflammatory medication for arthritis) can also lead to dysbiosis. Proton pump inhibitors increase the risk of Alzheimer’s disease by 44%.
Prebiotic fiber can prevent Alzheimer’s. Probiotics do the same.
Avoid sugar: even the Oompa Loompa knew that “If you eat sugar, you get fat”. Obesity and gut dysbiosis cause a higher risk of degenerative brain diseases.
Take magnesium supplements (250 mg twice per day) and DHA from fish oil capsules. It stabilizes your brain metabolism.
In severe, persistent cases of gut dysbiosis a fecal transplant can be considered by your gastroenterologist. This procedure takes place in more than 500 hospitals in the US.

Gut Bacteria Can Protect Your Brain

Conclusion

The diversity of gut bacteria is immensely important. As discussed, in rural areas of the world there is gut bacteria diversity. In civilized parts of the world dysbiosis of the gut flora frequently occurs. This can lead to gut inflammation and the inflammation eventually becomes internal and can even reach the brain. These are the points to remember: exercise; avoid GMO foods, use prebiotics and probiotics. Avoid antibiotics; also avoid meat from animals that were fed antibiotics for faster growth. Don’t eat processed foods and avoid sugar. A healthy gut creates a healthy body, and this includes a healthy brain as well.