My first video this 2018 is taken from page 1 of my upcoming ebook, Healing from within with the last 3 slides containing tips on arthritis, stress, skin and digestive issues.
As alternative medicine grows in popularity, people are beginning to search everywhere for natural, health-promoting foods and supplements. It seems apparent that organic food rises far above conventional in helping to maintain a healthy body, but even organic food is highly depleted in nutrients compared to decades ago. There is little way around natural supplementation today, as soil is depleted and mainstream vitamins provide little or no benefit. People can utilize the health benefits of turmeric, vitamin D, and cacao, but there are other very powerful supplements out there that will contribute to incredible health.
Papaya Leaf Extract a Powerful Health Booster
One supplement you should not overlook is Papaya Leaf Extract. Papayas are excellent sources of dietary fiber, vitamin C, vitamin A, vitamin E, and folate, while at the same time being rich in antioxidants, flavonoids, and carotenes. Papayas also contain high amounts of enzymes called papain and chymopapain, which are critical ingredients for a healthy body. Enzymes are responsible for almost every aspect of life and health, and are needed to help control all mental and physical functions.
So what are the real uses for papaya leaf extract ? The beneficial properties surrounding papaya have been known for generations, but they are now just gaining back some attention. Some of the healing properties papayas provide are:
- Increased quality of proteins in whole organism.
- Revitalization of the human body and a maintaining of energy and vitality.
- Encouraged renewal of muscle tissue.
- Supported cardiovascular system.
- Strengthened immune system
- Help with the digestive system by breaking down proteins and supporting production of digestive enzymes.
- Treatment for skin wounds that don’t heal quickly.
- Prevention of cataract formation.
- Lowered risk of emphysema in smokers and passive smokers thanks to high vitamin D content.
- Alleviated inflammation.
- Help with nausea and constipation.
- Fighting various cancers and aiding the cardiovascular and gastrointestinal systems.
>How do I tell the difference between a headache and a migraine?
A migraine is a common and especially debilitating type of headache, usually characterized by neurological symptoms called an aura, one sided pain and/or nausea. More than half of migraine sufferers haven’t been diagnosed and may identify simply as having headaches.
In the Global Burden of Disease Study, updated in 2013, migraines were found to be the sixth highest cause worldwide of years lost due to disability.
>>How do I know if my headaches are “chronic?”
There is a clinical definition of “chronic” (15 days per month or more) but it can simply mean headaches that are frequent, reoccurring or disruptive to your daily routine, family time and career goals. Not the once in a while headache you get from being dehydrated, but headaches that repeatedly make it hard to show up as your full, vibrant self for the things you want and need to do for the people you love.
Steps to a Cure
If I had to use one word to describe my approach to the successful treatment and elimination of migraine, that word would be “balance.” The approach involves an orchestrated and synchronized adjustment of the components and functions of several systems in the body to achieve that goal.
Those areas are as follows:
- Neurohormonal system: This area includes the activities of the hypothalamus, pituitary gland, and glands that produce steroid hormones, namely the ovaries, testes, and adrenal glands. Our goal is to restore the hormones produced by these glands to levels that are appropriate for the individual.
- Pineal gland: This gland balances the cyclic production of the neurotransmitter serotonin and the hormone melatonin, both of which are key players in migraine, so our goal here is to reset the function of the pineal gland.
- Digestive system: Given that 70% of migraineurs also have some type of gastrointestinal disorder, restoration of balance within the digestive system is a critical part of the Migraine Cure.
- Magnesium balance: Another factor in this part of the program is achieving a balance between two critical minerals, magnesium and calcium, since an imbalance between these substances is a crucial factor in migraine.
- Sympathetic and parasympathetic systems: As we work to balance the four systems mentioned above, we are also simultaneously working toward a balance between the sympathetic and parasympathetic nervous systems, which is the ultimate goal of The Migraine Cure.
Migraine headaches are recurrent, painful headaches often accompanied by nausea, photophobia (i.e., light sensitivity) and/or phonophobia (i.e., sound sensitivity). A migraine is often unilateral and pulsating, and may occur with or without an aura (Rakel 2011; Ferri 2012; NINDS 2012; Goldman 2011; NIH MedlinePlus 2012; Mayo Clinic 2011; D’Amico 2008; Univ. of Maryland Medical Center 2012).
About 23 million adults in the United States are reported to experience migraine headaches, and they are one of the most common complaints encountered by neurologists in day to day practice (Cutrer 2012; American Academy of Neurology 2012). Nonetheless, migraine disorder remains a commonly underdiagnosed and undertreated condition (Lipton 2011; Durham 2004; Moloney 2011; Diamond 2007).
Conventional pharmacologic migraine treatments often meet with limited success and may have intolerable side effects or be contraindicated with other common co-existing conditions (Chaibi 2011a; Magis 2011; Rothrock 2011; Sarchielli 2006).
On the other hand, avoiding migraine triggers such as intense emotional stress, poor sleep habits, and unbalanced hormone levels may reduce the occurrence of attacks (Shugart 2012b; Mayo Clinic 2011; Dzugan 2006). In addition, there are a variety of safe and effective natural treatment approaches available for migraine management (Schiapparelli 2010).
Upon reading this protocol, you will learn what causes migraine and how conventional medicine treats migraine headaches. You will also discover how to avoid common migraine triggers and read about natural options that can help you manage migraine headaches.
Migraine headache is often described as intense throbbing or pulsating head pain that interferes with a person’s ability to go about normal daily functioning (Rizzoli 2012; NINDS 2012). Migraine headache pain is often made worse by physical activity (Walling 2012).
Migraine sufferers frequently describe the pain as being limited to one side of the head (Digre 2011a). However, some people do experience migraines on both sides of the head (Digre 2011b). Migraine is commonly associated with nausea, as well as light and/or sound sensitivity (Cutrer 2012). Although migraine duration varies from patient to patient, a typical attack lasts for several hours, and sometimes persists for up to several (e.g. 2-3) days (Walling 2012).
Various physical and/or psychological changes sometimes precede the onset of a migraine headache by a few hours to a few days. This phase of a migraine is called prodrome. The experience of prodrome varies from person to person but can include such things as appetite changes, loss of balance, mood changes, tiredness, neck stiffness, and changes in alertness. The prevalence of a distinct prodrome phase is not entirely clear because studies have reported differing rates, but a significant portion of migraineurs indicate that they experience symptoms that predict the onset of migraine. Individuals who have experienced migraine preceded by prodrome in the past may be able to recognize an impending headache based upon their prodrome symptoms and plan accordingly for the next hours or few days by taking steps such as avoiding rigorous or stressful activity and ensuring that they have adequate stock of migraine relief medication (Rossi 2005).
Approximately 25% of migraineurs will experience a pre-migraine phenomena called aura, which is a neurologic abnormality causing mostly visual, but also other sensory and/or movement disturbances that manifests within a few hours of a migraine headache (Cutrer 2012; Digre 2011c). Most experts believe that migraine aura is caused by a phenomena in the brain called cortical spreading depression (CSD), a slowly progressing wave of excitability followed by long-lasting neuronal inhibition (Bogdanov 2011a).
Scientists have recently uncovered an alarming discovery: Migraines cause lasting brain damage that is closely related to the changes seen in seizures, strokes, and dementia.2,3 Indeed, having a history of migraines is turning out to be a risk factor for some of the most-feared chronic brain disorders.2,4-6
Current migraine treatments include drugs originally developed for treating epilepsy.7-9 Although these drugs are effective in the short term, they were never meant for long-term use, they are fraught with side effects, and they fail to address the underlying cause.7,9
As scientists searched for treatment alternatives to anti-epileptic drugs, they uncovered two ingredients that provide a therapeutic dual-action against the changes in the brain that lead to migraines.
By restoring chemical balance to the brain and improving brain blood flow, gastrodin and magnesium target the underlying mechanisms behind crippling migraine pain, providing safe and effective relief for crippling migraine pain.10-14
Getting to the Root of Migraine Pain
Brain imaging studies show that people with migraines have visible abnormalities that are similar to those seen in stroke victims and in people with dementia.15,16 And some large-scale epidemiological studies suggest that people with chronic migraines are at increased risk for strokes and dementia.17,18
An abrupt reduction in brain blood flow occurs during an ischemic stroke, and more gradually in the condition known as vascular dementia.19,20 Similarly, before and during a migraine attack, blood flow in specific brain regions begins to drop.21-23 In all three cases—stroke, vascular dementia, and migraines—the result is increased vulnerability of brain cells to dysfunction, degeneration, and eventually death.19-23
But brain blood flow disturbances are just part of the picture in migraine headaches. In addition to (and perhaps as a result of) those disruptions, people with migraines show a harmful imbalance in the brain’s excitatory and inhibitory chemical activity.4,24,25
The Migraine/Seizure Connection
Normally, your brain maintains a healthy balance between excitatory and inhibitory activity by modulating neurotransmitters such as GABA.
When you do not have enough GABA, you can end up with the uncoordinated electrical “storm” that presents itself as an epileptic seizure. We now know that a milder version of this process occurs during a migraine.3,26
Because the imbalance between excitatory and inhibitory neurotransmitters is common to both migraines and to seizures, anti-epileptic drugs might appear to be a promising treatment option for migraine sufferers. Such drugs generally elevate the GABA-related activity in the brain, which has a calming, inhibitory effect.8,9 They also reduce concentrations of excitatory neurotransmitters, further restoring a normal balance.
The problem is that seizure drugs are loaded with adverse effects and were never meant to be used on a long-term basis for the prevention of something like a migraine.7,9 In fact, the US Food and Drug Administration has issued a warning that all anti-epileptic drugs are associated with increased risk of suicidal ideation and behavior.7
Fortunately, magnesium formulations and gastrodin work to improve cerebral blood flow and restore neurotransmitter input as do anti-epileptic drugs…but with a much better safety profile.11-13,27-32 The result is a natural treatment that has been proven to reduce the number and severity of migraine attacks.30
Reduce the Number and Duration of Migraine Attacks
Gastrodin, originally extracted from the root of the orchid Gastrodia elata, has been used for centuries in traditional Chinese medicine, especially for disorders involving the central nervous system such as headaches and seizures as well as stroke and dementia.33 Now, these effects have been validated by modern science.
In one clinical trial, gastrodin was found to reduce the total number and the duration of migraine attacks—and was even more effective than the leading drug flunarizine.30Other studies have also shown that gastrodin has a higher overall effective rate when compared to flunarizine.34-36
How it Works
Studies show that gastrodin-based formulas improve brain blood flow, which is commonly reduced during migraines.12,29 In fact, due to gastrodin’s powerful effect on blood flow, doctors in China use it to treat stroke victims, whose decrease in brain blood flow is life-threatening.37,38
But perhaps gastrodin’s most exciting mechanism of action stems from its ability to modulate both excitatory and inhibitory neurotransmitters: It raises GABA levels to normal by blocking the enzymes that break it down,11,27 and it decreases levels of excitatory neurotransmitters.28,39,40
Restoring this balance has been shown to be neuro-protective, even against the massive decrease in brain blood flow seen in strokes.28,33,39
Clearly, gastrodin’s multiple mechanisms of action make it an effective choice in the treatment and prevention of migraine headaches. But as we’re about to see, adding magnesium enhances the benefits of gastrodin for comprehensive migraine prevention.
Magnesium for Migraine Relief
Magnesium supplementation has been proven to be effective at preventing and reducing the duration of migraine headaches—with one dramatic study demonstrating a complete disappearance of pain in 87% of those given intravenous magnesium sulfate—and 100% of patients responding to treatment.41
And in another impressive study, 80% of patients receiving intravenous magnesium sulfate experienced complete pain relief within 15 minutes of the injection, along with complete elimination of hypersensitivity to light or sound.42
Doctors in hospitals and clinics have even started using intravenous magnesium sulfate to treat an existing migraine headache.41-44
Clinical trials have demonstrated the benefits of oral magnesium as well. One study found that 360 mg of magnesium reduced the number of days women experienced headaches during their menstrual cycles,45 a study of both male and female migraine patients found that 600 mg/day of magnesium in the form of trimagnesium dicitrate significantly reduced the incidence of migraine headaches,46 and another study found that magnesium supplementation reduced the irritation of facial and neck muscles that is common in migraines.47
In total, more than a half a dozen solid clinical trials have now demonstrated the utility of oral magnesium for preventing migraines and reducing their severity.45-51
How it Works
Magnesium is increasingly being recommended for migraine prevention—and for good reason.13,50,51 When it comes to treating and preventing migraines, the mineral magnesium is able to work hand-in-hand with gastrodin to improve brain blood flow and to help balance the brain’s neurotransmitters.
Studies show that up to 50% of migraine patients are deficient in magnesium during an attack, and that they have a high ratio of calcium to magnesium.13,52 This imbalance sets the stage for the contraction of brain blood vessels resulting in a reduction of blood flow.52
Researchers using high-tech Doppler ultrasound to measure blood flow velocity in a major brain artery have definitively proven that supplementation with magnesium does increase both brain blood flow and its velocity.48,53
Like gastrodin, magnesium also has beneficial effects on the balance of excitatory to inhibitory neurotransmitters. Magnesium is a natural blocker of the excitatory receptor on brain cells, so when ample magnesium is available those receptors don’t trigger the excitatory electrical impulse.54-56 This allows the brain to move into its more balanced, calm mode.
Despite the fact that migraine headaches affect around 18% of American women and 6% of men, mainstream medicine has yet to find a safe, long-term way to prevent this debilitating condition.1
Connie’s comments: When I have a headache, it usually goes away after I eat a healthy meal. My brother has a migraine when he turned 17 and from then on, he started to have mild dementia.
- Scientists identified an enzyme in animal studies whose activity promotes weight gain and the loss of exercise capacity starting in mid-life.
- A drug that inhibits the enzyme prevented weight gain in mice, increased fitness levels, and reduced the incidence of obesity and type 2 diabetes.
- The findings could lead to more effective weight-loss medications.
Researchers have long known that losing weight and maintaining the capacity to exercise tend to get harder beginning between ages 30 and 40—the start of mid-life. Scientists have developed new therapies for obesity, including fat-fighting pills. However, many therapies have failed because of a lack of understanding about the biological changes that cause middle-aged people to gain weight, particularly around the abdomen.
Dr. Jay H. Chung, an endocrinologist at NIH’s National Heart, Lung, and Blood Institute (NHLBI), was always puzzled by the aging-weight gain paradox. An average adult in America gains 30 pounds from age 20 to 50, even though food intake usually decreases during this period. Chung and his associates thus searched for biochemical changes in middle-aged animals (human equivalent of 45 years). Their study appeared on May 2, 2017, in Cell Metabolism.
The team focused on an enzyme called DNA-dependent protein kinase, or DNA-PK. This enzyme is activated by a specific kind of DNA damage, but evidence has been mounting that DNA-PK has functions beyond DNA repair. One such function is in metabolism.
The scientists looked at levels of DNA-PK activity in the skeletal muscles of rhesus macaques and mice. These levels were low over time until middle-age, when they rose significantly. Further experiments showed that DNA-PK activity promotes the conversion of nutrients to fat and decreases the number of mitochondria, the tiny organelles in cells that turn fat into energy to fuel the body.
Mitochondria can be found in abundance among young people, but the numbers drop considerably in older people. Researchers know that fewer mitochondria can promote obesity as well as loss of exercise capacity.
The researchers theorized that reducing DNA-PK activity might increase the number of mitochondria and promote fat burning. They tested their theory with a drug that inhibits DNA-PK. Mice that received the inhibitor had a 40% decrease in weight gain when fed a high-fat diet. The drug boosted the number of mitochondria in the skeletal muscle, increased the fitness of obese and middle aged mice, and reduced the incidence of obesity and type 2 diabetes.
The team also examined the role of DNA-PK activity in calorie restriction and aerobic fitness, both of which can delay aging and protect against chronic diseases in animal models. Rhesus macaques on a calorie-restricted diet had lower levels of DNA-PK activity in skeletal muscle. Rats selectively bred to be strong runners also had reduced DNA-PK levels in their skeletal muscle—three-fold lower than poor rat runners.
“Our society attributes the weight gain and lack of exercise at mid-life (approximately 30-60 years) primarily to poor lifestyle choices and lack of will power, but this study shows that there is a genetic program driven by an overactive enzyme that promotes weight gain and loss of exercise capacity at mid-life,” Chung says.
These findings could lead to the development of a new type of weight-loss medication. However, DNA-PK inhibitors have yet to be tested this way in humans. Middle-aged people who are fighting obesity should continue to reduce calories and boost exercise.
Vegan vs American diet
Researchers in Finland have discovered what could be an important clue to what drives Parkinson’s disease (PD). Their new study has shown a reduced abundance of the Prevotellaceae bacteria family in the gut microbiome of PD patients compared with healthy control persons.
Dr Filip Scheperjans
Although the new findings only “scrape the surface,” they “give us good reason to dig deeper,” said lead author Filip Scheperjans, MD, PhD, Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Finland.
If further research verifies that PD is caused by a diminished number of Prevotellaceae in the gut, boosting levels of these bacteria might slow the progression of the disease, or even prevent it.
Their findings are published in the March issue of Movement Disorders.
“It’s an intriguing theory,” said Dr Scheperjans. “I think it’s something we will be looking at, because the ultimate goal of why we’re doing the study is that we want to find something that we can correct.”
However, perhaps a more pressing goal is to confirm that these changes in gut microbiome occur before patients develop PD.
It has already been shown that PD patients tend to have gastrointestinal dysfunction, particularly constipation, and that these symptoms may precede motor symptoms by several years. “So from a clinical point of view, we know that the gut is basically affected very early in PD, but we actually haven’t a clue really what is causing it,” said Dr Scheperjans.
According to background information in the article, the human body contains some 10 times more microbial cells than human cells, and these microbes carry about 100 to 200 times more protein- coding genes than the human genome. Almost all of these genes are of bacterial origin.
Intestinal microbiota influence the immune system and the absorption of nutrients, vitamins, medications, and toxic compounds.
There is mounting evidence of an intense bidirectional interaction between gut microbiota and the nervous system, influencing brain activity, behavior, and levels of neurotransmitter receptors and neurotrophic factors.
The new study included 72 PD patients (mean age, 65.3 years; 48.6% women), and 72 age- and sex-matched control individuals who were without signs of parkinsonism or potential premotor symptoms (mean age, 64.5 years; 50.0% women). The median time from motor symptom onset in PD patients was 5 years. All but two patients were receiving an antiparkinsonian medication.
The study excluded individuals living in the same household and so presumably having a similar diet.
From fecal samples collected from each study participant, researchers pyro-sequenced the V1-V3 regions of the bacterial 16S ribosomal RNA gene. They used random subsamples of 4500 sequences for analysis.
They found that the mean abundance of Prevotellaceae in the feces of PD patients was reduced by 77.6% compared with control individuals. This bacteria “is a normal inhabitant of the human gut,” with people having varying amounts of it, said Dr Scheperjans.
“It’s important to note that based on our data, PD patients have less of Prevotellaceae, but there were also controls who had low levels, so that alone doesn’t explain PD.”
The researchers did not find significant associations of bacterial abundances with age, body mass index, total Unified Parkinson’s Disease Rating Scale, and time from motor or nonmotor symptom onset.
The decreased abundance of Prevotellaceae was not explained by more severe constipation in PD patients, although the abundance of other bacteria, but not Prevotellaceae, was associated with degree of constipation, or by differences in comorbidities.
Less abundance of the bacteria also was not affected by medications. Dr Scheperjans noted that the COMT (catechol-O-methyl transferase) inhibitor was the only PD drug that was associated with changes in the gut microbiome.
“That was interesting, because that drug causes GI side effects like diarrhea,” he said. “But we accounted for that in our analysis, so the basic finding of the difference between PD patients and controls is not explained by the medications that patients are using.”
The study showed that another type of intestinal bacteria ― Enterobacteriaceae ― was linked to the severity of postural instability and gait difficulty (PIGD). These bacteria were significantly more abundant in patients with a PIGD phenotype than in patients with tremor dominant (TD) phenotype.
There is a wide variation in clinical manifestations in PD patients ― with some having mostly tremor, and others, rigidity ― and the question is whether these phenotypes represent the same disease. Itis possible, said Dr Scheperjans, that different PD subtypes are linked to different bacteria.
Dr Scheperans noted that it is not clear from this study whether the bacterial changes were present before patients developed PD or occurred after.
Role of Diet?
The role of diet is also not clear. Evidence in the literature does not suggest major differences between the diet of PD patients and that of other people, and studies of the impact on PD of particular nutrients or foods ― maybe with the exception of coffee ― have shown small effect sizes and contradictory results, said Dr Scheperjans.
What is known is that the level of Prevotellaceae bacteria increases when people consume foods high in fiber and certain carbohydrates ― for example, fruits and vegetables. And this bacteria has been found in oral plaque and has been linked to periodontal disease, although this could be a different strain of the bacteria.
“The difference between bacterial strains at the genetic level can be huge,” said Dr Scheperjans. “We don’t know if it’s the same bug that is healthy in the gut but bad in the mouth.”
Dr Scheperjans and his colleagues are now studying the dietary habits of patients and will be reporting on this later this year.
The idea that gut bacteria is involved in PD is intriguing, according to the authors. Alpha-synuclein, which is the hallmark protein for PD, has been found not only in the brain as the main component of Lewy bodies but also in the gut.
There is evidence, said Dr Scheperjans. that the alpha-synuclein “protein pathology” progresses “in a prionlike fashion,” migrating from the enteric nervous system to the central nervous system.
“There is a hypothesis that these pathological proteins can jump from one neuron to the next,” and that the vagal nerve is involved in the spread of the pathology, he said.
In the last 2 to 3 years, scientists have learned a lot about the presence and amount of these intestinal bacteria, “but we don’t know a lot about what they’re actually doing; that’s the next step,” said Dr Scheperjans.
To that end, he and his colleagues are following the study participants for 2 years to see whether the Prevotellaceae level continues to be reduced in PD patients or if it was just a temporary phenomenon.
“We’re specifically interested in seeing how they progressed,” said Dr Scheperjans. “We want to see if there’s an association between the microbiome configuration and disease progression.”
In an accompanying editorial, a group of authors, including Alberto Espay, MD, University of Cincinnati, in Ohio, point out that the demonstration that selected bacterial populations could influence disease and phenotype “is a remarkable finding” and could have important implications.
“For starters, Scheperjans and colleagues have given us the opportunity to envision a future in which specific motor features of PD could be modified by controlling the relative populations of certain species of microbiota.”
In addition to helping to shape novel treatment paradigms, gut microbiota also have the potential to inform the understanding of the etiopathogenesis of PD, they write.
It is “tempting” to speculate that gut microbiota might be in the pathogenic pathway that determines disease phenotypes and is “poised to become a target” for disease-modifying pharmacology, they note. “Gut microbiota may even have a role explaining the differences in PD prevalence between rural and urban environments, between countries and perhaps even between sexes.”
The study could not rule out the possibility that PD itself may change the microbial composition of the gut ― instead of vice versa ― or even that a third factor, such as an environmental trigger, initiates both PD and microbiota changes. But the new information adds to the evidence suggesting “that this may be the beginning of a leap forward in our understanding of and treatment options for PD,” the editorialists conclude.
Dr Scheperjans is an inventor on a Finnish patent application. The editorial writers have reported no relevant financial relationships.
Mov Disord. 2015;30:350-358, 296-298. Abstract, Editorial
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Contact Connie for holistic caregivers for homebound bayarea seniors, Motherhealth Inc at 408-854-1833 (text) and email@example.com