A cluster of conditions exist near the end of the luteal phase of the menstrual cycle. Over time doctors have referred to these conditions as “dysmenorrhea,” “Premenstrual Dysphoric Disorder” (PMDD) and “Premenstrual Syndrome” (PMS) to describe different levels of severity at different times in the cycle. Symptoms related to all of these conditions have been linked to changes in hormone levels that occur prior to menstrual bleeding caused by the physiological changes they initiate rather than by the hormones themselves. Because these symptoms are likely to have common causes it is then useful to treat them as one group when assessing the efficacy (or lack thereof) of various treatments. This article is an overview of current treatment options, and Lunapatch as a new solution for relieving menstrual pain without unwanted side-effects common in other treatment options.
Definition and Description of the Symptoms
The World Health Organization’s 2016 disease classification manual defines dysmenorrhea as “a disorder characterized by abnormally painful abdominal cramps during menses.” [1] Dysmenorrhea is a condition that has been found in medical studies to affect as many as 72.7% of women between menarche and menopause (Unsal et al.) [2].
The Mayo Clinic defines PMS as:
Premenstrual syndrome (PMS) has a wide variety of symptoms, including mood swings, tender breasts, food cravings, fatigue, irritability and depression. It’s estimated that as many as 3 of every 4 menstruating women have experienced some form of premenstrual syndrome.
Symptoms tend to recur in a predictable pattern. But the physical and emotional changes you experience with premenstrual syndrome may vary from just slightly noticeable all the way to intense.
Still, you don’t have to let these problems control your life. Treatments and lifestyle adjustments can help you reduce or manage the signs and symptoms of premenstrual syndrome. (Staff, Premenstrual Syndrome (PMS), 2014) [3]
The Mayo Clinic has listed a number of symptoms for PMS:
Emotional and behavioral symptoms:
- Tension or anxiety
- Depressed mood
- Crying spells
- Mood swings and irritability or anger
- Appetite changes and food cravings
- Trouble falling asleep (insomnia)
- Social withdrawal
- Poor concentration
Physical symptoms:
- Joint or muscle pain
- Headache
- Fatigue
- Weight gain related to fluid retention
- Abdominal bloating
- Breast tenderness
- Acne flare-ups
- Constipation or diarrhea” (Staff, Premenstrual Syndrome (PMS), 2014) [4]
The Mayo Clinic discriminates between PMDD and PMS as separate conditions, saying:
Premenstrual dysphoric disorder (PMDD) is a severe, sometimes disabling extension of premenstrual syndrome (PMS). Although regular PMS and PMDD both have physical and emotional symptoms, PMDD causes extreme mood shifts that can disrupt your work and damage your relationships. In both PMDD and PMS, symptoms usually begin 7-10 days before menstrual bleeding begins and continues for the first few days of bleeding.
In PMDD, however, at least one of these emotional and behavioral symptoms stands out:
- Sadness or hopelessness
- Anxiety or tension
- Extreme moodiness
- Marked irritability or anger (Thielen, 2015) [5]
Treatment of Pain
The most common treatments include over the counter NSAID (Non-steroidal Anti-inflammatory drugs) drugs such as aspirin, ibuprofen, acetaminophen, naproxen as well as other more recent drugs that inhibit the Cox family of enzymes. These drugs have their own downsides. A list of side effects includes:
Serious side effects of these drugs listed by the FDA (U.S. Food and Drug Administration, 2007) [6] include:
• “heart attack
• stroke
• high blood pressure
• heart failure from body swelling (fluid retention)
• kidney problems including kidney failure
• bleeding and ulcers in the stomach and intestine
• low red blood cells (anemia)
• life-threatening skin reactions
• life-threatening allergic reactions
• liver problems including liver failure
• asthma attacks in people who have asthma”
Many of these side effects are already problematic effects of PMS, side effects such as anemia, bleeding ulcers and edema will exacerbate the problems caused by PMS and menstruation.
Treating the symptoms of pain using more potent central nervous system pain relievers such as opiates have a laundry list of side effects. These have been reviewed by Benyamin et. al.
“Common side effects of opioid administration include sedation, dizziness, nausea, vomiting, constipation, physical dependence, tolerance, and respiratory depression. Physical dependence and addiction are clinical concerns that may prevent proper prescribing and in turn inadequate pain management. Less common side effects may include delayed gastric emptying, hyperalgesia, immunologic and hormonal dysfunction, muscle rigidity, and myoclonus.” (WebMD, LLC) [7]
Using opiates to treat the pain of PMS has more side effects and dangers than are reasonable for the treatment of premenstrual disorders.
Treatment of Bloating
Diuretics offer a poor option, as this may lead to non-selective depletion of nutrients such as magnesium, which have a renal route of excretion. Products that combine diuretics with NSAIDs have some strong side effects that impair the user’s mental state and alertness.
A list of common side effects of Pamprin Max from Web MD:
- “Chronic Trouble Sleeping
- Conditions of Excess Stomach Acid Secretion
- Feel Like Throwing Up
- Heartburn
- Irritation of the Stomach or Intestines
- Nervous
- Stomach Cramps
- Throwing Up” (WebMD, LLC) [8]
Treatments for Depression and Mental Distress
Antidepressants are described as a treatment for PMS, but have too broad an effect with too little benefit to be really practical. Antidepressants have become the poster child for the mismanagement of the medical profession’s arsenal of medications. It is common to receive prescription of an antidepressant by the doctor with no plan for eliminating the medication as symptoms are remedied.
In a recent article entitled, “Are Antidepressants Just Placebos with Side Effects?” more evidence unfolds for the poor choice that antidepressants provide.
“After analyzing all the FDA studies, Kirsch concluded that placebos are 82 percent as effective as antidepressants. According to Kirsch, this difference vanishes if antidepressants are compared to “active placebos,” which are compounds such as atropine, an alkaloid that blocks certain nerve receptors and causes dry mouth and other symptoms, that have distinct side effects.”
Additionally:
“Although Prozac was touted for its relatively mild side effects, it causes sexual dysfunction in as many as three out of four consumers.” (Horgan, 2011) [9]
With this dizzying number of side effects, how does one relieve the pain and other symptoms of PMS without facing unreasonable risks?
Natural Alternatives to Pharmaceuticals
Magnesium supplementation has been found to improve the symptoms of PMS/PMDD in several studies. One study states that it found results “contrary to prior reports”. This study illustrates how poorly this conclusion is supported and does a disservice to women by dissuading them from using a simple, safe and effective treatment.
One study by American researchers (Khine, Rosenstein, Elin, Neimela, Schmidt, & Rubinow, 2005) [10] reported as a conclusion:
“Contrary to prior reports, we found no evidence of Mg2+ deficiency in women with PMDD compared with control subjects. Furthermore, Mg2+ was not superior to placebo in the mitigation of mood symptoms in women with PMDD.”
Upon careful examination of the data, there was a trend toward greater magnesium retention of the administered intravenous dose in PMDD sufferers than in controls. This difference did not reach statistical significance, but it was certainly not contrary to prior reports and data did not support a conclusion that there was “no evidence of Mg2+ deficiency”.
Likewise, subjects saw no worsening of their symptoms upon magnesium supplementation, while most reported an improvement, but again this did not reach the threshold of statistical significance in this small group of 17 affected women. It is possible that the similarities between the control and experimental treatments may have been due to the 5% dextrose (glucose) used as the placebo and as the carrier for intravenous magnesium. Injecting 5% glucose is likely to be mood elevating, and it is quite commonly understood that PMS and a craving for sweets often occur simultaneously. This was a very poor placebo, and administration of saline as an additional control might have revealed the poor choice of 5% glucose as a carrier.
Also of interest in this study: “the mean baseline 24-hour urinary magnesium output was below the lower limit of the reference range in both patients (2.14 ± .53 mmol/24 hour) and healthy control subjects (2.35 ± .60 mmol/24 hr; reference range 3.0 – 4.25 mmol/24 hour).”
This means that compared to previous studies on magnesium metabolism and retention, both groups (affected and unaffected by PMDD) exhibited very low urinary excretion of magnesium.
After supplementation of magnesium intravenously, an additional difference was noted between groups regarding the amount of magnesium they retained.
“Although the mean of the patients (31.5% retention) exceeded the normal threshold of 27.5%, the mean of the control subjects was exactly at the upper limit of normal (27.5% retention) and did not differ from that of the patients. Thus, our data failed to support the hypothesis that Mg2+ depletion causes PMDD.”
When using this level of infused magnesium, all of the patients and the controls showed a very low level of magnesium excretion. Some affected individuals were much, much lower, as we can extrapolate from the fact that 6 of the 17 affected women were not deficient in magnesium. The authors did not do the obvious and separate those with magnesium deficiency from those who did not demonstrate a deficiency to analyze them as subgroups. Their presumption that the diagnosis they made via questionnaire could so finely divide subjects so that there would be only one cause of PMDD or that their diagnosis was so precise that it excluded any other disorders is flawed. What the dogmatic belief in the survey allowed was the inclusion of a heterogeneous group of affected individuals. This is often the case in science, where defining the sample group becomes dogmatically correct and the groups henceforth cannot be subdivided, even when evidence of heterogeneity surfaces. To reanalyze data of comorbid PMDD and magnesium deficiency and then calculate the level of the response would have provided a much more meaningful result. In clinical practice, it is very practical to have someone with a PMDD diagnosis undergo some additional testing to determine whether they are also magnesium deficient. The only hypothesis these researchers tested was that all PMDD is caused by magnesium deficiency and that all PMDD could be remedied by a single dose of magnesium. These patients with both a magnesium deficiency and PMDD are likely to improve significantly when supplemental magnesium is given. Those without magnesium deficiency are unlikely to improve, but even for these patients, the cost/benefit ratio for magnesium supplementation is very low.
In short, methods in this study are predisposed to short-sighted results and the wording of the conclusions are very strong compared to the information contained within the data. The data all trend toward a positive effect of magnesium supplementation, even if this does not achieve statistical significance. The clumsy analytical “blandness” employed by not subdividing the PMDD group into two groups of magnesium deficient versus those who were not deficient makes this study appear to have a contrary result compared to previous studies that showed benefits of long-term magnesium supplementation, even though the trends in the data actually support a positive impact of magnesium upon many markers of PMS and PMDD.
This study administered its magnesium dosage intravenously, a method not normally used to introduce magnesium, and this was done only acutely, without long-term supplementation. Given the critical role of magnesium in a vast number of metabolic cycles, short supplementation bursts with this low level of magnesium are unlikely to make significant changes in the status of the women and whether they were actually satisfying the deficiency. Following this intravenous injection study with dietary supplementation until all subjects reached magnesium sufficiency might have revealed a recovery from symptoms of PMDD seen in other studies. As it stands, this study clearly did not bring women to the level of magnesium sufficiency that would actually show whether magnesium supplementation would help PMDD. They simply showed that giving a low dose of magnesium for a short time to severely magnesium deficient women experiencing PMDD did not significantly change their outcome. This is not a great surprise.
There are enough poor choices about experimental design and data analysis to make the motivations of the authors in this study suspect as the data they had in hand could have been subjected to a much more refined analysis.
In contrast, an Italian study by Facchinetti et. al. (Facchinetti, Borella, Sances, Fioroni, Nappi, & Genazzani, 1991) [11] found:
“To evaluate the effects of an oral Mg2+ preparation on premenstrual symptoms, we studied, by a double-blind, randomized design, 32 women (24-39 years old) with PMS confirmed by the Moos Menstrual Distress Questionnaire. After 2 months of baseline recording, the subjects were randomly assigned to placebo or Mg for two cycles. In the next two cycles, both groups received Mg2+. Magnesium pyrrolidone carboxylic acid (360 mg Mg2+) or placebo was administered three times a day, from the 15th day of the menstrual cycle to the onset of menstrual flow. Blood samples for Mg2+ measurement were drawn premenstrually, during the baseline period, and in the second and fourth months of treatment. The Menstrual Distress Questionnaire score of the cluster “pain” was significantly reduced during the second month in both groups, whereas Mg2+ treatment significantly affected both the total Menstrual Distress Questionnaire score and the cluster “negative affect.” In the second month, the women assigned to treatment showed a significant increase in Mg2+ in lymphocytes and polymorphonuclear cells, whereas no changes were observed in plasma and erythrocytes. These data indicate that Mg2+ supplementation could represent an effective treatment of premenstrual symptoms related to mood changes.”
In this study, it is clear that the effects of magnesium supplementation do not relieve symptoms in the first month. This study was done prior to the study by Khine et. al. yet those authors designed their study to only observe the effects of supplementation at most 2 days after infusion of magnesium. Expecting to see results in a short period when previous studies have observed results only after more than a month of supplementation is a very poor design.
Another study conducted in the United Kingdom by Walker et. al. (Walker, De Souza, Vickers, Abeyasekera, Collins, & Trinca, 1998) [12] again showed no effect in the first month of supplementation, but in the second month found significant impact of magnesium upon bloating, one of the more difficult to manage symptoms of PMS, since diuretics often produce unwanted side-effects.
“Analysis of variance for 38 women showed no effect of Mg2+ supplementation compared with placebo in any category in the first month of supplementation. In the second month there was a greater reduction (p = 0.009) of symptoms of PMS-H (weight gain, swelling of extremities, breast tenderness, abdominal bloating) with Mg2+ supplementation compared with placebo.”
It is again of interest that this study was cited by Khine et. al, but its conclusions were not incorporated into the design of their study. If two independent studies by different research groups show no effect in the first month of supplementation, then why would you design a study that can only observe effects within two days of administration?
Since the studies by Khine et. al., additional research has been done on the role of magnesium as a factor in the severity of PMS and PMDD. Ebrahimi et. al. (Ebrahimi, Motlagh, Nemati, & Tavakoli, 2012) [13] found that at the end of two months of magnesium supplementation all scores of PMS were reduced compared to placebo. Symptoms of craving, water retention and anxiety achieved a statistically significant difference compared to placebo. Symptoms of depression and somatic changes both were reduced, but did not achieve statistical significance at this sample size.
This study also evaluated the effects of vitamin B6, which showed a pattern of symptom relief similar to magnesium supplementation, but had a greater impact upon depression symptoms than magnesium. B6 has roles as a cofactor in many enzyme reactions in amino acid, glucose, and lipid metabolism. One role for B6 beyond its functions as an enzyme cofactor is as an antioxidant. (Bilski, Li, Ehrenshaft, Daub, & Chignell, 2000) [14]
Morris et. al. (Morris, Picciano, & Selhub, Plasma pyridoxal 5′-phosphate in the US population: the National Health and Nutrition Examination Survey, 2003–2004, 2007) [15] measured blood levels of vitamin B6 as plasma pyridoxal 5′- phosphate (PLP) and noted a stark contrast in plasma PLP levels between women of childbearing age (ages 13 to 54) and their male peers. “When we looked specifically at the plasma PLP levels in women of childbearing age, we noticed they were significantly lower than in males in approximately the same age group.” Morris continues, “Most importantly, the data suggest that oral contraceptive users have extremely low plasma PLP levels. Three quarters of the women who reported using oral contraceptives, but not vitamin B6 supplements, were vitamin B6 deficient.”
A pattern of low vitamin B6 status also surfaced in menstruating women who reported using oral contraceptives but who were no longer using them at the time of the NHANES survey. Among women in this sub-group who were not taking vitamin B6 supplements, 40 percent demonstrated plasma PLP blood levels below the cut-off for vitamin B6 inadequacy.
To further support their findings, Morris and colleagues measured homocysteine levels in the blood and compared them against the plasma PLP measures. Homocysteine is an amino acid that can accumulate in the blood if vitamin B6 levels are too low. Though study participants using oral contraceptives at the time of the survey did not demonstrate elevated homocysteine levels, the homocysteine concentrations of former users were significantly higher than those of women who had never used oral contraceptives. Morris says this could mean that oral contraceptive use has an effect on vitamin B6 status that is masked during use by acute effects of the exposure. (Tufts University, Health Sciences, 2008) [16]
Homocysteine (Hcy) levels are markers of inflammation and are correlated with other inflammatory markers such as HsCRP (P<0.001), IL-6 (P<0.001) and TNFα (P<0.001) in patients with acute coronary syndrome (ACS). All of these markers were positively correlated with the number of diseased vessels. (Oudi, et al., 2010) [17]
A recent study by Bertone-Johnson et. al. (Bertone, et al., 2014) [18] determined that markers of chronic inflammation were associated with menstrual symptom severity and premenstrual syndrome (PMS).
“Affective menstrual symptom score was linearly related to levels of IL-2 (percentage difference at 75th percentile versus 25th percentile = 31.0%; P = 0.02), while physical/behavioral symptom score was linearly related to levels of IL-4 (19.1%; P = 0.03) and IL-12 (33.2%; P = 0.03). Additionally, mean levels of several factors were significantly higher in women meeting PMS criteria compared with women meeting control criteria, including IL-4 (92% higher in cases versus controls; P = 0.01); IL-10 (87%; P = 0.03); IL-12 (170%; P = 0.04) and IFN-γ (158%; P = 0.01).”
These results indicate that the severity of PMS is quantitatively linked to levels of inflammation. While this study did not examine levels of homocysteine, there are excellent data from the study by Morris et. al. (Morris M. , Picciano, Jacques, & Selhub, 2007) [19]
Treating Inflammation
Treatments for inflammatory states are typically through NSAIDs, but these drugs only stop the enzymes within the person’s body from feeding the flames of inflammation. Smoking, for instance is a well understood source of inflammatory oxidation and free radicals, and the effects of NSAIDs do not counter this exogenous source of free radical damage. Taking NSAIDs is akin to preventing people at the campground from feeding a campfire, but does nothing to prevent the blaze all around them. It is no coincidence that smoking is positively correlated to the severity of PMS symptoms as seen in a study by Ju et. al. among Australian women (Ju, Jones, & Mishra, 2014) [20]
Antioxidants can be supplemented to directly eliminate the oxidation effects of free radicals that include pain, protein damage, DNA damage and other physical and psychological discomforts. One vitamin that does double duty as both an enzyme cofactor and as an antioxidant is Vitamin B6. This water soluble vitamin is critical to human health as an enzyme cofactor, but in a person suffering from periodic inflammation, it may be destroyed before it gets to its proper locations in an enzyme and is instead consumed as an antioxidant.
Adequate intake of vitamin B6 is difficult, especially since absorption via the digestive tract is variable when co-administered with other drugs. A large number of medicines and other substances negatively affect the absorption and metabolism of vitamin B6, vitamin B12 and folic acid, particularly of folic acid and vitamin B6. A few examples are the contraceptive pill, alcohol, various barbiturates and a number of chemotherapeutics (mainly methotrexate). Pancreatic extract can also negatively affect folic acid absorption, and has to be taken separately from the aforementioned B vitamins. Other interactions with mainstream or natural medicines are also possible. (Natura Foundation) [21]
Review of typical dosing of B6 also reveals a very wide therapeutic index, that is, the difference between the dosage that is necessary for therapeutic effect versus the dosage necessary for overdose. The US RDA for B6 is between 1.2 and 1.7mg per day as defined by table 1 from the National Institutes of Health factsheet on vitamin B6.
Age | Male | Female | Pregnancy | Lactation |
---|---|---|---|---|
Birth to 6 months | 0.1 mg* | 0.1 mg* | ||
7 – 12 months | 0.3 mg* | 0.3 mg* | ||
1 – 3 years | 0.5 mg | 0.5 mg | ||
4 – 8 years | 0.6 mg | 0.6 mg | ||
9 – 13 years | 1.0 mg | 1.0 mg | ||
14 – 18 years | 1.3 mg | 1.2 mg | 1.9 mg | 2.0 mg |
19 – 50 years | 1.3 mg | 1.3 mg | 1.9 mg | 2.0 mg |
51+ years | 1.7 mg | 1.5 mg |
This level of adequate intake is suspect due to the unusually low blood level of 20nmol/L B6 used to calibrate the level of intake.
“PLP concentrations of more than 30 nmol/L have been traditional indicators of adequate vitamin B6 status in adults (Shils, Shike, Ross, Caballero, & Cousins, 2012) [23]. However, the Food and Nutrition Board (FNB) at the Institute of Medicine of the National Academies (formerly National Academy of Sciences) used a plasma PLP level of 20 nmol/L as the major indicator of adequacy to calculate the Recommended Dietary Allowances (RDAs) for adults (Institute of Medicine, 1998) [24]” (National Institutes of Health) [25]
The Tolerable Upper Intake Level (UL) of B6 supplementation for adults is 100 milligrams. This is half of the amount found to have no adverse effects on study subjects.
“Studies in patients treated with vitamin B6 (average dose of 200 mg/day) for up to 5 years found no evidence of this effect. Based on limitations in the data on potential harms from long-term use, the FNB halved the dose used in these studies to establish a UL of 100 mg/day for adults.” [26] (National Institutes of Health)
Even with a 100 milligram UL, the highest RDA dose of 1.7 mg the therapeutic index for this vitamin is 58.8. Using the quantity that has shown toxicity of reversible neuropathy at 500mg/day gives a therapeutic index of 294; an exceptionally safe vitamin by any standard.
Transdermal Administration
Interactions between orally consumed medications and orally consumed vitamins is a common problem. One common complaint prior to menstruation is diarrhea, which can impair absorption of B6, which may make the oral administration hit and miss. These problems with oral administration have a very simple answer- topical administration.
In 1985, Russian researchers Gurochkina et. al. (Gurochkina, Koroleva, Avakumov, & Smirnova, 1985) [27] found that pyridoxal phosphate had vitamin B6 activity when applied to the skin of rats. This form of vitamin B6 is therefore likely to have much more reliable absorption and consistent bioavailability compared to other forms of B6 administered orally.
Pyridoxal phosphate has another important advantage over pyridoxine, it has reduced or completely eliminated toxicity when compared to pyridoxine. According to studies conducted by Levine and Saltzman:
“The coenzyme (pyridoxal 5-phosphate) did not cause clinical signs or lesions similar to those produced by pyridoxine even when injected in maximum tolerated doses. Neither a protein-deficient diet nor bilateral nephrectomy changed the results with the vitamers.” (Levine & Saltzman, 2004) [28]
Topical application is therefore an effective and safe means for B6 administration. However, bioavailability of topical applications are typically low, since the only factors driving the movement of these compounds through the skin are the forces of diffusion and translocation by transporters. Enhancing the rate of B6 movement through the skin would allow this route of administration to be much more effective. Penetrating agents can be utilized to enhance delivery, such as glycerin. (Theratech I. , 1993) [29]
Iontophoresis is an additional method of improving permeability of skin to drugs using a flow of ions induced by electrochemical activity. Translocation of pyridoxine phosphate through the epidermis of the skin is predicted to occur for solutions below a pH of 4 (positively charged) and above a pH of 7 (negatively charged). See figure 1 below from dos Santos et. al. (Sci Flo Brazil, 2010) [30]
Figure 3 – Fractional distribution of pyridoxine hydrochloride in its possible forms according to pH values, according to the experimentally determined Ka1 and Ka2 values.
Iontophoresis of pyridoxine hydrochloride and pyroxidine-5 phosphate should be quite efficient for transport of these vitamers through the skin. Typical iontophorisis utilizes a positive and negative pad with a battery or other power source to create ions under these pads via electrolysis of water to H+ and OH– ions. The H+ ions drive the positively charged vitamin into the skin at the anode or positive (+) side of the device and simultaneously drive the negatively charged vitamin into the skin at the cathode or negative (-) side of the device.
The Naked Electron’s Distinct Advantages Over Both Typical Molecular Antioxidants and NSAIDs.
- They leave no waste material behind – Unlike a molecular antioxidant, which upon donating its electron becomes waste, a naked electron gets wholly consumed by the free radical.
- They are able to act at a distance – Molecular antioxidants need to come into direct contact with a free radical to donate their electron, whereas the naked electron from magnesium metal can utilize its high reducing potential voltage (2.37V), to push the electrons and neutralize free radicals away from the source.
- Unlike NSAIDs, they can quench any oxidizing agent regardless of the source – By their nature, NSAIDs can only inhibit enzymes that produce oxidizers. To use an analogy, NSAIDs prevent people at the campground from adding fuel to the campfire, but can do nothing about sources of inflammation that are exogenous. Exogenous sources would be excess sugars, radicals from cigarette smoking, or toxins such as paraquat or pollution. The naked electron doesn’t discriminate when it comes to the source of the radicals, and will neutralize any radicals that occur within the range of the patch.
- Can bypass the digestive system and provide highly targeted relief and vitamin delivery – Most dietary vitamins and antioxidants get destroyed as they make their way through the digestive system, while the ones that do make it through are distributed diffusely throughout the body, with no strong way to direct where they go. NSAIDs take a heavy toll on the user’s digestive system and liver, plus they create the potential for lots of side effects if taken in excess. The amount of naked electrons being delivered far exceeds any dose of antioxidants that is possible to be eaten and absorbed through the digestive system. As such, the patch is able to provide effects that are not reproducible by normal antioxidant intake and will neutralize the free radicals and create a potent anti-inflammatory effect within the vicinity of the patch. The patch also has the ability to deliver positive ions like magnesium and potassium directly to desired areas to help initiate various enzymatic effects.
- Allow vitamins to fulfill their higher purpose – Many vitamins double as antioxidants and play a crucial role as enzyme cofactors. By being in the presence of large amounts of powerful antioxidants via the naked electrons, the vitamins are protected from oxidation and no longer need to be reduced to the role of a simple antioxidant. Naked electron therapy allows vitamins like B6 to fulfill their specialized role as an enzyme cofactor instead thus making them more useful to the user.
Final Words
Because Lunapatch provides naked electrons and minerals in a concentrated manner via transdermal delivery, there is a great deal of pain and symptom relief that can be targeted to the area where the pain occurs. Because menstrual pain from cramps is localized and because the cause of the pain is understood by the user, there is a reduced risk that the source of the pain will be misidentified. This technology has shown itself to be an extremely potent anti-inflammatory, as such, it is important to remember there is actually a protective role of inflammation for conditions such as infection and beneficial immune response. We do not recommend that human half-cell electron donation technology be used for medical conditions or unidentified sources of pain, and if pain does not resolve within 3 days, we strongly suggest that you contact your health practitioner and investigate other underlying medical conditions that might be the real culprit.
Menstrual pain is particularly suited to naked electron therapy because it has a predictable onset as well as a predictable endpoint. If you experience symptoms that continue beyond the end of menstrual bleeding, please obtain a healthcare practitioner’s advice and seek a more specific treatment for your condition.
Works Cited
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Bilski, P., Li, M., Ehrenshaft, M., Daub, M. E., & Chignell, C. F. (2000). Vitamin B6 (Pyridoxine) and Its Derivatives Are Efficient Singlet Oxygen Quenchers and Potential Fungal Antioxidants. Retrieved from National Science Foundation: https://cals.ncsu.edu/plantbiology/Faculty/mdaub/bilski2000.pdf
Ebrahimi, E., Motlagh, S., Nemati, S., & Tavakoli, Z. (2012). Effects of Magnesium and Vitamin B6 on the Severity of Premenstrual Syndrome Symptoms. U.S. National Library of Medicine National Institutes of Health , 4 (1).
Facchinetti, F., Borella, P., Sances, G., Fioroni, L., Nappi, R., & Genazzani, A. (1991, August). Oral magnesium successfully relieves premenstrual mood changes. U.S. National Library of Medicine National Institutes of Health .
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Oudi, M., Aouni, Z., Mazigh, C., Khockkar, R., Gazoueni, E., Haouela, H., et al. (2010). Homocysteine and markers of inflammation in acute coronary syndrome. U.S. National Library of Medicine National Institutes of Health , 2 (15).
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Footnotes
[1] http://apps.who.int/classifications/icd10/browse/2015/en#/N94.6
[2] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2853792/
[3] http://www.mayoclinic.org/diseases-conditions/premenstrual-syndrome/basics/definition/con-20020003
[4] http://www.mayoclinic.org/diseases-conditions/premenstrual-syndrome/basics/symptoms/con-20020003
[5] http://www.mayoclinic.org/diseases-conditions/premenstrual-syndrome/expert-answers/pmdd/faq-20058315
[6] http://www.fda.gov/downloads/Drugs/DrugSafety/ucm089162.pdf
[7] http://www.webmd.com/drugs/2/drug-151686/pamprin-max-oral/details/list-sideeffects
[8] http://www.webmd.com/drugs/2/drug-151686/pamprin-max-oral/details/list-sideeffects
[9] http://blogs.scientificamerican.com/cross-check/are-antidepressants-just-placebos-with-side-effects/
[10] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1509101/
[11] http://www.ncbi.nlm.nih.gov/pubmed/2067759/
[12] http://www.ncbi.nlm.nih.gov/pubmed/9861593/
[13] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161081/
[14] http://cals.ncsu.edu/plantbiology/Faculty/mdaub/bilski2000.pdf
[15] http://ajcn.nutrition.org/content/87/5/1446.long
[16] http://www.sciencedaily.com/releases/2008/05/080520103435.htm
[17] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898531/
[18] http://www.ncbi.nlm.nih.gov/pubmed/25035435
[19] http://ajcn.nutrition.org/content/87/5/1446.long
[20] http://www.ncbi.nlm.nih.gov/pubmed/25403655
[21] http://www.naturafoundation.co.uk/monografie/Vitamin_B6_B12_and_folic_acid.html
[22] https://ods.od.nih.gov/factsheets/VitaminB6-HealthProfessional/
[25] https://ods.od.nih.gov/factsheets/VitaminB6-HealthProfessional/
[26] https://ods.od.nih.gov/factsheets/VitaminB6-HealthProfessional/
[27] http://www.ncbi.nlm.nih.gov/pubmed/4085632
[28] http://www.ncbi.nlm.nih.gov/pubmed/15558839