TRUTH: The “tendencies” that cause RLS are passed down from parent to child. These tendencies are VERY changeable. They are not hard-coded.
Epigenetics are the switches that turn these tendencies OFF or ON.
Science now knows with absolute certainty that genetics play a much smaller role than previously thought.
Here’s a quote from Newsweek Magazine about the new exciting world of epigenetics.
“Roll over, Mendel. Watson and Crick. They are so your old man’s version of DNA. And that big multibillion-dollar hullabaloo called the Human Genome Project? To some scientists, it’s beginning to look like an expensive genetic floor pad for a much more intricate – and dynamic – tapestry of life that lies on top of it.” - Newsweek Magazine, June 2009
Genetics determine certain traits that are passed on to children, such as hair color, the shape of the nose etc. (as we all learned in school) but beliefs, tendencies and conditions that are passed on are passed through what is called “epigenetics.” These are the switches that determine how our genes are going to act.
For instance, if a parent was extremely negative, those negative switches would be already turned on in the child’s genetic makeup, even before it was born. The child would have to take an action to change the switches to turn the positive genes on and the negative genes off.
In the case of RLS, the bad switches could be on because of diet, environment, and in a lot of cases, stress. This would create inflammation in the parent, and at some point in the child’s life, sometimes very early. These switches would cause inflammation to build until actions were taken and changes were made.
Here’s a quote from a 2012 study:
“Phenocopies in families with essential tremor and restless legs syndrome challenge Mendelian laws. Epigenetics might provide answers.” Zimprich A. Parkinsonism Relat Disord. 2012 Jul;18(6):711-6.
“There is increasing evidence that epigenetic modifications, which refer to changes in gene expression without changes in DNA sequence, can be transmitted to the next generation. Moreover, epigenetic information can be transferred from one allele of a gene to the other allele of the same gene; if then inherited to the next generation, the offspring consequently presents phenotypic properties related to the untransmitted allele.”
Note that if a parent had inflammatory tendencies in the way they lived their life, the inflammation could eventually manifest in the child in a number of ways. It could become RLS as well as hundreds of other inflammatory conditions including depression, ADHD, Parkinson’s etc.
For an extensive look at epigenetics visit:
TRUTH: There is only ONE type of RLS. RLS is ALWAYS caused by inflammation, not by another condition.
Having chronic inflammation in your body is like spilling a coffee on your keyboard. Something unpleasant is going to happen, you’re just not sure what.
In the now famous 2012 study by Dr. Leonard Weinstock titled “Restless Legs Syndrome: Theoretical Roles of Inflammatory and Immune Mechanisms” it was shown that 36 of the 41 RLS-associated conditions (88%) have been associated with inflammatory and/or immune changes.
According to the study “The fact that the majority of highly RLS associated conditions are also associated with inflammatory/immune changes suggests the possibility that RLS may be mediated or affected through these mechanisms.”
Parkinson’s, IBS, SIBO, Cancer or any of the other secondary conditions the study refers to do not cause RLS. Inflammation is causing BOTH of the conditions.
Keep in mind that inflammation can manifest as one condition, two conditions or more if it’s not addressed.
You can read about the study at the website below, which also includes some additional data that shows why the results should have shown that 100% of the conditions are associated with inflammation.
TRUTH: The inflammation causing the RLS also affects iron levels.
The medical text “Hyperkinetic Movement Disorders: Differential Diagnosis and Treatment” by Alberto Albanese and Joseph Jankovic (John Wiley & Sons, 2012) is a scholarly work written for pediatric and adult endocrinologists, orthopaedic surgeons, roentgenologists, workers in rheumatology clinics, geneticists, nutritionists and very specialized osteologists. The book is a collection of data and observations made through a variety of scientific studies.
Chapter 20 of the book focuses on Restless Legs Syndrome. On page 311, Arthur S. Walters M.D. of the Vanderbilt Department of Neurology is quoted.
“Most recently we have noted that RLS patients have an increased prevalence of Irritable Bowel Syndrome (IBS) and an increased prevalence of Small Intestinal Bacterial Overgrowth (SIBO) compared to controls. This led us to review the 40 or so secondary causes of RLS. Independent of RLS, the vast majority of these secondary causes are associated with either iron deficiency, SIBO or inflammatory/immune abnormalities.
This suggests that inflammation and immune attacks on the peripheral or central nervous system in RLS could be pathogenetic to RLS.
An alternative explanation is that inflammation may lead to iron deficiency which may in turn lead to RLS.”
It is well known in the scientific community that inflammation can affect iron levels. Below are a couple of studies that support this idea:
“Influence of acute inflammation on iron and nutritional status indexes in older inpatients.” MM Chiari et al. J Am Geriatr Soc. 1995 Jul;43(7):767-71.
“Patients with acute inflammation present altered iron status indexes that resemble those observed in the anemia of chronic disease.”
“Interpretation of biochemical tests for iron deficiency: diagnostic difficulties related to limitations of individual tests.” Frank Firkin, Director of Clinical Haematology; and Bryan Rush, Director of Laboratory Haematology, St Vincent’s Hospital, Melbourne.
“Most cases of iron deficiency can be diagnosed with simple tests. The concentration of serum iron does not fall until the body’s iron stores are exhausted. As the stores are depleted, the concentration of transferrin rises while the concentration of ferritin falls.
Caution is required when assessing patients with inflammatory disease as a low serum iron may not represent iron deficiency. These patients often have reduced concentrations of transferrin.”
TRUTH: The dopamine imbalance and the Restless Legs are BOTH caused by INFLAMMATION.
A dopamine imbalance can be caused by low iron levels or directly from inflammation as is stated in the following studies:
“CSF iron, ferritin and transferrin levels in restless legs syndrome.” Soichi Mizuno et al. Department of Psychiatry, Shimane University School of Medicine, Shimane, Japan, February 2004.
“The results of this MRI study suggest that idiopathic RLS patients may have a dysfunction of dopamine production induced by the iron deficiency in a dopamine-related specific area of the brain, and support the iron-dopamine model of this syndrome.
“Iron deficiency alters expression of dopamine-related genes in the ventral midbrain in mice” L.C. Jellena et al. Neuroscience, Volume 252, 12 November 2013, Pages 13–23
“A clear link exists between iron deficiency (ID) and nigrostriatal dopamine malfunction. This link appears to play an important role in at least restless legs syndrome (RLS) if not several other neurological diseases.”
“Iron deficiency alters dopamine uptake and response to L-DOPA injection in Sprague–Dawley rats.” Laura E. Bianco1 et al. Journal of Neurochemistry, Volume 106, Issue 1, pages 205–215, July 2008.
“Iron deficiency (ID) disrupts brain dopamine (DA) and norepinephrine (NE) metabolism including functioning of monoamine transporters and receptors.”
“Inflammation induces mitochondrial dysfunction and dopaminergic neurodegeneration in the nigrostriatal system.” RL Hunter et al. Journal of Neurochemistry. 2007 Mar;100(5):1375-86.
“Evidence suggests that chronic inflammation, mitochondrial dysfunction, and oxidative stress play significant and perhaps synergistic roles in Parkinson’s disease (PD), where the primary pathology is significant loss of the dopaminergic neurons in the substantia nigra.”
“Systemic Infusion of Naloxone Reduces Degeneration of Rat Substantia Nigral Dopaminergic Neurons Induced by Intranigral Injection of Lipopolysaccharide.” Bin Liu et al. The Journal of Pharmcology and Experimental Therapeutics Vol. 295, No. 1, JPET 295:125-132, (2000).
“A massive degeneration of dopamine-containing neurons in the substantia nigra (SN) in the midbrain is characteristic of Parkinson’s disease. Inflammation in the brain has long been speculated to play a role in the pathogenesis of this neurological disorder.”
TRUTH: RLS is a BIOMARKER indicating that your body is dangerously INFLAMED and that ACTIONS must be taken to prevent further damage.
RLS is now officially Willis-Ekbom Disease (WED). The name change occurred a few years ago to give it more credibility, but the truth is it’s an uninspiring name and is rarely used by anyone outside of RLS.org.
The body is an incredibly complex machine and one of its survival mechanisms is its ability to send our warning signals when something is not right underneath the hood.
For example, frequent headaches indicate that something beneath the surface needs to be attended to, whether it be stress, lifestyle, a tumor, inflammation or something else.
In the case of RLS, your body is telling you that you have too much inflammation and that it must be dealt with. If no changes are made, the inflammation will increase and lead to additional conditions.
A nationally-recognized sleep expert has published an editorial describing Restless Legs Syndrome (RLS) as a possible biomarker for underlying disease. The editorial appears in the March 5, 2014 issue of Neurology the medical journal of the American Academy of Neurology and was authored by Boston Medical Center neurologist Sanford H. Auerbach, MD.
Auerbach suggests that restless leg syndrome is a meaningful biomarker for serious disease, and that RLS screening may become more common as a tool for primary care providers to identify patients at risk.
Find out more here:
TRUTH: The RLS is caused by the HIGHER presence of INFLAMMATION in pregnant women.
As the studies below demonstrate, inflammation levels tend to increase in pregnant women.
“Vaginal cytokines in normal pregnancy.” G. Gilbert et al. American Journal of Obstetrics and Gynecology, vol. 189, no. 5, pp. 1433–1438, 2003.
“A significant increase of proinflammatory cytokines (IL-6 and IL-8) is produced in the third trimester. These cytokines act as chemoattractants of polymorphonuclear leukocytes stimulating the expression of prostaglandins in response to delivery preparation.”
“C Reactive Protein levels are elevated in the Third Trimester in Preeclamptic pregnant Women.” Zaima Ali et al. Dept. of Physiology, Lahore Medical and Dental College, Department of Obstetrics and Gynecology, Jinnah Hospital, Lahore.
“Pregnancy is a complex process which leads to a number of systemic changes. During normal pregnancy all these changes are very well regulated. Preeclampsia is a very common disorder of pregnancy and is characterized by hypertension and proteinuria that begins at more than 20 weeks of gestation. Poor placentation with inadequate cytotrophoblast invasion results in widespread maternal endothelial dysfunction. There is increasing evidence that preeclampsia is accompanied by exaggerated maternal systemic inflammatory response to this poor placentation.”
“Prokineticin-1: A Novel Mediator of the Inflammatory Response in Third-Trimester Human Placenta.“ Fiona C. Denison et al. Endocrinology. 2008 July; 149(7): 3470–3477. doi: 10.1210/en.2007-1695
“Prokineticin-1 (PK1) is a recently described protein with a wide range of functions, including tissue-specific angiogenesis, modulation of inflammatory responses, and regulation of hemopoiesis. The aim of this study was to investigate the localization and expression of PK1 and PK receptor-1 (PKR1), their signaling pathways, and the effect of PK1 on expression of the inflammatory mediators cyclooxygenase (COX)-2 and IL-8 in third-trimester placenta.
Our study demonstrates that PK1 and PKR1 are highly expressed in third-trimester placenta with PK1 up-regulating expression of IL-8 and COX-2 potentially via activation of PKR1 and cross-talk with EGFR. The latter finding is supported by double-immunofluorescent immunohistochemistry studies that show that PKR1 colocalizes with IL-8 and COX-2 in placenta. Together, these data suggest that PK1 may be a novel paracrine mediator of the inflammatory response in third-trimester placenta.”
TRUTH: The RLS is caused by the HIGHER presence of INFLAMMATION in elderly people.
As the studies below demonstrate, inflammation levels tend to be higher in the elderly population.
“Inflammation in aging: cause, effect, or both?” NS Jenny. Discov Med. 2012 Jun;13(73):451-60.
“Aging is a progressive degenerative process tightly integrated with inflammation.”
“Chronic Low-Grade Inflammation in Elderly Persons Is Associated with Altered Tryptophan and Tyrosine Metabolism: Role in Neuropsychiatric Symptoms.” L. Capuron et al. Biol Psychiatry. 2011 Jan 28.
“Our findings show that chronic low-grade inflammation in aging is associated with alterations in enzymatic pathways involved in monoamine metabolism and suggest that these alterations might participate in the pathophysiology of neuropsychiatric symptoms in elderly persons.”
“Age-related alterations in retinal neurovascular and inflammatory transcripts.” CA Van Kirk et al. Mol Vis. 2011;17:1261-74.
“The commonalities in retinal age-related and diabetes-induced molecular alterations provide support for the hypothesis that diabetes and aging engage some common para-inflammatory processes.”