Dr. Tom Greenfield

Dear Dr. Greenfield,

I am a 42 year old woman with RLS. I have it since I was 20, with alternating good and bad periods.

It affects me especially in my sleep. I am a 0+, Gatherer.

Are there any natural supplements I can take which could make a difference?

Thanks and kind regards,

Petra

Restless legs syndrome (RLS) and periodic limb movement disorder are characterized during waking by an irresistible urge to move the legs while awake, and involuntary leg movements while asleep.

For people with a family history of RLS, it is worth considering whether there is a genetic influence on the condition: researchers have found several genetic loci associated with RLS in an autosomal dominant inheritance pattern [1].

One of the genetic influences may involve an increased need for folate [2]. Individuals with polymorphisms for folate metabolism often do better taking an active form of folic acid such as folinate, rather than the commonly available folic acid supplements. Although folic acid improves methylation in all GenoTypes, GT4 Explorers are more prone to folic acid deficiency anaemia; GT1 Hunters and GT6 Nomads may also need folate to slow down their rapidly aging genes [3].

Researchers have also found that iron supplementation may improve the symptoms of RLS [2], reducing fluctuations in dopamine levels in the brain at night. Patients with RLS have lower levels of dopamine and respond to iron administration [4]. Caffeine, nicotine, alcohol and medication that affects dopamine levels may induce RLS as a side effect. It is recommended to check ferritin (iron storage) levels before supplementing with iron, as ferritin levels are often lower than average in RLS sufferers. There are strong indications that a gene regulating dopamine beta hydroxylase activity is linked to the ABO blood group locus [5], and altered dopamine levels may be associated with blood type.

Finally, osteopathic manipulative therapy has been found to decrease spinal facilitation in a small pilot study, relieving symptoms in many patients with RLS [6].

References:
1. Dhawan V, Ali M, Chaudhuri KR. "Genetic aspects of restless legs syndrome." Postgrad Med J. 2006 Oct;82(972):626-9. PubMed
2. Lee KA, Zaffke ME, Baratte-Beebe K.J. "Restless legs syndrome and sleep disturbance during pregnancy: the role of folate and iron." Womens Health Gend Based Med. 2001 May;10(4):335-41. PubMed
3. Dadamp, P. The GenoType Diet. Broadway Books, 2007, ISBN 978-0-7679-2524-2
4. Patrick LR. "Restless legs syndrome: pathophysiology and the role of iron and folate." Altern Med Rev. 2007 Jun;12(2):101-12. PubMed
5. Wilson AF, Elston RC, Siervogel RM, Tran LD. "Linkage of a gene regulating dopamine-beta-hydroxylase activity and the ABO blood group locus". Am J Hum Genet 1988;42:160-166. PubMed
6. Peters T W, "Restless Legs", Osteopathy Today, October 2001. P12-13.

An extract of the seaweed Lithothamnion corallioides from Ireland has been the subject of a clinical trial with patients suffering from osteoarthritis of the knee.[1] The seaweed extract containing minerals was compared to glucosamine sulfate, and both products demonstrated improvements in those taking them.

Comparing 6-Minute Walking Distances and the WOMAC Knee and Hip Osteoarthritis Index, 70 subjects with moderate to severe osteoarthritis of the knee were placed into 4 random groups and took either the seaweed mineral extract (2400 mg), glucosamine sulfate (1500 mg), both, or a placebo. The seaweed mineral and glucosamine groups demonstrated significant improvements in 6 minute walking distances, but the placebo and combination groups did not.

The WOMAC index grades pain, stiffness and physical function over specific activities. Significant differences were found between groups for pain scores after 12 weeks of treatment. The seaweed extract treatment group showed significantly improved WOMAC pain, stiffness, activity and composite scores over the course of the 12-week treatment. No significant improvements were found for subjects in the placebo group or for subjects in the combination treatment group.

The authors hypothesize that there could be an interaction in the stomach between the alkaline seaweed minerals and the acid glucosamine, which has to ionize in the stomach to be effective.

NAP Phytocal and Clearcal contain minerals from Lithothamnion corallioides, and are suitable for specific or all blood groups.

References:
1. Frestedt JL, Walsh M, Kuskowski MA, Zenk JL. "A natural mineral supplement provides relief from knee osteoarthritis symptoms: a randomized controlled pilot trial." Nutr J. 2008 Feb 17;7:9. PMID 18279523

The UK Food Standards Agency (FSA) has issued a press release advising pregnant mothers to limit their intake of coffee and caffeine-containing substances.[1] "Pregnant women are advised to limit their daily caffeine intake to 200mg a day – roughly two mugs of coffee a day" due to a potential link with Foetal Growth Retardation (FGR). This is a reduction from the previous advice of 300 mg per day, following an updated report from the FSA's independent Committee on Toxicity (COT).[2] According to the committee, if there is a causal link then there may be no lower 'safe' limit, but a caffeine intake of less than 200 mg per day during pregnancy may reduce the risk of FGR to less than 2%. FGR is defined as failure of the baby to attain its growth potential as determined by genetic and environmental factors.

The FSA funded research published by the British Medical Journal[3] which measured caffeine intake from all sources (coffee, tea, colas and medication) in pregnant women, and then measured their babies when they were born. The xenobiotic caffeine can be detoxified from the body in four main ways, 3-demethylation being quantitatively the most important: caffeine is converted to paraxanthine by the enzyme cytochrome P450 1A2 (CYP1A2). This is one of the enzymes which often has low activity in the GT4 Explorer GenoType, and is responsible for Explorers being up all night after drinking coffee. The researchers measured the CYP1A2 enzyme activity as the main form of caffeine clearance in the mothers taking part in the study. They found that the mothers with the highest CYP1A2 activity passed the most caffeine and caffeine metabolites to their foetus via the placenta. CYP1A2 activity is absent in the placenta and the fetus.[4] This means that like the GT4 Explorer, the unborn baby won't get much sleep after their mother has drunk coffee.

What is the problem with having smaller babies? It is a well known epigenetic risk factor, as the COT study says:

FGR is an important outcome because it is associated with an increased risk of perinatal mortality and morbidity, including perinatal asphyxia. Moreover, there is epidemiological evidence that FGR correlates with adverse effects in adult life. For example, affected individuals have an increased incidence of metabolic syndrome, manifesting as obesity, hypertension, hypercholesterolemia, cardiovascular disease, and type 2 diabetes.

Smoking and alcohol intake also have a significant effect on the risk of FGR.

References:

1. Food Standards Agency. "Food Standards Agency publishes new caffeine advice for pregnant women." Press release, Monday 3 November 2008.
2. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment. "Statement on the reproductive effects of caffeine". COT statement 2008/04
3. CARE Study Group. "Maternal caffeine intake during pregnancy and risk of fetal growth restriction: a large prospective observational study" BMJ 2008;337:a2332
4. Aldridge A, Aranda JV, Neims AH. "Caffeine metabolism in the newborn." Clin Pharmacol Ther. 1979 Apr;25(4):447-53. PMID: 428190

With great fanfare, the establishment medical journal The New England Journal of Medicine (NEJM) published a paper "Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein."[1] Rosuvastatin (Crestor) is a drug marketed by the pharmaceutical company AstraZeneca as a HMG-CoA reductase inhibitor (they called it a 'super-statin'). AstraZeneca funded this study, and the lead author is one of the patent holders for the high sensitivity C-Reactive Protein test (hs-CRP),[2] a sensitive blood marker of inflammation. Of course there are no real vested interests apart from the health of the nation, and as such, the American Heart Association meeting wondered whether it should be "put in the water".[3] This harks back to the PolyPill hypothesis,[4] where it was suggested everyone should take pharmaceutical medication before they inevitably get ill. Shares in AstraZeneca rose since the NEJM publication,[3] as it would cost $116 USD per month for an individual (over $1,300 USD per year) to take it daily, according to USA Today.[5] This means that each life saved would cost approximately $557,000 (if you believe the studies). AND that does not include the cost of the patented hs-CRP test (more expensive than a cholesterol test). And according to The Blog of Michael R Eades MD,[6] the drug might only give a little protection to a very few people:

If you believe the data from this study..., it indicates that men over 50 and women over 60 with normal LDL-cholesterol levels AND elevated C-reactive protein levels who took the very expensive ($3.50 per day) statin drug rosuvastatin (Crestor) minimally reduced their risk of developing heart disease or dying of any cause as compared to those who took placebo.

So what else should we put in the water - the toxic chemical fluoride? But that's another story ...

What is counted by medics as 'high' cholesterol has been gradually dropping over the years as drug companies push the 'benefits' of statins as a simple magic bullet to the ubiquitous deaths from heart disease. Yet simple epigenetic cardiovascular disease risks such as low birth weight in males who regain a normal or above average Body Mass Index in childhood,[7] or men with shorter legs[8] or shorter index fingers than ring fingers[9] (high 2D:4D ratio) are ignored until the individual becomes a patient with heart disease later in life.

Back to the paper, which was dubbed the JUPITER trial: "The primary objective of the Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) was to investigate whether treatment with rosuvastatin, 20 mg daily, as compared with placebo, would decrease the rate of first major cardiovascular events." Eades translates this as "by God we’re going to prove that statins prevent something. "[6]

And what it did prove is that more people taking Crestor got diabetes than the people not taking Crestor:

We did detect a small but significant increase in the rate of physician-reported diabetes with rosuvastatin, as well as a small, though significant, increase in the median value of glycated hemoglobin. Increases in glucose and glycated hemoglobin levels, the incidence of newly diagnosed diabetes, and worsening glycemic control have been reported in previous trials of pravastatin, simvastatin, and atorvastatin.

Even though physician-reported diabetes was been significantly increased in this and previous Crestor studies, and statins are given to people who have diabetes because they have diabetes, the authors say that "further study is needed before any causative effect can be established or refuted." Eades suggests that this is why the study was stopped when it was by outside observers. Ok, let's further poison our water supply with an expensive drug that gives people diabetes (not to mention muscle pain) all in the name of health.

References:

1. Ridker PM, Danielson E, Fonseca FA, et. al. Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein. N Engl J Med. 2008 Nov 9.

2. US Patent 6040147 - Systemic inflammatory markers as diagnostic tools in the prevention of atherosclerotic diseases and as tools to aid in the selection of agents to be used for the prevention and treatment of atherosclerotic disease. Paul M Ridker.

3. "Cholesterol Pills in the Water? Crestor Market Widens (Update3)". Bloomberg.com news, Nov 10 2008.

4. Wald NJ, Law MR. "A strategy to reduce cardiovascular disease by more than 80%". BMJ 2003;326:1419 (28 June), doi:10.1136/bmj.326.7404.1419

5. "Crestor would save lives at $500,000 each" Steve Sternberg, USA Today, Nov 10 2008.

6. Eades, M. Weblog: "Truth versus hype in the Jupiter study" 10. November 2008.

7. Eriksson JG, Forsén T, Tuomilehto J, Winter PD, Osmond C, Barker DJP "Catch­up growth in childhood and death from coronary heart disease: longitudinal study." BMJ 1999;318;427-431

8. Davey Smith G, Greenwood R, Gunnell D, Sweetnam P, Yarnell J, Elwood P. "Leg length, insulin resistance, and coronary heart disease risk: The Caerphilly Study." J. Epidemiol. Community Health 2001;55;867-872 doi:10.1136/jech.55.12.867

9. Manning JT, Bundred PE, Flanagan BF. "The ratio of 2nd to 4th digit length: a proxy for transactivation activity of the androgen receptor gene?" Med Hypotheses. 2002 Sep;59(3):334-6. Pubmed 12208164