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From the Townsend Letter
June 2012

briefed by Jule Klotter
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Aquamin Mineral Supplement
Aquamin, derived from the red marine alga Lithothamnion corallioides, has been the subject of recent, manufacturer-sponsored studies. The Marigot Ltd. product, which contains calcium, magnesium, and 72 trace minerals, reduces inflammation. Aquamin inhibited the lipopolysaccharide-induced secretion of inflammatory cytokines TNF-a (tumor necrosis factor-alpha) and IL-1b (interleukin-1 beta) in cultures of rat cortical glial cells in a 2010 Irish study. Aquamin has also been tested on people with knee osteoarthritis.

Researchers at the University of Minnesota conducted two pilot studies on people with moderate to severe knee osteoarthritis. In the larger study, 70 patients were randomized into four double-blind treatment groups: (1) glucosamine sulfate (1500 mg/d); (2) Aquamin (2400 mg/d); (3) combined glucosamine-Aquamin treatment; (4) placebo. Fifty completed the study. WOMAC (Western Ontario and McMaster Universities) osteoarthritis scores and 6-minute walking distances were measured at baseline, 4 weeks, 8 weeks, and 12 weeks (end of treatment).

Both Aquamin and glucosamine groups had significant improvement in WOMAC pain and activity scores when compared with their baseline scores. Both the Aquamin group and the glucosamine group also showed significant improvement in the 6-minute walking distance test. The Aquamin subjects walked 101 feet (+7%) farther after 12 weeks of treatment, and the glucosamine group walked 56 feet (+3.4%) farther. The Aquamin group was the only one to show significant improvement in WOMAC stiffness by the study's end. Neither the placebo group nor the combined treatment group displayed any significant improvements. Aquamin is very basic (pH 10) compared with glucosamine sulfate (pH 3.5 to 5), and the authors think that the two therapies may interact in some way, preventing effectiveness.

The second University of Minnesota trial was a small, double-blind, placebo-controlled pilot study to investigate the effect of Aquamin on the use of NSAIDs (non-steroidal anti-inflammatory drugs) for pain relief. Participants with moderate to severe knee osteoarthritis underwent a two-week screening period during which they were asked to stop using all prescription, over-the-counter, or alternative pain management therapies except for a NSAID of their choice. The researchers intended to enroll 50 people, but patients were unwilling to volunteer upon learning that NSAID use would be gradually discontinued during the 12-week study. Only 14 of 22 subjects completed the study. Five of the 14 in the placebo group and 1 of 6 in the Aquamin group quit because of increasing pain levels; two other patients withdrew early in the study because of inability to follow the protocol.

After two weeks of using 50% of baseline NSAID dose, the Aquamin group had higher adjusted mean values for knee range of motion compared with the placebo group: 173 degrees vs. 168 degrees for passive and active extension (p = 0.028). The Aquamin group also walked farther during the 6-minute distance test – 1408 feet, an 8.7% improvement over baseline – compared with the 1295 feet for the placebo group (p = 0.03). "[T]he positive results did not continue once NSAID use was abolished completely," the researchers write. "… Aquamin cannot entirely replace NSAIDs as a treatment for [osteoarthritis]. However, Aquamin may allow for a reduced need for NSAIDs which may have substantial health benefits including a reduction in many of the adverse and well documented side effects of NSAIDS."

These small pilot studies suggest that the minerals or possibly some other factor in Aquamin can reduce inflammation and pain.

Frestedt JL, Kuskowski MA, Zenk JL. A natural seaweed derived mineral supplement (Aquamin F) for knee osteoarthritis: A randomized, placebo controlled pilot study. Nutr J. February 2, 2009. Available at Accessed March 20, 2012. (Bad link)
(Editor note: Try this link: )

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. February 17, 2008. Available at Accessed January 4, 2010.

Marigot Ltd. What is inflammation? Available at Accessed March 20, 2012.

Ryan S, O'Gorman DM, Nolan YM. Evidence that the marine-derived multi-mineral Aquamin has anti-inflammatory effects on cortical glial-enriched cultures. Phytother Res. 2010. Available at Accessed March 20, 2012.

Cholesterol Sulfate Hypothesis
Cholesterol sulfate deserves far more attention than it has received, if Stephanie Seneff is correct. While immersing herself in medical literature about cholesterol and its biological roles, she became intrigued with two sulfur compounds: cholesterol sulfate and vitamin D sulfate. Seneff, who has a BS degree in biophysics and a PhD in electrical engineering, is a senior research scientist in the Computer Science and Artificial Intelligence Laboratory at MIT.

Cholesterol sulfate is synthesized in skin. Unlike fatty cholesterol, cholesterol sulfate is water-soluble and does not need LDL transport to tissues. The compound enters cell membranes with ease. It is known to be part of the protective barrier in the skin that prevents the entry of harmful microbes. Despite its ubiquitous presence, cholesterol sulfate's full purpose remains uncertain.

Cholesterol sulfate may be the precursor of water-soluble vitamin D sulfate. The two sulfate compounds are nearly identical, and research by Magnus Axelson and others indicates that "25-hydroxvitamin D3 is not readily sulphated by man in vivo"; vitamin D3 sulfate needs to be made from a compound that already contains sulfur. Researchers are unclear about vitamin D3 sulfate's purpose, but Seneff believes that this is the form that protects against cancer and heart disease. Unlike 25-hydroxvitamin D3, sulfated vitamin D does not transport calcium and prevent rickets. 

Seneff hypothesizes that cholesterol sulfate plays important roles in fat and muscle cells' metabolism of glucose. Glucose enters cells through "special cholesterol rich sites in the cell wall called lipid rafts." Seneff believes that water-soluble cholesterol sulfate supplies the extra cholesterol to form these "rafts," packing the lipoproteins in the cell wall closer together and thereby exposing less of their surface area to damage from glucose (a reducing agent) and from the oxygen used to break it down. (Cells' mitochondria use hydrogen peroxide to metabolize glucose.)

When the cholesterol portion of the compound forms a lipid raft, the sulfate portion enters the cell. Seneff believes that the sulfur bonds to iron present in myoglobin, which stores oxygen in muscle cells. This iron sulfate molecule works with hydrogen peroxide to break down glucose in a way that safeguards cellular proteins: "… the sulfur molecule's charge would be driven down from +6 to -2, releasing energy and absorbing the impact of the reducing effects of glucose, and therefore serving as a decoy to protect the proteins in the cell from glycation damage."

"I would predict," Seneff writes, "that deficiencies in cholesterol sulfate lead to severe defects in muscle metabolism, and this includes the heart muscle. My theory would explain the protective role of cholesterol sulfate in heart disease and muscle wasting diseases." She refers to a 2008 study by Yongjie Ma and colleagues which showed that "the sulfate ion attached to oxidized forms of cholesterol is highly protective against fatty streaks [in coronary arteries] and atherosclerosis."

Most Americans believe that cholesterol is bad. They avoid eggs (which are also rich in sulfur) and other cholesterol-rich foods and take cholesterol-lowering drugs. Furthermore, commercial agriculture practices reduce the soil's sulfur content, a lack that is passed on to plant foods normally rich in the mineral: onions, garlic, kale, and broccoli. As a result, cells throughout the body lack protection from the damage of glycation that cholesterol sulfate appears to prevent.

Seneff believes that sulfur deficiency and the ongoing drive to lower cholesterol levels are contributing to several modern-day disorders, including obesity, heart disease, Alzheimer's disease, and chronic fatigue syndrome. She may be right. Certainly, she is calling attention to an important element – sulfur – that has been largely overlooked.

Axelson M. 25-hydroxyvitamin D3 3-sulphate is a major circulating form of vitamin D in man. FEBS Letters. October 1985:191(2);171–175. Available at Accessed March 21, 2012.

Seneff S. Could sulfur deficiency be a contributing factor in obesity, heart disease, Alzheimer's and chronic fatigue syndrome? September 15, 2010. Available at Accessed February 6, 2012.

Stephanie Seneff [Web page]. Accessed February 6, 2012.

Dietary Fiber and Diverticulosis
Contrary to expectation, people who eat a high-fiber diet are more likely to have asymptomatic diverticulosis, according to a 2011 University of North Carolina-Chapel Hill study. In itself, diverticulosis, a condition in which pouches form in the colon wall, usually produces no symptoms – unless fecal matter gets stuck in a pouch and produces infection (diverticulitis). For decades, doctors have recommended high-fiber diets to prevent constipation, which is believed to contribute to diverticula formation.

A UNC research team, led by Anne F. Peery, interviewed 2104 patients (aged 30–80) who underwent outpatient colonoscopy at UNC Hospitals from 1998 to 2010. They gathered data about diet, bowel movements, and physical activity. The prevalence of diverticulosis was 30% higher in those with the highest fiber intake compared with those with the lowest intake.

In addition, frequent bowel movements, not constipation, were linked to the condition. "Compared to those with fewer than seven bowel movements per week, individuals with more than 15 bowel movements per week were 70 percent more likely to develop diverticulosis," according to a UNC Health Care News report. The researchers found no connections between diverticulosis and physical activity, dietary fat consumption, or red meat intake. This study clearly disproves the prevailing belief that constipation and a low-fiber diet lead to diverticulosis. Instead, the UNC researchers suggest that gut flora may play a role.

In their 2007 editorial "Fiber and Colorectal Diseases: Separating Fact from Fiction," Drs. Kok-Yang Tan and Francis Seow-Choen write: "… what we have all been made to believe about fiber needs a second look. We often choose to believe a lie, as a lie repeated often enough by enough people becomes accepted as the truth. We urge clinicians to keep an open mind. While there are some benefits of a diet high in natural fiber, one must know the exact indications before recommending such a diet."

Diets high in fiber won't protect against diverticulosis [online press release]. UNC Health Care. January 23, 2012. Accessed March 23, 2012.

Kok-Yang T, Seow-Choen F. Fiber and colorectal diseases: separating fact from fiction. World J Gastroenterol. August 21, 2007;13(31):4161–4167. Available at

Peery AF, Barrett PR, Park D, et al. A high-fiber diet does not protect against asymptomatic diverticulosis [abstract]. Gastroenterology. February 2012; 142(2); 266-272 e1. Available at Accessed March 23, 2012.

Exercise and Low-Grade Inflammation
Chronic low-grade inflammation has been linked to several disorders, including cardiovascular disease, metabolic syndrome and insulin resistance, neurodegeneration, and tumor growth. Danish researchers have been investigating myokines – anti-inflammatory cytokines released by muscle cells during exercise. "Today, it appears that skeletal muscle has the capacity to express several myokines," Claus Brandt and Bente K. Pedersen state in a 2010 review article. "The list includes IL-6, IL-8, IL-15, BDNF, and LIF. In addition, Kenneth Walsh, Boston, has recently identified the myokines FGF21 and Follistatin-like-1."

The first anti-inflammatory myokine to be identified – and the first to be released during exercise – is interleukin-6 (IL-6).  IL-6 in monocytes or macrophages is one of the pro-inflammatory cytokines activated by TNF-a (tumor necrosis factor-alpha) during an immune response. IL-6 in skeletal muscle, however, is anti-inflammatory. Circulating IL-6 "increases … up to 100 fold in response to exercise," according to Neha Mathur and Bente K. Pedersen. Muscle-cell IL-6 stimulates production of anti-inflammatory cytokines IL-1ra and IL-10. It also inhibits pro-inflammatory TNF-a and IL-1. TNF-a promotes inflammation and alters insulin signal transduction, inhibiting glucose uptake and metabolism. Healthy volunteers displayed insulin resistance in skeletal muscle after receiving an infusion of TNF-a, according to a study led by P. Plomgaard (Diabetes. 2005;54(10):2939–2945). In contrast, muscle IL-6 increases glucose uptake and fat oxidation.

Pedersen and colleagues tested the anti-inflammatory effect of IL-6 and exercise in a 2003 study (FASEB Journal, 17[8]:884–886). The researchers randomly assigned healthy volunteers to rest or to stationary bicycling for three hours. At the 2.5 hour point, all volunteers were injected with a low dose of Escherichia coli endotoxin to create low-grade inflammation. Circulating TNF-a levels increased "2- to 3-fold" in the resting subjects but did not increase at all in the cycling group. The researchers found that using an infusion of IL-6 in place of cycling had the same effect. (One would not want to "blunt" TNF-a with exercise or an IL-6 infusion if the body were fighting a true infection.)

I know that exercise improves mood, relieves stress, and helps people lose weight; but this is the first time that I've heard that skeletal muscles actually release anti-inflammatory cytokines during exercise. The question is whether regular exercise can prevent chronic low-grade inflammation. And if so, how much and what kind of exercise is most effective?

Brandt C, Pedersen BK. The role of exercise-induced myokines in muscle homeostasis and the defense against chronic disease. J Biomed Biotechnol. 2010. Available at Accessed March 24, 2012.

Mathur N, Pedersen BK. Exercise as a mean to control low-grade systemic inflammation. Mediators Inflamm. 2008. Available at Accessed March 24, 2012.

Inflammation, Insulin Resistance, and Metabolic Syndrome
Metabolic syndrome has been associated with low-grade inflammation unrelated to infection, tissue trauma, or autoimmunity. Inflammation is known to contribute to insulin resistance. Two possible contributors to this low-grade inflammation are adipocyte (fat cell) dysfunction and systemic oxidative stress.

In a 2010 review article, Portuguese biochemists Rosário Monteiro and Isabel Azevedo explain how adipocyte dysfunction, due to excessive nutrient intake, can produce inflammation and insulin resistance. When adipocytes hold too many fatty acids, their stressed cell walls weaken and burst, setting off an inflammatory response as the body tries to clean up the dead cells. In addition, adipocytes have toll-like receptors (TLRs) that produce pro-inflammatory cytokines, such as TNF-a, when activated by fatty acids. "It is very likely that the activation of TLRs takes place in hyperlipidemic states, resulting in amplified inflammation and contributing to the development or aggravation of the metabolic syndrome," they state.

Systemic oxidative stress is another cause of inflammation and insulin resistance. In their 2007 review article, Mohammed Qatanani and Mitchell A. Lazar define systemic oxidative stress "as a persistent imbalance between the production of highly reactive molecular species (chiefly oxygen and nitrogen) and antioxidant defenses." Reversing that imbalance by providing antioxidants – such as N-acetylcysteine and RAC-a-lipoic acid – has decreased insulin resistance caused by hyperglycemia in rodents and humans. Qatanani and Lazar do not claim that oxidative stress is the sole or even primary cause of insulin resistance: "… the view that one factor is primarily responsible for the link between obesity and insulin resistance is clearly simplistic."

The cycle of insulin resistance and inflammation in metabolic syndrome appears to be self-perpetuating. What are we doing that has made metabolic syndrome and insulin resistance increasingly common? Monteiro and Azevedo point to the "modern Western lifestyle," consisting of long-term and continuous psychological stress; excessive energy intake (sugar and fat) with low physical activity; low-quality, nutrient-poor food; and sleep disruption.

Monteiro R, Azevedo I. Chronic inflammation in obesity and the metabolic syndrome. Mediators Inflamm. 2010. Available at Accessed March 22, 2012.

Qatanani M, Lazar MA. Mechanisms of obesity-associated insulin resistance: many choices on the menu.  Genes Dev. 2007;21:1443–1455. Available at Accessed March 21, 2012.

Intention-Host Device Research
"[F]or this past ~400 years, human consciousness and intent have been rejected [by "establishment science"] as possible and significant experimental variables in physical reality," write physicist William A. Tiller, PhD, and geochemist Walter E. Dibble Jr., PhD, in "White Paper I: A Brief Introduction to Intention-Host Device Research." Tiller, now retired from Stanford University, began investigating human intention while teaching and researching traditional science at the school's Department of Materials Science and Engineering nearly 40 years ago. Dibble worked with Tiller as a postdoctoral student in the early 1980s and later as a visiting scholar. He is now employed at Ditron LLC and the William A. Tiller Foundation for New Science.

In recent years, Tiller and colleagues have been using intention-host devices to investigate the effects of human intention on physical reality. Unlike Princeton Engineering Anomalies Research (PEAR) in which subtle energy and intention affect the outcomes of a random number generator, the intention-host device produces effects on a variety of organic and inorganic targets. The intention-host device is programmed, via meditation, to hold a specific intention in its electrical circuit. This device primarily consists of a RAM computer chip in an oscillating electrical field. By placing the device near the intended target, Tiller and colleagues have used the device to raise or lower the acid/alkaline balance (pH) of water; increase the chemical activity of the liver enzyme alkaline phosphatase (ALP) by 25% to 30% (in vitro); and increase the ATP/ADP ratio in fruit fly larvae by 15% to 20%, thereby decreasing the time it took the flies to reach adult stage by 20% to 25%.

The pH study was replicated using 10 sites in the US and Europe. Initially, researchers set up host devices in Arizona, Missouri, and Kansas with control sites 2 to 20 miles away. The control sites had the same equipment and water but no intention-host device. All three device sites showed an exponential increase in pH over time. Curiously, the control sites also showed increases in pH. The researchers hypothesized that information entanglement had occurred between the host sites and control sites, so they set up new control sites for the US intention devices in London, England, and three months later in Milan, Italy. "Within 3 weeks the [change in pH] had increased by ~1 pH unit at the London-site and, 3 months later the Milan site went online and within 1 week the [change in pH] at that site had increased exponentially to ~1 pH unit. Thus, this information entanglement phenomenon had now been proved to extend at least 6000 miles," Tiller and Dibble state. They add, "The fact that all of the control sites exhibited non-zero values for [excess thermodynamic free energy change used to measure aqueous H+-ion] demonstrates very clearly that the control sites are informationally connected to the intention-host device sites even over such huge distances."

Tiller and his colleagues are working to understand how human consciousness and intention work in the physical world. The two researchers say, "… from our experimental work of the past ten years, we have discovered that there are actually two levels of physical reality and not just the one with which we are all familiar. It is this new [spacetime] level of physical reality that can be significantly influenced by human intention – not our familiar electric atom/molecule level!" These two levels of physical reality interpenetrate, become "coupled," when using conscious intention in a meditative state.
For more information about this research and the use of intention-host devices, see

McTaggart L. The creative observer. In: The Field. New York: HarperCollins; 2008:105–112.

Tiller WA, Dibble WE Jr. White paper I: a brief introduction to intention-host device research [online document]. 2009. Accessed January 6, 2012.

Microbial Exposures in Infancy and C-reactive Protein
Recognizing that environmental factors during infancy affect how a person's immune system copes with pathogens, Thomas W. McDade (Northwestern University, Evanston, IL) and colleagues decided to look at another part of the immune response: inflammation. They used prospective data from a Philippine birth cohort to "test the hypothesis that microbial exposures in infancy are associated with high sensitivity C-reactive protein (CRP) in adulthood." CRP has become a marker for low-grade inflammation characteristic of chronic diseases, such as cardiovascular disease.

The study began in 1983, when the 1461 participants were still in utero. Participants' exposure to respiratory and GI microbes during the first two years of their lives was assessed by asking their mothers about recent illnesses during bimonthly in-home interviews. Follow-up surveys continued throughout childhood and into adulthood. Information about household economic demographics, education, environment, and health was collected in 1983 and again in 2005. As adults in their early 20s, participants were questioned about health behaviors related to CRP (smoking, alcohol consumption, oral contraceptive use) and whether they were currently experiencing any sign of infection or illness. Body fat was assessed before taking blood samples to measure CRP levels.

The researchers reported that median CRP concentration for the entire group was 0.2 mg 1−1 with no significant difference between men and women. (In comparison, a 2003 study reported a mean CRP level of 0.9 mg 1−1 for 20– 29-year-old American men.) The researchers had expected a greater exposure to microbes during the first two years of life to produce a higher CPR level in adulthood. In fact, the opposite was true: "… individuals with elevated CRP as adults were exposed to lower levels of animal faeces in the home, had fewer episodes of diarrhea in their second year, and were less likely to be born in the dry season." (Microbes spread more readily during wet weather.) In addition, low birth weight corresponded to higher adult CRP levels independent of adult health behaviors and body fat: "Birth weight … remained a significant predictor of CRP in adulthood, with each kilogram increase in birth weight associated with a 29 per cent reduction in the odds of elevated CRP."

The results of this study supports the hygiene hypothesis which asserts that exposure to diverse environmental microbes early in life " … is critical to immune development, and the absence of such exposure is the key factor leading to immune dysregulation." This study does not, however, prove that lower CRP levels in young adults produces lowered risk to inflammatory-associated conditions such as cardiovascular disease.

McDade TW, Rutherford J, Adair L, Kuzawa CW. Early origins of inflammation: microbial exposures in infancy predict lower levels of C-reactive protein in adulthood. Proc Biol Sci. 2010;277:1129–1137.
Available at http:/ Accessed March 23, 2012. Bad link.
(Editor note:

Diet and Muscle Stimulation for MS
When internist Terry Wahls, MD, was diagnosed with multiple sclerosis in 2000, her doctor offered her interferon and copolymer-1 as a way to slow progressive degeneration, characteristic of the disease. She took the drugs and began a four-year search through medical literature to investigate neurodegeneration and mitochondrial failure – a primary contributor to MS disability in her view. She began to experiment with B vitamins, omega-3 fatty acids, alpha-lipoic acid, coenzyme Q10, L-carnitine, and other supplements. Her decline slowed but did not halt. In 2003, she began using a cane and an ankle-foot orthotic for left foot drop. Her diagnosis changed to secondary progressive multiple sclerosis; no FDA-approved treatments were capable of restoring her lost function. In 2004, fatigue led her to use a scooter in place of the cane. Her back tired so quickly that she began to use a zero gravity chair for meals and desk work.

"Then in the summer of 2007," she writes, "another metamorphosis began. Reviewing a study protocol for the University of Iowa's Institutional Review Board, I learned about neuromuscular electrical stimulation and wondered if it might help me." Neuromuscular electrical stimulation (NMES) detects small electrical signals in paralyzed muscles (such as in stroke patients) and uses those signals as a prompt for electrical stimulation that can actually make the muscles move. Wahls convinced her physical therapist to let her add NMES to her exercise program.

At the same time, Wahls took a second look at nutrition. She added more micronutrients such as sulfur amino acids, kelp (iodine), resveratrol (flavonoids), and vitamin D. She also began "to think more critically about food." She decided to concentrate on eating foods which contained the nutrients that she was taking as pills. She started eating three cups of greens and three cups of sulfur-rich cruciferous vegetables (600 grams total) per day. She also ate three cups of brightly-colored fruits or vegetables (300 grams) and 60 to 100 grams of grass-fed beef, poultry, or wild-caught fish daily. A weekly serving of seaweed took the place of her kelp supplement. Wahls also decided to avoid milk, eggs, and gluten-containing grains – all of which are common allergens. She began taking supplements that would help her body excrete mercury, pesticides, and other neurodegenerative toxins. The supplements included glutathione (2 grams), N-acetyl-cysteine (2 grams), taurine (2 grams), lithium orotate (300 mg/twice a day), methylated folate, and B12.

"Two months after starting my e-stim and intensive nutrition, I could again sit in a standard desk chair without being exhausted – for the first time in years," she writes. "At three months, I could walk between exam rooms in the clinic. At five months, I could walk to the clinic, and at seven months, I could bicycle around the block. A year after start e-stim and intensive nutrition, I was able to bicycle 18 miles. …" She has noticed an energy decline and decreased mental focus within 48 hours if her diet or access to NMES therapy is disrupted.

Her physical therapists and neurologist wrote up her case for Cases Journal. In their conclusion, they wrote, "This case suggests that the nutritional intervention and NMES were synergistic. Whether either NMES alone or nutrition alone would have yielded as many functional gains is unknown." Wahls and colleagues have since conducted a small pilot study on the use of NMES in people with secondary and primary progressive multiple sclerosis. Wahls's nutritional and NMES program is now being tested on patients with secondary progressive multiple sclerosis.

ENG triggered NMES, ES or TENS for stroke rehabilitation: what are the differences? [Web page] Accessed March 21, 2012.

Reese D, Shivapour ET, Wahls TL, Dudley-Javoroski SD, Shields R. Neuromuscular electrical stimulation and dietary interventions to reduce oxidative stress in a secondary progressive multiple sclerosis patient leads to marked gains in function: a case report. Cases J. 2009; 2;7601. Available from Accessed March 21, 2012. Bad link.
Editor note:

Wahls TL. Diet to support mitochondria [online video]. Available at Accessed March 22, 2012.

The seventy percent solution. J Gen Intern Med. January 21, 2011 [online article]. Available at Accessed March 21, 2012.

Wahls TL, Reese D, Kaplan D, Darling WG. Rehabilitation with neuromuscular electrical stimulation leads to functional gains in ambulation in patients with secondary progressive and primary progress multiple sclerosis: a case series report [abstract]. J Altern Complement Med. December 2010; 16(12):1343–1349. Available at Accessed April 5, 2012.


Jule Klotter


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