Letter from the Publisher

Why Shouldn’t We Use LDN for All Neurological Conditions?

The medical profession cringes whenever a treatment is touted as a panacea, a cure-all. Such remedies are generally little more than snake oil offered by hucksters to a vulnerable and suffering population. Still most medications not only have limited benefit but usually are accompanied by minor and major adverse effects including, not infrequently, death. There is something to be said about a drug that has a broad range of symptomatic benefit with very few side effects none of which are lethal. That Rx is naltrexone and the dosing of the pharmaceutical is low dose, hence low dose naltrexone (LDN). For a few individuals it may even be ultra-low dose naltrexone. Wouldn’t that be a boon for medicine to have a medication that not only relieves symptoms, especially pain, and poses no ill effects? It is time that neurologists and physicians as a whole take LDN seriously and prescribe it not as a last resort, but as a first resort.

Linda Elsegood is one individual who has greatly benefitted from LDN when no other medication provided any relief at all. She developed the full range of symptoms characteristic of multiple sclerosis as a 40+ year old mother and wife. Her life was entirely hampered by physically disabling symptoms and cognitive impairment. She needed assistance with nearly all her day-to-day tasks including clothing herself, going to the bathroom, and eating. Too weak to stand she became confined to a wheelchair—she barely made it through her daughter’s wedding celebration. Medications for MS were limited in the late 1990s, and they offered very little to reverse her course. Pain medication lived up to its reputation and simply made her dopey. By chance she read of a promising treatment in the US that individuals were posting on some blogs. That treatment was LDN; and after much consultation and cajoling of her physicians in the British National Health Service, she succeeded in arranging a prescription for it. Within three weeks there was a major change in her symptoms; within two years the wheelchair was gone. Linda is now the chairperson of the LDN Research Trust and very actively providing patient and physician education about LDN internationally. Her MS has remained in remission now for more than 13 years!

Peripheral neuropathy is a debilitating and painful condition for most individuals. Despite the best efforts of individuals who have diabetes, neuropathy frequently complicates their condition. A patient who has type 2 diabetes had been opting to manage her condition without the use of medication. Unfortunately, her glucose control was sub-optimal with an elevated hemoglobin-a1c. She noted that her most difficult symptom had been insomnia caused by intractable foot pain. She agreed to abide by a much more restrictive, low-carbohydrate diet. Additionally, she was agreeable to using a substantial nutraceutical regimen both morning and night, intended to help control her glucose levels. She also elected to have i.v. chelation treatment as she did have a low-grade burden of toxic elements, including lead and mercury. As time proceeded, she did experience improvement in her diabetic control, hypertension, weight management, and general state of well-being. She was able to exercise with more vigor. However, her feet pain persisted despite several administration of herbals and homeopathics to abate the discomfort. Eventually she agreed to try LDN at a very low dose.

Within weeks there was a marked reduction in her discomfort and improvement in her insomnia. Dosing of the LDN was increased from once to three times daily. She experienced further pain reduction and less interrupted sleep.

LDN has not only been helpful in MS and peripheral neuropathy but in other neurologic conditions as well. For those who would like a primer on the topic read The LDN Book edited by Elsegood and published by Chelsea Green Publishing. Additional reading material and videos are available on the website, ldnresearchtrust.org.

How Safe is that Avobenzone You Are Absorbing with the Sunscreen Spray?

The short answer is no one knows. According to Jo McGinty’s August 3rd Wall Street Journal column (“The Numbers”). we do know, based on a study published in JAMA in May, that four commercial brands caused volunteers’ blood levels of avobenzone to exceed “acceptable limits” after just one day of application. That limit is 0.5 nanograms per ml of the ingredient. In the products under study, which all listed the concentration of avobenzone to be 3%, the measured blood levels were 4.0 ng/ml for the spray, 4.3 ng/ml for the lotion, and 1.8 ng/ml for the cream. Similarly, other sunscreen chemicals were determined to yield high blood levels after one day use. Oxybenzone demonstrated far higher blood levels measuring 200 ng/ml for the spray and 169 ng/ml for the lotion. Octocrylene had average levels of 5 ng/ml for the spray, 5.7 ng/ml for the lotion, and 5.7 ng/ml for the cream.

Now that we know that we absorb these chemicals quite nicely by spraying or slathering ourselves with these products, one needs to know what effect these chemicals are having on us. The industry would have us believe that they are inert but we know better. Anne Marie Fine, MD, wrote about the skin’s role as an underappreciated route of entry for toxicants in the June 2019 issue of the Townsend Letter. Fine broadly considered how absorbed chemicals act as endocrine disruptors, neurotoxins, and carcinogens. Additionally, the chemicals might cause birth defects—think of all the pregnant women basking in the sun after carefully applying sunscreen. Any possibility that the avobenzone might be impacting the fetus?

Well the FDA wants to find out and find out this year. A rule set to go into effect this November is ordering manufacturers of all these sunscreen products to do the testing for each of the major chemicals. There are 16 of them; zinc and titanium oxide are deemed safe while PABA and trolamine salicylate are not. As you might imagine the industry is fighting back, seeking to avoid testing of their chemicals. This is a $2 billion industry so one can imagine the lawyers will be offering all sorts of reasons not to test.

Much as I don’t like to concur with FDA policy making—the draconian restrictions it is imposing on compounding hormones and injectables are awful—this is one time when mandated testing for safety makes sense.

Fluoride and Brain Decay—No Problem as Long as We Prevent Cavities

Although I approve of the FDA investigating avobenzone in sunscreen lotions I am not a fan of their ignorance or, would that be, denial of fluoride’s toxicity. Ever since the dental profession joined forces with the aluminum industry who needed a good way to dispose of fluoride industrial waste, fluoride has become the central means to preventing cavities. We are encouraging young parents to use fluoride toothpaste on toddlers. Much worse, however, has been the widespread fluoridation of community water systems. Strangely enough, despite the herculean efforts and sanctimonious testimony of public health officials, nearly half the municipalities in the US have not signed on for water fluoridation. Of course, the need to fluoridate remains a mandate for these good doers—many non-fluoridating cities are besieged every five years or so by a full-tilt propaganda campaign to get on board with the fluoridators and stop threatening the dental health of children. Nevertheless, the large number of towns that don’t fluoridate makes for an interesting comparison with those that do. And the difference is not only surprising but makes for a compelling argument to not fluoridate.

Researcher and citizen advocate, John MacArthur, who has written several times before about the mischief caused by fluoride in the Townsend Letter, writes in this issue about the devilry achieved by fluoride on the brain and its cellular functioning. The dental profession treats fluoride very cavalierly as though it is a knight in armor despite the fact that excessive fluoride application results in dental fluorosis. Chemically one of the harshest agents on the lab bench is hydrofluoric acid, which is capable of reacting with ordinary glassware. In the operating room the administration of a particular anesthetic, sevoflurane, is capable of rendering a patient delirious post-surgically. One of the most abrasive chemotherapy agents is 5-fluorauracil. You get the idea—fluoride transforms a compound that has a certain level of toxicity and amplifies that toxicity many-fold.

MacArthur examines the evidence of how the fluoride that we absorb from our toothpaste and, without consent, from our drinking water insults our brain cells and the blood brain barrier and the synaptic proteins that enable neuron communication. When you compare states that have the largest number of fluoridating cities to those that have the least, there is more neurological disease in the states that are heavy fluoridators. This includes that great scourge befuddling researchers and doctors, Alzheimer’s disease. Shouldn’t that be a reason to give the fluoridating stalwarts pause? Maybe a reason for the FDA to investigate? Yes, avobenzone may be harsh, but what about fluoride? And if Alzheimer’s isn’t your thing, MacArthur’s examination of the statistics shows a similar picture of increased death from hypertension, stroke, and kidney disease in states that push fluoridation versus those that don’t.

We have tests available that assess mercury and lead, pesticide and solvent, and mycotoxin levels. We need some tool capable of determining fluoride toxicity. Of course, that might be heckled by the dental profession.

We Don’t Have a Treatment for Alzheimer’s But We Might Have One to Prevent It

One of the most frustrating aspects of treating a patient with Alzheimer’s disease is the paucity of treatment options. The pharmaceutical world offers several drugs, none of which leads to good control of the condition much less reversal. The progressive deterioration of dementia is heart breaking for the patient and the family; it is so painful to experience a person’s vitality and competency break down especially with the memory of someone so full of life and creativity. While researchers seek some remedy that may stop the B-amyloid deposition and the tau protein neurofibrillary tangles, we do have a remedy, a natural one at that, very likely to slow if not prevent the development of Alzheimer’s. This is not new experimental work—but it is work that has been largely ignored by public health authorities despite its low cost and dearth of adverse effects.

James Greenblatt, MD, has a special interest in integrative medicine, especially in how it applies to managing psychiatric disorders. Greenblatt has written frequently about depression, anxiety, suicide prevention, attention deficit disorders, and optimizing brain health in this publication as well as in other journals and books. His most recent text is titled Integrative Medicine for Alzheimer’s. His research reveals extensive evidence that individuals with higher nutritional intake of a “non-essential” nutrient have a far lower incidence of Alzheimer’s than those with a lower intake of that nutrient. The need for it is not related to genetic errors of metabolism—it is simply those getting more of it have less Alzheimer’s, those with less have more. If the evidence confirms that there is a reduction in Alzheimer’s with intake of this nutrient, shouldn’t it be a mandatory part of our dietary enrichment, just like fortifying white bread with thiamine and salt with iodine? I would think so, but you make up your own mind after reading this issue’s article by Greenblatt.

Cover Story: Assessing Non-Genetic Factors Leading to Alzheimer’s Disease

Families with a high number of relatives having Alzheimer’s disease at an early age clearly have a genetic basis for the disorder. Genomic testing has determined that certain mutations appear to increase the risk for developing Alzheimer’s. However, the ever-increasing number of individuals succumbing to dementia in the elderly population suggests that genetics cannot be the key cause. Greenblatt’s discussion of a nutrient deficiency may represent a major public health breakthrough in Alzheimer’s prevention. The question remains, however, as to how one can assess the risk for developing Alzheimer’s and would such information be useful in its prevention or at least in slowing its development.

Aristo Vojdani, PhD, director of Immunosciences Lab, would argue “yes” on both points. He would make the case that testing would be very useful in appraising one’s risk for developing Alzheimer’s and that such abnormalities would not depend on the disease imminently becoming symptomatic. Instead, immunologic abnormalities would be evident years, if not decades, before memory loss is prominent. It has long been acknowledged that there has been an association between aluminum and Alzheimer’s. Yet the evidence remains weak that the two are directly tied together. Vojdani’s work asserts that it is not the mere presence of aluminum that is the issue. Instead, it is the immune system’s recognition of aluminum binding to tissue proteins, leading to antibody formation against the aluminum-tissue protein complex. Such antibodies cross react with amyloid precursor protein, a signaling peptide capable of producing fibril formations that result in amyloid plaque formation. Vojdani’s article in this issue provides a detailed discussion of how not just metals, like aluminum, and chemicals, like phthalate, but also microbial infections are all capable of creating bound-tissue complexes, leading to immune system recognition and production of antibodies against these metal-tissue complexes or pathogen-tissue complexes. It is the cross reactivity of these antibodies with amyloid-beta peptide that leads to amyloid plaque deposition as well as tau neurofibrillary deformation. Testing to determine the presence of such antibodies offers important clues as to whether neurodegenerative changes are occurring and to what degree. Moreover, beyond chemical and microbial risk factors, foods form tissue-bound complexes also leading to antibody formation cross reacting with brain tissue. Not surprisingly, gluten is frequently found to have very high antibody formation.

Vojdani’s treatise makes a compelling argument for the immunoreactivity of a variety of environmental toxins, pathogens, and food proteins contributing to the early development of dementia. The fact that these antibody abnormalities can be screened decades before cognitive impairment offers an important tool not just for risk assessment but also prevention.

Jonathan Collin, MD