A recent study showed that osteoarthritis may boost the risk of heart disease. Interestingly, other recent articles, seemingly unrelated and likely ignored, provide a clue: Colchicine, not allopurinol, cuts the risk of heart attacks in half, and Ayurdevic treatment of gut problems alleviates migraines. What is going on? The researchers linking arthritis and heart disease hypothesized that inflammation may be the common denominator, but they were not sure.
If you have been reading this newsletter for a while you know the answer. It is the subject of the cover issue of the June 2012 J. Scientific American: bacteria in our body, most of which are in the GI tract, outnumber our body’s cells 10:1. Their genetic material outnumbers ours by 150:1. So, who is in control? This article is quoted below. It is likely to become a watershed study.
Treat your friendly bacteria well and they will work for you. They are the reason we get inflammation problems because they are 2/3 of your immune system. They start in the gut and spill over to every organ of the body, including our joints, and our heart. Yes, you have heard it before; but, when it makes it to the cover issue of Scientific American you have a right to demand that your Health Care provider helps you along these lines.
P.S. The herb Butterbur, an anti inflammatory, is now “level A” treatment for migraines.
Hugo Rodier, MD
“How Bacteria in Our Bodies Protect Our Health: Researchers who study the friendly bacteria that live inside all of us are starting to sort out who is in charge-microbes or people?” J. Scientific American June 2012, p7
- “Bacterial cells in the body outnumber human cells by a factor of 10 to 1. Yet only recently have researchers begun to elucidate the beneficial roles these microbes play in fostering health.
- “Some of these bacteria possess genes that encode for beneficial compounds that the body cannot make on its own. Other bacteria seem to train the body not to overreact to outside threats.
- “Advances in computing and gene sequencing are allowing investigators to create a detailed catalogue of all the bacterial genes that make up this so-called microbiome.
- “Unfortunately, the inadvertent destruction of beneficial microbes by the use of antibiotics, among other things, may be leading to an increase in autoimmune disorders and obesity.
“Biologists once thought that human beings were physiological islands, entirely capable of regulating their own internal workings. Our bodies made all the enzymes needed for breaking down food and using its nutrients to power and repair our tissues and organs. Signals from our own tissues dictated body states such as hunger or satiety. The specialized cells of our immune system taught themselves how to recognize and attack dangerous microbes-pathogens-while at the same time sparing our own tissues.
“Over the past 10 years or so, however, researchers have demonstrated that the human body is not such a neatly self-sufficient island after all. It is more like a complex ecosystem-a social network-containing trillions of bacteria and other microorganisms that inhabit our skin, genital areas, mouth and especially intestines. In fact, most of the cells in the human body are not human at all. Bacterial cells in the human body outnumber human cells 10 to one. Moreover, this mixed community of microbial cells and the genes they contain, collectively known as the microbiome, does not threaten us but offers vital help with basic physiological processes-from digestion to growth to self-defense.”
Shedding More Light on the Immune System
I am stepping out of the way on this one; just read the following quote:
Early studies on vitamin D showed promise that various forms of the “vitamin” may be protective against chronic disease. A number of studies have suggested that patients with autoimmune diagnoses are deficient in 25-hydroxyvitamin D (25-D) and that consuming greater quantities of vitamin D, which further elevates 25 D levels, alleviates autoimmune disease symptoms. Some years ago, molecular biology identified 25 D as a secosteroid. Secosteroids would typically be expected to depress inflammation, which is in line with the reports of symptomatic improvement. The simplistic first-order mass-action model used to guide the early vitamin studies is now giving way to a more complex description of action. When active, the Vitamin D nuclear receptor (VDR) affects transcription of at least 913 genes and impacts processes ranging from calcium metabolism to expression of key antimicrobial peptides. Additionally, recent research on theHuman Microbiome shows that bacteria are far more pervasive than previously thought, increasing the possibility that autoimmune disease is bacterial in origin. Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D’s ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.
Translation: vitamin D, a pro-hormone, improves the health of the gut flora, which IS your immune system. This is why vitamin D lowers the risk of Multiple Sclerosis if you get your blood level around 75. Levels under 30 are associated with osteoarthritis. More proof:
“Associations of 25-Hydroxyvitamin D2 and D3 with Cardiovascular Risk Factors in Childhood,”
“Vitamin D Levels Predict All-Cause and Cardiovascular Disease Mortality in Subjects With the Metabolic Syndrome,”
“Vitamin D-Related Genetic Variation and Risk of Lethal Prostate Cancer.”
Some Don’t Like it Hot
Menopausal hot flashes are believed to be due to a change in sex hormones levels. While there is some truth to this, it ignores the fact that healthy women (2%) have no problems while undergoing “the change.” Why? They have less inflammation and oxidation at the cellular level because they eat a lot of plant-based foods and stay away from processed garbage, especially sugars. They also exercise and handle stress better. The article “Increased Vascular Inflammation in Early Menopausal Women Is Associated with Hot Flush Severity” proves the point. So, think of changing hormone levels as exacerbating the underlying arterial inflammation.
While treatment with synthetic or bioidentical hormones, and supplementation with curcumin, omega oils,(olive oil,) vitex agnus, black cohosh, soy isoflavones, B complex, tryptophan and DHEA are helpful, it is always best to eliminate the source of the inflammation: processed foods. Also, you may want to eliminate toxins like Benzophenones in sunscreen; they have been linked to hormonal problems like endometriosis. I find cruciferous veggies particularly helpful in eliminating them from the body; they are high in Indole-3-Carbinol (supplement) and sulpharanes (MSMS sufur.)
BTW, a study showed that pelvic floor exercises are better than drugs for urinary incontinency and, of course, have fewer side effects.
The same inflammation behind hot flashes may affect our brain, causing problems like Alzheimer’s disease. An early warning that your brain may be on fire is a loss of smell. Can you imagine growing demented and not being able to tell you are passing gas? Speaking of gas, remember that this newsletter has repeatedly documented that excessive gas correlates with an overgrowth of noxious organisms in the gut that may be responsible for the inflammation that ends up not only in the brain, but all over our body.
In addition to keeping your brain agile, eating well and supplements to lower inflammation like omega oils, CoQ10, Sage, Huperzine A, consider eating a lot of berries; they have been linked to a delay in cognitive decline. The common denominator to all the above may well be the optimizing of glutathione levels. As reported previously, this “master” antioxidant is vital for optimal function in any organ. Suboptimal levels of glutathione induce “neurotoxicity,” which has been observed in neurodegenerative diseases. See previous newsletters for a list of nutritional glutathione precursors.
 “Osteoarthritis may boost heart risk, but why,” J. Family Practice News May 1st 2012 p1
 J. Family Practice News April 15th 2012 p26. Colchicine is an anti-inflammatory; allopurinol is not
 “Ayurvedic Medicine, a Complementary approach to Headache Care,” J. Neurology Reviews May 2012 p17 & “GERD Prevalence in Migraine Patients and the Implication for Acute Migraine Treatment,” J. Headache Pain 2009;10:35
 “Has the Microbiota Played a Critical Role in the Evolution of the Immune System?” J. Science 2010;330:1768
 “The Gut-Joint Axis,: J. Gut 2006;55:1240
 “Cardiovascular Disease: the diet-microbe morbid union,” J. Nature 2011;472:40
 “Vitamin D: the alternative hypothesis,” J. Autoimmunity Reviews 2009;8:639
 J. Neurology News, April 2012, p10
 J. Family Practice News April 15th 2012 p24
 J. Clinical Endocrinology Metabolism 2012;97:1563
 J. Diabetes Care May 2012;35:1158
 Journal Metabolism Clinical and Experimental 2012;61:661
 J. National Cancer Institute 2012;104:690
 J. Clinical Endocrinology Metabolism 2012;97:E760
 “Protection of LDL from oxidation by olive oil polyphenols is associated with a downregulation of CD40-ligand expression and its downstream products in vivo in humans,” Am J Clin Nutr 2012;95:1238
 J. Environmental Science and Technology May 2012
 JAMA 2012;307:2016
 “Inflammatory markers and neuropsychological functioning: the Framingham Heart Study,” J. Neuroepidemiology 2011;37(1):21
 “Disruption of odour quality coding in piriform cortex mediates olfactory deficits in Alzheimer’s disease,” J. Brain 2012;133(9):2714
 “Gut Reaction: environmental effects on the human microbiota,” J. Environmental Health Perspectives 2009 volume 117, Number 5 & “The Gut’s Clostridium Cocktail,” J. Science 21 January 2011: 289
 “Systemic inflammation and disease progression in Alzheimer disease,” J. Neurology 2009;73(10):768
 J. Annals of Neurology, April 25th 2012
 “Depletion of GSH in glial cells induces neurotoxicity: relevance to aging and degenerative neurological diseases,” FASEB J. 2010 24: 2533 & “A glutathione deficit alters dopamine modulation of L-type calcium channels via D2 and ryanodine receptors in neurons,” J. Free Radic Biol Med 2008;44(6):1042