November 5, 2001 Research Update

James Bogash, D.C. Mesa, AZ
info@lifecarechiro.com
www.lifecarechiro.com

Short-Chain Fatty Acids Induce Intestinal Epithelial Heat Shock Protein

I know this is one of those long, complicated titles, but the take home message here is clear. SCFAs definately protect the lining of the GI tract (this is a rat study but there have been many such studies in humans). To get SCFAs, we need a combination of both healthy bacterial flora and soluble fiber. Gastroenterology -- Abstracts: REN et al. 121 (3): 631 http://www.gastrojournal.org/cgi/content/abstract/121/3/631

GI Cancer After Cholecystectomy: Is Bile Involved in Carcinogenesis?

Considering the large number of patients who come through my office lacking their gall bladders, this article has some serious implications. Remember that the gallbladder is designed to collect bile as it is made by the liver and then release it in response to a fatty meal to help absorb the digested fat. Without a gallbladder (which mainstream medicine sometimes appears to consider as a vestigial organ...) the bile leaks into the GI tract as it is produce by the liver--this will occur at times when nothing is present in the GI tract for the bile acids to emulsify. It appears that these bile acids doing nothing increase the risk of not only intestinal cancer, but also esophageal cancer. This study is incredibly large and therefore the results are more likely to hold true for everyone. Gastroenterology -- Abstracts: LAGERGREN et al. 121 (3): 542 http://www.gastrojournal.org/cgi/content/abstract/121/3/542

Acute GI permeability responses to different NSAIDs

This is one of those topics regarding NSAIDs that has such a potentially harmful impact on our systemic health and yet is never address and few patients are aware of it. Note that the dosages used in this study were not large and changes were seen within two days. Worst in this class was naproxen (aka Alieve...) which also affected gastric permeability. Maintaining intestinal permeability is so important to keeping the immune response to things we eat to a mininum. With increased intestinal permeability ("leaky gut syndrome") the immune system is very likely to react and overreact to food antigens; this abnormal response sets the tone for immune upregulation and autoimmune responses. All this from two days of anti-inflammatories. Do they seem so harmless now? Gut -- Abstracts: Smecuol et al. 49 (5): 650 http://gut.bmjjournals.com/cgi/content/abstract/49/5/650

Animal Products and Risk of Esophageal and Gastric Cancer

This is another of those "How much did we spend on this?" studies. How many more studies do we need to show that a more plant based diet is protective and animal based diet is harmful? This study does note that nitrate intake (very common in processed foods and lunchmeats...) increases risk of gastric cancer. How do you think Dr. Atkin's weighs in on this one? CEBP -- Abstracts: Mayne et al. 10 (10): 1055 < ahref="http://cebp.aacrjournals.org/cgi/content/abstract/10/10/1055" class="roll" target="_blank">http://cebp.aacrjournals.org/cgi/content/abstract/10/10/1055

HRT and Heart Disease

Here's another study not able to find a benefit of HRT on heart disease indices. Any women desiring to take HRT needs to fully evaluate what diseases she hopes to altered the path to. If lowering risk of heart disease is the reason then there are 20 other things this woman can do to lower her risk that are very clear cut, do not potentially increase risk of other diseases and are less controversial (and much cheaper!!). Besides, just ask that mare that's been confined most of her life while she is maintained in a state of almost constant pregnancy which methods she would prefer... Synergy : Clinical Endocrinology 55 (5), 673-682 http://www.blackwell-synergy.com/Journals/content/abstracts/cen/2001/55/5/abstract_cen1382.asp?journal=cen&issueid=7461&artid=136269&cid=cen.2001.11&ftype=abstracts

Glutathione rescues homocystine-induced endothelial dysfunction

This is a perfect example of why a natural approach can be so effective. Any natural approach to cardiovascular disease is going to take homocyteine into account an ensure adequate intake of folic acid, Vit B6 and Vit B12. In addition, antioxidant therapy to include high intakes of Vit C and fresh fruits and veggies would also be a part of this plan. This study suggests that, in the presence of high levels of homocysteine, high levels of glutathione peroxidase (an exzyme that quenches free radicals) may counteract the damage that would otherwise have occurred. High levels of Vit C are known to regenerate glutathione levels. PNAS -- Abstracts: Weiss et al. 98 (22): 12503 http://www.pnas.org/cgi/content/abstract/98/22/12503

Esophageal Cancer Prevention in Zinc-Deficient Rats

Just happened to come across this one by accident. This article attributes abnormal cell proliferation and it's reversal to a deficiency of only one nutrient - zinc. Considering that the typical Western diet is very deficient in zinc, this raises some very interesting concerns, does it not?? J Natl Cancer Inst -- Abstracts: Fong et al. 93 (20): 1525 http://jnci.oupjournals.org/cgi/content/abstract/93/20/1525

Night Shift Work, Light at Night, and Risk of Breast Cancer

This article is included as an FYI. There are many people in today's society that believe that breast cancer has no controllable risk factors. Things like cruciferous vegetable intake, exercise, refined carb intake, whole grain intake and smoking are definate risk factors for breast cancer that are modifyable. J Natl Cancer Inst -- Abstracts: Davis et al. 93 (20): 1557 http://jnci.oupjournals.org/cgi/content/abstract/93/20/1557

Bone Markers Indicate Early Response to Osteoporosis Therapy

I believe that the authors of this study have been living in a cave for at least 5 or more years. The concept of using markers of bone breakdown found in the urine has been using by functional medicine practioners for many years now. In any of my osteroporosis presenations in the community, I always point out that checking only for bone mineral density is not only slow, it is incomplete. A patient needs to know how dense their bones are, but also how fast or slow that bone is being broken down. In addition, these markers can be used to determine if an osteoporosis program (note I said "program", not calcium supplementation...) is having a positive effect on bone turnover. It is a simple urine test that costs under $100.

23rd Annual Meeting of the American Society for Bone and Mineral Research New findings suggest that assessment of bone resorption markers during the first 3 to 6 months of osteoporosis treatment may be a useful alternative to the conventional method of evaluating therapeutic response, measurement of bone mineral density after 2 years. At the 23rd Annual Meeting of the American Society for Bone and Mineral Research, Dr. Richard Eastell of the University of Sheffield in the UK presented the results of a study that measured N-telopeptide and C-telopeptide of type I collagen in urine samples from 2442 women with postmenopausal osteoporosis who had sustained at least one vertebral fracture. All of the women had been treated with a calcium supplement (and vitamin D, if needed), and they had been randomized to risedronate 5 mg/day or placebo for 3 years. Decreases in bone turnover measured 3 to 6 months after the start of treatment accounted for approximately 50% of risedronate's 1-year effect against vertebral fractures and about 66% of the vertebral fracture risk reduction associated with the medication over 3 years, the researchers reported. The results also showed that the relationship between fracture risk and bone resorption rate was not linear and that reduction beyond 60% was associated with no additional decrease in fracture risk. As in prior trials, risedronate was shown to suppress bone resorption by a mean of 50% to 60%. "This is the first time that we can document a link between decreases in bone resorption markers and reductions in fracture risk," said Dr. Eastell . The findings suggest that measuring bone resorption markers may serve as a useful tool for evaluating response to osteoporosis therapy, he added. Besides the 1- to 2-year period of uncertainty, Dr. Eastell noted, the standard method of evaluating osteoporosis therapy is limited in that increases in bone mineral density are responsible for only about 20% of the fracture risk reduction seen with current therapies.