naturopathydigest.com -- Critical Research

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Critical Research

Critical Research is a regular feature in Naturopathy Digest. Each month, we provide abstracts from studies published in the top peer-reviewed journals; each abstract includes the complete citation and an online link to the journal. Whenever possible, this link directs you to a page where you can order the full text of the study, if desired.

This Month's Featured Abstract

Metabolic syndrome compared with type 2 diabetes mellitus as a risk factor for stroke: The Framingham Offspring Study.

Robert M. Najarian, MD; Lisa M. Sullivan, PhD; William B. Kannel, MD; et al.

Background: Metabolic syndrome (MetS) has been recognized as a prediabetic constellation of symptoms and an independent risk factor for cardiovascular disease.
Methods: To evaluate the age-adjusted risk of stroke and population-attributable risk associated with MetS and compare with those of overt type 2 diabetes mellitus (hereinafter, "diabetes"), we determined the prevalence of MetS alone, diabetes alone, and both in 2,097 subjects in the Framingham Offspring Study, ages 50 to 81 years and free of stroke. Age-adjusted risk ratios, 10-year incidence, and population-attributable risks of stroke were estimated for men and women with MetS alone, diabetes alone, and both.
Results: Criteria for MetS were met in 30.3% of men and 24.7% of women. Twenty-four percent of men had MetS alone; 7% had diabetes alone; and 6% had both. Twenty percent of women had MetS alone; 3% had diabetes alone; and 5% had both. Over 14 years of follow-up, 75 men and 55 women developed a first stroke; all but four events were ischemic. Relative risk (RR) of stroke in persons with both diabetes and MetS (RR, 3.28; confidence interval [CI], 1.82-5.92) was higher than that for either condition alone (MetS alone: RR, 2.10; CI, 1.37-3.22; diabetes alone: RR, 2.47; CI, 1.31-4.65). The population-attributable risk, owing to its greater prevalence, was greater for MetS alone than for diabetes alone (19% vs. 7%), particularly in women (27% vs. 5%).
Conclusions: Metabolic syndrome is more prevalent than diabetes and is a significant independent risk factor for stroke in people without diabetes. Prevention and control of MetS and its components are likely to reduce stroke incidence.
Source: Archives of Internal Medicine 2006;166:106-111.

Melatonin improves bowel symptoms in female patients with irritable bowel syndrome: a double-blind placebo-controlled study.

Lu W.Z., Gwee K.A., Moochhalla S., Ho K.Y.

Background: Melatonin is involved in the regulation of gastrointestinal motility and sensation.
Aim: To determine the potential therapeutic effects of melatonin in irritable bowel syndrome (IBS).
Method: Seventeen female patients satisfying the Rome II criteria for IBS were randomized to receive either melatonin 3 mg nocte or identically appearing placebo 1 nocte for eight weeks, followed by a four-week washout period and placebo or melatonin in the reverse order for another eight weeks. Three validated questionnaires - the GI symptom, the sleep questionnaires and the Hospital Anxiety and Depression Scale - were used to assess symptom severity and to compute the IBS, sleep and anxiety/depression scores, respectively.
Results: Improvements in mean IBS scores were significantly greater after treatment with melatonin (3.9 2.6) than with placebo (1.3 4.0, P = 0.037). Percent response rate, defined as percentage of subjects achieving mild-to-excellent improvement in IBS symptoms, was also greater in the melatonin-treated arm (88% vs. 47%, P = 0.04). The changes in mean sleep, anxiety, and depression scores were similar with either melatonin or placebo treatment.
Conclusions: Melatonin is a promising therapeutic agent for IBS. Its therapeutic effect is independent of its effects on sleep, anxiety or depression.
Source: Alimentary Pharmacology & Therapeutics, November 2005;22(10):927.

Relation of body composition, fat mass, and serum lipids to osteoporotic fractures and bone mineral density in Chinese men and women.

Yi-Hsiang Hsu, Scott A. Venners, Henry A. Terwedow, et al.

Background: Higher fat mass may be an independent risk factor for osteoporosis and osteoporotic fractures.
Objective: We aimed to determine the independent contribution of fat mass to osteoporosis and to estimate the risk of osteoporotic fractures in relation to body weight, lean mass, and other confounders.
Design: This was a community-based, cross-sectional study of 7,137 men, 4,585 premenopausal women, and 2,248 postmenopausal women ages 25-64 years. Total-body and hip bone mineral content (BMC) and bone mineral density (BMD) and body composition were measured by dual-energy X-ray absorptiometry. Serum lipids were measured. Sex- and menopause-specific multiple generalized linear models were applied.
Results: Across 5-kg strata of body weight, fat mass was significantly inversely associated with BMC in the whole body and total hip. When we compared the highest quartile with the lowest quartile of percentage fat mass in men, premenopausal women, and postmenopausal women, the adjusted odds ratios (95% CIs) of osteoporosis defined by hip BMD were 5.2 (2.1, 13.2), 5.0 (1.7, 15.1), and 6.9 (4.3, 11.2), respectively. Significant linear trends existed for higher risks of osteoporosis, osteopenia, and nonspine fractures with higher percentage fat mass. Significant negative relations were found between whole-body BMC and cholesterol, triacylglycerol, LDL, and the ratio of HDL to LDL in all groups.
Conclusions: Risks of osteoporosis, osteopenia, and nonspine fractures were significantly higher for subjects with higher percentage body fat independent of body weight, physical activity, and age. Thus, fat mass has a negative effect on bone mass in contrast with the positive effect of weight-bearing itself.
Source: American Journal of Clinical Nutrition, January 2006;83(1):146-154.

Exercise and postprandial lipemia: effect of continuous compared with intermittent activity patterns.

Miyashita M., Burns S.F., Stensel D.J.

Background: Guidelines state that accumulated physical activity is beneficial for health, but a minimum duration of 10 minutes per activity bout is recommended. Limited information regarding the effects of short (<10 min.) bouts of activity on health is available, and no studies of the effects of such short bouts of activity on postprandial lipemia have been conducted.
Objective: The objective was to compare the effects of accumulating 10 three-minute bouts of exercise with those of one 30-minute bout of exercise on postprandial plasma triacylglycerol concentrations.
Design: Ten men ages 21-32 years completed three two-day trials 1 week apart in a randomized repeated-measures design. On day 1, the subjects rested (no exercise) or ran at 70% of maximum oxygen uptake in either 10 three-minute bouts (30 minutes rest between each) or one continuous 30-minute bout. On day 2, the subjects rested and consumed test meals (0.69 g fat, 0.95 g carbohydrate, 0.31 g protein, and 46 kJ/kg body mass) for breakfast and lunch. Venous blood samples were obtained in the fasted state and for seven hours postprandially on day 2.
Results: Postprandial plasma triacylglycerol concentrations were lower throughout day 2 of both the accumulation exercise trial and the continuous exercise trial than during the control trial (main effect of trial: P < 0.001, 2-factor analysis of variance).
Conclusions: Accumulating multiple short bouts of exercise throughout the day effectively reduce postprandial plasma triacylglycerol concentrations to an extent similar to that of a single 30-min session of exercise in healthy young men.
Source: American Journal of Clinical Nutrition, January 2006;83(1):24-29.

Specific probiotic therapy attenuates antibiotic-induced visceral hypersensitivity in mice.

Verdu EF, Bercik P, Verma-Gandhu M, et al.

Background and Aim: Abdominal pain and discomfort are common symptoms in functional disorders and are attributed to visceral hypersensitivity. These symptoms fluctuate over time, but the basis for this is unknown. Here, we examine the impact of changes in gut flora and gut inflammatory cell activity on visceral sensitivity.
Methods: Visceral sensitivity to colorectal distension (CRD) was assessed at intervals in healthy mice for up to 12 weeks, and in mice before and after administration of dexamethasone or non-absorbable antibiotics with or without supplementation with Lactobacillus paracasei (NCC2461). Tissue was obtained for measurement of myeloperoxidase activity (MPO), histology, microbiota analysis, and substance P (SP) immunolabelling.
Results: Visceral hypersensitivity developed over time in healthy mice maintained without sterile precautions. This was accompanied by a small increase in MPO activity. Dexamethasone treatment normalised MPO and CRD responses. Antibiotic treatment perturbed gut flora, increased MPO and SP immunoreactivity in the colon, and produced visceral hypersensitivity. Administration of Lactobacillus paracasei in spent culture medium normalised visceral sensitivity and SP immunolabelling, but not intestinal microbiota counts.
Conclusion: Perturbations in gut flora and in inflammatory cell activity alter sensory neurotransmitter content in the colon, and result in altered visceral perception. Changes in gut flora may be a basis for the variability of abdominal symptoms observed in functional gastrointestinal disorders and may be prevented by specific probiotic administration.
Source: Gut February 2006;55(2):182-90.

Etiology of Crohn's disease: do certain food additives cause intestinal inflammation by molecular mimicry of mycobacterial lipids?

F. Traunmüller

Crohn's disease is a chronic granulomatous inflammation of the gastrointestinal tract that was first described in the beginning of the 20^th century. The histological similarity with intestinal tuberculosis has led to the assumption of an involvement of mycobacteria and mycobacterial antigens, respectively, in the etiology. A major defense mechanism against mycobacterial lipid antigens is the CD1 system, which includes CD1 molecules for antigen presentation and natural killer T cells for recognition and subsequent production of cytokines like interferone-gamma and tumour necrosis factor-alpha. These cytokines promote granulomatous transformation.
Various food additives, especially emulsifiants, thickeners, surface-finishing agents and contaminants like plasticizers, share structural domains with mycobacterial lipids. It is therefore hypothesized that these compounds are able to stimulate by molecular mimicry the CD1 system in the gastrointestinal mucosa and to trigger the pro-inflammatory cytokine cascade. The understanding of Crohn's disease as a CD1-mediated delayed-type hypersensitivity to certain food additives would lead to strong emphasis on a dietary treatment. Related aspects of pathology, physiology and epidemiology of Crohn's disease are presented.
Source: Medical Hypotheses 2005;65(5):859-64.

Acidosis affects tumor cell survival through modulation of nitric oxide release.

Ljubica Harhaji, Dusan Popadic, Djordje Miljkovic, et al.

The influence of environmental pH on the production of tumoricidal free radical nitric oxide (NO) was investigated in mouse fibrosarcoma L929 and rat glioma C6 cell lines. A combination of IFN- and IL-1 induced a significant NO release and subsequent reduction of cell viability in tumor cell lines. Acidification of cell culture medium reduced tumor cell NO production in a pH-dependent manner. While the inhibitory effect of acidosis on NO production in C6 cells was associated with a further decrease in cell viability, it completely rescued L929 cells from NO-dependent apoptotic and necrotic death. Acidic pH diminished IFN-+ IL-1-induced expression of inducible NO synthase (iNOS) mRNA and protein, and abolished the activation of iNOS transcription factor IRF-1 in L929 cells. Moreover, extracellular acidosis significantly impaired cytokine-induced phosphorylation of MAP kinase p44/42 (ERK1/2) and subsequent expression of transcription factor c-Fos in L929 cells. Finally, mild acidosis (pH 6.8) augmented, while severe acidosis (pH 6.0) reduced, IFN--induced iNOS activation/NO release and NO-dependent anticancer activity of rat and mouse macrophages. Taken together, our findings indicate that modulation of macrophage and tumor cell iNOS by an acidic microenvironment might influence the progression of NO-sensitive solid tumors.
Source: Free Radical Biology and Medicine, Jan. 15, 2006;40(2):226-35.

Immune mechanisms of allergen-specific sublingual immuno-therapy.

P. Moingeon, T. Batard, R. Fadel, et al.

Sublingual immunotherapy has been shown in some clinical studies to modulate allergen-specific antibody responses (with a decrease in the immunoglobulin E/immunoglobulin G4 [IgE/IgG4] ratio) and to reduce the recruitment and activation of proinflammatory cells in target mucosa. Whereas a central paradigm for successful immunotherapy has been to reorient the pattern of allergen-specific T-cell responses in atopic patients from a T helper (Th)2 to Th1 profile, there is currently a growing interest in eliciting regulatory T cells, capable of downregulating both Th1 and Th2 responses through the production of interleukin (IL)-10 and/or transforming growth factor (TGF)-.
We discuss herein immune mechanisms involved during allergen-specific sublingual immunotherapy (SLIT), in comparison with subcutaneous immunotherapy. During SLIT, the allergen is captured within the oral mucosa by Langerhans-like dendritic cells expressing high-affinity IgE receptors, producing IL-10 and TGF-, and upregulating indoleamine dioxygenase (IDO), suggesting that such cells are prone to induce tolerance. The oral mucosa contains a limited number of proinflammatory cells, such as mast cells, thereby explaining the well-established safety profile of SLIT. In this context, second-generation vaccines based on recombinant allergens in a native conformation formulated with adjuvants are designed to target Langerhans-like cells in the sublingual mucosa, with the aim to induce allergen-specific regulatory T cells. Importantly, such recombinant vaccines should facilitate the identification of biological markers of SLIT efficacy in humans.
Source: Allergy: European Journal of Allergy and Clinical Immunology, February 2006;61(2):151.