Chris Oliver

Bovine lactoferrin supplementation supports immune and antioxidant status in healthy human males

Dietary supplements of bovine lactoferrin are purported in consumer literature to enhance and support the immune system response through their antioxidant, antibacterial, and antiviral properties. Our aim was to investigate more fully the potential immune modulating properties and antioxidant activity of an oral supplementation of bovine lactoferrin in humans. Using an intraindividual repeated measure design, 8 healthy males aged 30 to 55 years, self-administered daily for 21 days, one capsule of placebo for 7 days, followed by 100 mg of lactoferrin for 7 days, followed by 200 mg of lactoferrin for 7 days. Peripheral blood lymphocyte subset counts, T-cell activation, natural killer (NK) cell cytotoxicity, serum cytokine levels (tumor necrosis factor [TNF]-alpha, interferon [IFN]-gamma, interleukin [IL]-2, IL-4, IL-6, and IL-10), and serum hydrophilic, lipophilic, and total antioxidant capacity were repeatedly measured before and after each progressive supplementation. Statistically significant increases were found between presupplementation levels and levels after 200 mg of supplementation in total T-cell activation (as measure by CD3(+)) (P < .001), helper T-cell activation (as measure by CD4(+)) (P < .001), cytotoxic T-cell activation (as measured by CD8(+)) (P < .001), and hydrophilic antioxidant capacity (P < .05). No significant changes were seen in the other parameters measured. These results support the proposal that oral supplements of bovine lactoferrin may be a useful adjunct toward modulation of immune activity, in particular T-cell activation and antioxidant status.

The Neuropharmacology of L-Theanine(N-Ethyl-L-Glutamine)

L-theanine (N-ethyl-L-glutamine) or theanine is a major amino acid uniquely found in green tea. L-theanine has been historically reported as a relaxing agent, prompting scientific research on its pharmacology. Animal neurochemistry studies suggest that L-theanine increases brain serotonin, dopamine, GABA levels and has micromolar affinities for AMPA, Kainate and NMDA receptors. In addition has been shown to exert neuroprotective effects in animal models possibly through its antagonistic effects on group 1 metabotrophic glutamate receptors. Behavioural studies in animals suggest improvement in learning and memory. Overall, L-theanine displays a neuropharmacology suggestive of a possible neuroprotective and cognitive enhancing agent and warrants further investigation in animals and humans.

Dietary intake of antioxidant supplements modulate antioxidant status and heat shock protein 70 synthesis

Abstract The physiological effects and efficacy of dietary intake of antioxidant supplements in humans remains controversial. Experiments involving dietary, often high, intake of a single antioxidant or vitamin may be seriously flawed given the interactive nature of antioxidants in vivo. The present studies were conducted on individuals (35-60 years of age) taking a commercial antioxidant mixture in a double-blind, placebo-controlled, cross-over study. Intake was two capsules per day, for 4 weeks, with a 4-week washout period in between active dose or placebo. Intake of antioxidants was associated with little change in superoxide dismutase activity, but an increase in glutathione peroxidase was noted. Haemolysis of red blood cells (erythrocytes) induced by the free radical generator AAPH was significantly reduced in individuals on antioxidant supplements. In lymphocytes isolated from individuals taking supplements, there was a marked increase, as compared with individuals on placebo, in the synthesis of heat shock protein 70 (hsp70) following heat shock from 37°C to 42.5°C. We conclude that dietary intake of a mixed antioxidant supplement leads to modulation of cellular redox status resulting in decreased oxidative stress and increased ability of lymphocytes to mount a stress response.

Comment on “Effects of different omega-3 sources, fish oil, krill oil, and green-lipped mussel against cytokine-mediated canine cartilage degradation” In Vitro Cell Dev Biol Anim. 2017 doi: 10.1007/s11626-016-0125-y.

Dear Editor, We read with interest a recent paper by Buddhachat et al. (Buddhachat et al., 2017) who evaluated three marine lipid sources (fish oil, krill oil and green-lipped mussel oil) in an in vitro cartilage degradation model and who then concluded with a clinical recommendation as to the relative efficacy of these lipid substances. Putting aside whether the model used in this paper is appropriate in terms of the substances tested, a basic error was made in the comparison of samples. The proprietary green-lipped mussel oil (GLM) used in this experiment was sampled from a commercially available capsule (Antinol®) which is a mixture of the pure supercritical fluid extracted mussel oil and olive oil carrier used to assist encapsulation. The capsules tested contained 50 mg of GLM oil and 100 mg of olive oil carrier and 0.025 mg alphatocopherol (vitamin E). By the protocol used in sampling these capsules, the GLM oil was diluted, against EPA and DHA, by a factor of three, and the 250, 500, 1000 μg/mL samples used were actually 83, 167, 333 μg/mL of equivalent GLM oil. As the samples contained twice as much olive oil to GLM oil, it makes sense that these in vitro results could equally be attributed to olive oil. Due to this unfortunate error, the results and conclusions the authors have reached are not valid. It is important to note that there are in vivo canine trials which demonstrate the clinical effectiveness of Antinol in osteoarthritis (Kwananocha et al., 2016; Mongkon & Soontornvipart, 2012; Soontornvipart et al., 2015). Further work attempting to elucidate mechanisms of action and the effects of Antinol on cartilage degradation are warranted.

Response to “Acute Hepatitis Induced by Lyprinol, the Lipid Extract of the Green-Lipped Mussel (Perna canaliculus), in a Patient with Polyarthrosis”

The title of the case report “Acute hepatitis induced by lyprinol, the lipid extract of the green-lipped mussel (Perna canaliculus), in a patient with polyarthrosis” [1] asserts a definitive causal relationship between Lyprinol and acute hepatitis. We are concerned that the report itself does not provide evidence that supports a definitive or highly probable association. As no rechallenge was undertaken definitive causality is impossible to prove.

Not being able to see the muscle for the fat.

At its simplest, we can express body weight or body composition as comprising of adipose tissue, muscle tissue and skeletal tissue. Body weight and body mass index (BMI) of populations of all ages have been increasing for close to half a century, leading to the present obesity epidemic. The causal pathways linking excessive body fat to serious chronic diseases, including diabetes and heart diseases is now well established. A recent editorial citing body composition data from Li et al. [1] asked the question “Are Normal-Weight Americans Over-Fat?” [2]. This interpretation of the data from Li et al. reinforces an adipocentric view giving adipose tissue primacy; perhaps there is a different view, a sarcocentric view that proposes that people are perhaps becoming under-muscled rather than just over-fat. Data from Canada [3] and Germany [4] indicate that children and adults are getting fatter at the same body weight or BMI. If we are fatter at the same body weight and BMI then the other two tissues, muscle and or bone must be diminishing. Given that this increased body fatness at the same weight is most likely a proxy for decreased physical activity, it is a good bet that muscle is the tissue that has diminished most. The loss of muscle is of great physiological importance as proper-functioning muscle is responsible for most glucose disposal and required to stave off insulin resistance [5, 6]. Proper functioning muscle has been highlighted as important for longevity even after accounting for respiratory fitness and BMI [7]. Therefore it is important to remind those with an adipocentric perspective that a low body fat in itself is not necessarily healthy if it coexists with poor-quality muscle and bone. This is important given various body composition states such as metabolically normal obese individuals [8] and thin persons with significant ectopic fat [9]. We may have better health outcomes if we focus more on the causes and sequelae of body dyscomposition, especially the diminution of muscle mass and function even in the young, rather than assuming the problems of body composition in the general population largely lie in terms of adiposity. The retention and maintenance of muscle and muscle function is coming under increasing scrutiny in our ageing society because of the looming epidemic of sarcopenia and the financial and social impact that this will have. However, the discussion around the diagnosis and prevalence on sarcopenia is centred on the target clinical population, i.e., the elderly [10]. Nevertheless, the data cited above from the USA, Canada and Germany studies highlight that on current form, a number of our children may not meet their genetic potential of muscle mass and by inference muscle function. The medium-term consequences of this muscle shortfall as a risk factor for type 2 diabetes alone is of concern; the longer-term consequences of any muscle shortfall to sarcopenia prevalence and its possible inception at a younger age should be of even greater concern. Those concerned with sarcopenia, including this journal, perhaps need also to focus more on prevention even starting with childhood.