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Fish Oil and HMB Supplementation in COPD

Not Applicable
Completed
Conditions
Chronic Obstructive Pulmonary Disease
Interventions
Dietary Supplement: Capsule + Powder supplementation
Other: stable tracer infusion
Registration Number
NCT03796455
Lead Sponsor
Texas A&M University
Brief Summary

In the present study, the role of chronic (10 weeks) intake of low dose (2g/day) of EPA+DHA in whole body protein metabolism, and functional performance and systemic inflammation will be examined, and whether adding either HMB at 3.0 g/d to the low dose of EPA+DHA (2.0 g/d) will enhance these effects even more.

Detailed Description

Weight loss commonly occurs in patients with Chronic Obstructive Pulmonary Disease (COPD), negatively influencing their quality of life, treatment response and survival. Furthermore, limb muscle dysfunction (weakness and/or enhanced fatigue) is a major systemic comorbidity in patients with Chronic Obstructive Pulmonary Disease (COPD), negatively affecting their exercise performance, physical activity, quality of life, and mortality. As nutritional abnormalities are main contributors to muscle loss and dysfunction in COPD, nutritional support is viewed as an essential component of integrated care in these patients.

Although nutritional support is effective in the treatment of weight loss in COPD, attempts to increase muscle mass and function in COPD by supplying large amounts of protein or calories to these patients have been small. This suggests that gains in muscle mass and function are difficult to achieve in COPD unless specific metabolic abnormalities are targeted. The investigators and other researchers found that low muscle mass in COPD was strongly associated with elevated whole body protein turnover and increased myofibrillar protein breakdown rates indicative of muscle contractile protein loss. The investigators have extended this finding recently to normal weight COPD patients characterized by muscle weakness using a more precise and accurate pulse method of tau-methylhistidine tracer.

A substantial number of COPD patients, underweight as well as normal weight to obese, are characterized by an increased inflammatory response as evidenced by elevated levels of the pro-inflammatory cytokines (Tumor Necrosis Factor (TNF)-α, Interleukin (IL) 6 and 8, and the soluble TNF-α receptors (55 and 75). Furthermore, CRP levels are elevated in COPD and associated with reduced quadriceps strength, lower maximal and submaximal exercise capacity and increased morbidity.

One of the few agents capable to suppress the generation of pro-inflammatory cytokines are eicosapentanoic acid (EPA) and docosahexanoic acid (DHA), primary ω-3 fatty acids found in fish oils.

Previous experimental research and clinical studies in cachectic conditions (mostly malignancy) indicate that polyunsaturated fatty acids (PUFA) are able to attenuate protein degradation by improving the anabolic response to feeding and by decreasing the acute phase response. Eicosapentaenoic acid (EPA), in combination with docosahexaenoic acid (DHA), has been shown to effectively inhibit weight loss in several disease states, however weight weight and muscle mass and function increase was not present or minimal. Also in healthy older adults, fish oil can slow the decline in muscle mass and function. A randomized clinical trial in COPD patients showed that extra nutritional supplementation with PUFAs daily of 1000 mg EPA+DHA as adjunct to exercise training during 8 weeks enhanced exercise capacity but did not lead to muscle mass gain. The patients who did not respond adequately (\< 2% gain in weight), had a higher TNF-α level than those who did gain sufficient weight, which is in line with previous data in COPD showing an association between an increased systemic inflammation with non-response to nutritional therapy.

Although previous studies support the concept of EPA+DHA supplementation to ameliorate the systemic inflammatory response and decrease protein breakdown, there is no information present on the effects of EPA+DHA supplementation on whole body and muscle protein metabolism in COPD. The investigators have recently examined the dose-response effects of 0, 2 and 3.5 g of EPA+DHA intervention ( EPA / DHA) for 4 weeks in stable moderate to severe COPD patients (8pts /group) (unpublished data) but were not able to find a positive effect of muscle mass and strength, even with the highest dose, likely related to the relatively short (4 week) supplementation period. The effect of EPA+DHA intervention on whole body and muscle protein synthesis and breakdown rates is currently being analysed.

Although numerous animal studies have shown the benefit of HMB in downregulating muscle protein breakdown under catabolic conditions, there is very little data in COPD patients. Others have tested HMB (3g/d) in COPD patients in the ICU and reported anti-inflammatory benefits and improvement in pulmonary function. In patients with bronchiectasis, 24 week supplementation with an ONS containing HMB (1.5g/d) versus standard of care during pulmonary rehabilitation program, resulted in benefits on body composition, muscle strength and QoL. A combination of HMB and EPA/DHA in a mouse model of cancer cachexia showed a synergy between the two ingredients on preventing muscle loss and downregulation of muscle protein degradation.

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
54
Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
Fish Oilstable tracer infusion2.0 g EPA + DHA / day + placebo powder
PlaceboCapsule + Powder supplementation3 g/d soy oil: corn oil (50:50 ratio) + placebo powder
Placebostable tracer infusion3 g/d soy oil: corn oil (50:50 ratio) + placebo powder
Fish OilCapsule + Powder supplementation2.0 g EPA + DHA / day + placebo powder
Fish Oil and HMBCapsule + Powder supplementation2.0 g EPA + DHA + 3.0 g HMB / day
Fish Oil and HMBstable tracer infusion2.0 g EPA + DHA + 3.0 g HMB / day
Primary Outcome Measures
NameTimeMethod
Changes to net whole body protein metabolismbaseline and after 10-week supplementation

whole body protein synthesis and myofibrillar protein breakdown measured by labeled amino acids on each study day via blood drawn at time 4, 10, 15, 20, 30, 40, 60, 120, 180, 240 minutes of infusion

Secondary Outcome Measures
NameTimeMethod
respiratory muscle strength15 minutes on baseline visit, visit at week 5 of supplement intake, and after 10-week supplementation

Micro-respiratory pressure meter to measure maximum inspiratory and expiratory pressure

muscle mass15 minutes on baseline visit, visit at week 5 of supplement intake, and after 10-week supplementation

Body composition as measured by Dual-Energy X-ray Absorptiometry

limb muscle strength15 minutes on baseline visit, visit at week 5 of supplement intake, and after 10-week supplementation

kin-com 1-leg test

functional performance via six minute walk testbaseline visit, visit at week 5 of supplement intake, and after 10-week supplementation

walk a predetermined loop of 69.77 meters (228.89 feet) at self-selected pace for six minutes

resting energy expenditurebaseline visit and after 10-week supplementation

Oxygen consumption and carbon dioxide production will be calculated from the airflow in a transparent plastic (Plexiglas) hood to determine concentration differences between inhaled and exhaled air

systemic inflammatory markersbaseline visit and after 10-week supplementation

blood sample will be taken to measure c-reactive protein levels

Trial Locations

Locations (1)

Texas A&M University-CTRAL

🇺🇸

College Station, Texas, United States

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