Creatine Benefits for Non Athletes

Creatine is a naturally occurring amino acid that is found in meat and fish, and also made by the human body in the liver, kidneys, and pancreas. It is converted into creatine phosphate or phosphocreatine and stored in the muscles, where it is used for energy.

Creatine is primarily used by athletes to be able to train harder and longer! Few people though realize that creatine has other uses. Some of the other uses are:

Creatine for heart disease

A clinical study suggests that creatine supplements may help lower levels of triglycerides in men and women.

In few other clinical studies of people with heart failure, those who took creatine, in addition to standard medical care, were able to increase the amount of exercise they could do before becoming fatigued, compared to those who took placebo. Getting tired easily is one of the major symptoms of heart failure. One clinical study of 20 people with heart failure found that short-term creatine supplementation in addition to standard medication lead to an increase in body weight and an improvement of muscle strength.

Creatine has also been reported to help lower levels of homocysteine. Homocysteine is associated with heart disease, including heart attack and stroke.

Creatine for Chronic Obstructive Pulmonary Disease (COPD)

Chronic obstructive pulmonary disease (COPD) is one of the most common lung diseases. If you have COPD you have difficulty breathing. There are two main forms of COPD:

Chronic bronchitis, is a long-term cough with mucus

Emphysema, involves destruction of the lungs over time

Most people with COPD have a combination of both conditions.

In one double-blind study, people with COPD who took creatine increased muscle mass, muscle strength and endurance, and improved their health status compared with those who took placebo. They did not increase their exercise capacity. More studies are needed to see whether creatine has any benefit for people with COPD.

Creatine for Muscular dystrophy

The muscular dystrophies (MD) are a group of more than 30 genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles that control movement. Some forms of MD are seen in infancy or childhood, while others may not appear until middle age or later.

People who have muscular dystrophy may have less creatine in their muscle cells, which may contribute to muscle weakness. One study found that taking creatine led to a small improvement in muscle strength. However, other studies have found no effect.

Creatine for Parkinson’s disease

People with Parkinson’s disease have decreased muscular fitness including decreased muscle mass, muscle strength, and increased fatigue. A small clinical study found that giving creatine to people with Parkinson’s disease improved their exercise ability and endurance. In another clinical study, creatine supplements boosted participants’ moods and they didn’ t need to increase their medicine dose as much as those who didn’ t take creatine. More research is needed in this area.

Creatine has been used primarily since the mid 80s, so it is relatively new and that is part of the reason that many outside of the sport world are not familiar with creatine!

Chronic Obstructive Pulmonary Disease. Copd

Plan of Attack
Goals of Management
Managing Stable COPD
Managing Acute Exacerbations of COPD

A disease state characterized by airflow limitation that is not fully reversible. Airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Symptoms, functional abnormalities, and complications of COPD can all be explained on the basis of this underlying inflammation and the resulting pathology.
Chronic Bronchitis (clinical)
Sputum production more days than not for at least 3 months a year for at least 2 years
Emphysema (pathologic)
Parenchymal destruction airspace walls distal to terminal bronchioles, without fibrosis
Important: You can have either, but to have COPD you MUST demonstrate obstruction (thus the O in COPD)

Fourth leading cause of death in U.S.
100,000 American deaths each year
15-20% of chronic smokers develop COPD
2.5% mortality for COPD hospital admissions
COPD with acute respiratory failure:
24% in hospital mortality
59% one year mortality
If you have COPD and PaCO2 > 50mmHg:
67% chance of being alive in 6 months
57% chance of being alive in 12 months

Sputum production (especially in the morning)
Recurrent acute chest illnesses
Headache in the morning possible hypercapnia
Cor pulmonale (Right heart failure)

Goals Of Management
Identifying and ameliorating (if possible) the cause of the acute exacerbation
Optimizing lung function by administering bronchodilators and other pharmacotherapy
Assuring adequate oxygenation and secretion clearance
Averting the need for intubation, if possible
Preventing complications of immobility, such as thromboemboli and deconditioning
Addressing nutritional needs at the time of the acute illness, most patients are in negative nitrogen balance, which is exacerbated by steroid therapy

Prolonged expiratory time
Expiratory wheezes
Increased AP diameter of chest
Decreased breath sounds (especially upper lung fields)
Distant heart sounds
End stage: accessory muscles, pursed lip breathing, cyanosis, enlarged liver and pedal edema (in case of cor pulmonale).

Chest X-ray
Hyperinflated lung fields more radiolucent
Bullae, often bilateral upper lobes in smokers
Flat diaphragms (best seen on lateral) and retrosternal airspace can indicate air trapping
High Resolution CT of Chest
Most sensitive to detect above changes
No role in routine care of COPD patients
Can be useful for giant bullous disease surgeries or lung volume reduction surgery planning

Pulmonary Function Testing
Spirometry: Decreased FEV1/FVC
FEV1 percent predicted defines severity
Lung volumes: Increased TLC, RV, RV/TLC
DLCO: Decreased

Gold Staging Criteria
Stage O: Normal spirometry; chronic sx
Stage 1 (Mild):
FEV1/FVC 80% predicted
Stage 2 (Moderate):
2A: FEV1 50-80% predicted
2B: FEV1 30-50% predicted

Stage 3 (severe):

American Thoracic Society Spirometry
Low FEV1/FVC defines obstruction
FEV1%predicted Category

35-50% Severe
50-60% Moderately Severe
60-70% Moderate
70-80% Mild
80-100% Mild vs. Normal variant
> 100% Normal

Managing Stable COPD
Smoking Cessation Is KEY!
YOUR intervention will make a difference must address at each visit
Two therapies ONLY have been shown to improve mortality in stable COPD:
1) Smoking Cessation
2) Oxygen Therapy

Bronchodilator Technique
MDIs get better drug deposition than nebs
Use a spacer device with MDIs
Technique is key important for patient and doctor
Inadequate dosing can hamper treatment

Beta-2 selectivity is good
Some additive vs. slightly synergistic effects of combining beta-2 agonist and ipratropium (Combivent)
Some data to support decreased H.influenzae pneumonia incidence with Serevent
Anticholinergic Agents (Atrovent, glycopyrrolate)
Similar ability to bronchodilate (in appropriate doses) as beta-agonists
Also reduces sputum volume; no change in viscosity
Usually under dosed
Recommend 2 (36 mcg) puffs qid
glycopyrrolate which is manufactured for IV/IM use for other indications, is available only “off label” for nebulized use in COPD (1 to 2 mg every two to four hours).
Aminophylline and theophylline are not recommended for the management of acute exacerbations of COPD. Randomized controlled trials of intravenous aminophylline in this setting have failed to show efficacy in excess of that afforded by therapy with inhaled bronchodilators and corticosteroids

Mucokinetic agents
There is little evidence supporting the use of mucokinetic (mucolytic) agents, such as N-acetylcysteine or iodide preparations, in acute exacerbations of COPD. In fact, some drugs of this class may worsen bronchospasm.

Oxygen. Yes.
Demonstrated to improve exercise performance, symptom indices and mortality
Goal in hypercapnic patients for SpO2 need not be greater than 88-90%
Always test COPD patients for oxygenation with ambulation if baseline at rest room air SpO2 ok

Systemic Corticosteroids
Never demonstrated to significantly impact mortality or exercise capacity
Slight improvements in symptom indices
Significant side effects
Rarely of benefit, generally of harm to your patient
Occasionally useful in a small subset failing other therapies AND with demonstrated bronchodilator response on PFTs

Inhaled Corticosteroids
Jury still out
Lots of recent research with some favorable data supporting its use
May be part of standard regimens in the future

Pneumovax, annual flu shots
Chronic antibiotic therapy BAD IDEA
Nutritional status Important
Pulmonary Rehabilitation
Improved exercise capacity, symptom scores
Lung Volume Reduction Surgery

Managing Acute Exacerbations of COPD
Common precipitants:
Infection esp viral or bacterial
Acute bronchospasm

Who To Admit
Countless studies, few definite answers
Worsening hypoxemia and/or hypercapnia
Otherwise, mostly a clinical decision
Key points to consider:

Neb or MDI neb MAY be better in acute setting, but MDIs have better drug deposition overall
Continuous nebulizer treatments confer no benefit over treatments every 1-2 hours
Generally should avoid subcutaneous beta-agonists
BEWARE: Hypokalemia, tachycardia (occasional)
Levalbuterol still with weak clinical data few situations where it is clinically indicated

ATROVENT (anticholinergic bronchodilator)
May decrease secretions
Few significant side effects
Usually significantly under dosed emerging data supports much higher doses than usually used currently

Corticosteroids Parenteral corticosteroids are frequently used in treating acute exacerbations of COPD. Methylprednisolone (60 to 125 mg intravenously, two to four times daily) or the equivalent glucocorticoid dose of other steroid preparations commonly is given.
Corticosteroids Utilization in this setting was initially based upon small randomized trials in which only a minority of patients benefit and the degree of improvement is modest
A randomized, placebo-controlled trial of 271 patients has confirmed the benefits of systemic corticosteroids given for up to 2 weeks to hospitalized patients with COPD exacerbation

Winnipeg Criteria (give for 2-3 of the following):
Increased cough
Increased purulence
Increased sputum production
Antibiotics accelerate improvement in peak expiratory flow rates and lessen the rate of recrudescence in this setting
Amoxicillin, Doxycycline, TMP/SMX, Azithromycin, Clarithromycin, Levaquin for 10 days

Mucokinetic Agents JUST SAY NO.
N-acetylcysteine is actually contraindicated in patients with airway obstruction
No significant clinical benefit ever demonstrated
Chest PT, intermittent positive pressure breathing and postural drainage may actually be harmful in the setting of acute obstruction

Methylxanthines (Theophylline, Aminophylline)
Not recommended for acute exacerbations
No significant benefit ever demonstrated in large, prospective trials

Oxygen: YES!
Generally a good thing cells like that stuff
If requiring a significant increase in FiO2 over baseline requirement, start hunting for something other than just COPD exacerbation
BEWARE of CO2 RETAINERS! (goal SpO2 90%, PaO2 of 60 to 65 mmHg )
1) Altered V/Q relationships
2) Haldane effect (Hgb*O2 holds less CO2 goes out into plasma)
3) Decreased ventilatory drive (least impt mechanism)

Non-Invasive Positive Pressure Ventilation
Set FiO2, inspiratory (IPAP) and expiratory (EPAP)
Difference between IPAP and EPAP augments tidal volume, therefore improving minute ventilation. CO2 then gets blown off
MORTALITY BENEFIT in patients who will tolerate

Mechanical Ventilation
Respiratory distress
Acidemia that does not correct quickly with therapy
Inability to oxygenate adequately
Often a clinical decision relative to patients work of breathing