The Catabolic Process: Consequences and Treatments
Consequences of the Catabolic Process
Patients suffering from a catabolic process condition, depending on the level of severity, are at increased risk of:
- Diminished quality of life in general with loss of vitality
- Falls due to frailty
- Infection as the immune system lacks the nutrient to be optimized
- Much lower capacity for exercise due to lack of muscle mass
- Poor and/or slower healing of wounds
- Significantly lower breathing capacity as intercostal muscle function declines
Consequences of a catabolic process state, whether clinical or subclinical, include:
- Worsening of the underlying condition, such as Adrenal Fatigue Syndrome
- Gradual loss of muscle mass that easily leads to frailty causing adverse effects on a number of medical outcomes
- Compromising various bodily organs, including cardiac and respiratory function
- Continued weight loss, although unintended
- Ultimately death
Stress and the Catabolic Process
Glucocorticoids, primarily cortisol, are steroidal hormones produced by the adrenal glands in response to stress. With chronic stress, the adrenal glands become weakened after its effort to compensate by increasing anti-stress hormone cortisol fails. Cortisol output there varies as AFS progresses. It is usually high in stages 1 and 2 of adrenal fatigue. As adrenal fatigue progresses, cortisol output is often pushed to its limit. A chronically high cortisol output can lead to a state of catabolism because cortisol causes the breakdown of proteins in order to generate energy over time. As AFS enters Stage 3 and beyond, cortisol levels tend to stay low as AFS advances further.
This metabolic cycle is deranged when under stress with AFS. The emergency mobilization of quick nutritional resources, cortisol release, norepinephrine, epinephrine prepares the body for the fight-or-flight alarm response. It is a way to ensure that our energy needs are covered when survival is perceived to be at risk. At the same time, this mobilization is handled under stress, the levels or cortisol and adrenaline go up while the levels of DHEA and testosterone go down. The net effect is in favor of catabolism if all else is equal.
In advanced stages of adrenal fatigue, the rebuilding process, normally carried out by testosterone, estrogen, DHEA, and pregnenolone, is overwhelmed by the amount of catabolic hormone damage. While laboratory tests may show low cortisol at this time, the vicious cycle of catabolism is well entrenched with its downward decompensatory cascade reinforced by a destabilizing positive feedback loop. Therefore, the rebuilding process will be exceedingly slow and sluggish.
In other words, the catabolic process mode is self-driven once entered. Less muscle mass means reduced exercise capacity. This further reduces the incentive to exercise as frustration and fatigue sets in. Fatigue drives further inactivity. Muscle mass loss is exaggerated with disuse. The vicious cycle continues. Furthermore, muscles torn from normal wear and tear are not adequately repaired on a timely basis. Collagen is broken down without significant compensatory replenishment. Outwardly, wrinkles start to develop as premature aging sets in. Internally, organs and muscle breakdown leads to chronic muscle and joint pain of unknown origin, especially after strenuous exercise or heavy lifting. Reduced muscle mass can lead to chronic pain syndrome, joint pain, chronic fatigue, and fibromyalgia.
As the collagen structures of internal organs break down, their functions are compromised. Gastrointestinal tract motility and contraction forces are reduced. Adrenal fatigue is often associated with the poor ability to digest proteins and common symptoms include indigestion and irritable bowel syndrome. The amount of acid production in the body may not be sufficient to help break down the digested foods, resulting in further improper digestion. Clearly, the root pathophysiology is a body in catabolic state of the metabolic cycle. Unless reversed, the health consequences can be devastating.
Laboratory Tests for a Catabolic State
The basic normal laboratory workup for diagnosing catabolism includes a complete blood count, IGF-1 (a surrogate marker for growth hormone); cytokine panel, CRP, CBC, chemistry panel, sedimentary rate, chemistry panel, liver panel, thyroid function, free testosterone, DHEA-S and electrolytes. Those with advanced AFS should also have a 24-hour 4-point cortisol saliva test.
The following are good markers of catabolic process:
- BUN-to-creatinine ratio with normal creatinine
Urea is the final breakdown product of the protein and amino acid metabolism. This is the most important catabolic pathway for eliminating excess nitrogen from within. This test is frequently accompanied by serum creatinine testing. Clinicians frequently calculate the urea nitrogen/creatinine ratio: serum bun in mg/dL/serum creatinine in mg/dL. For a normal healthy individual on a standard diet, the normal ratio ranges between 12 and 20. A low BUN: Cr ratio suggests inadequate protein intake, reduced urea synthesis as in advanced liver disease, and increased creatinine production as in rhabdomyolysis. High ratio with normal creatine is noted with a catabolic state of tissue breakdown.
- Free testosterone
When the body spends excessive amounts of time in a catabolic state, injuries, illness and reduced performance levels are typical symptoms. In addition to high cortisol and low DHEA, testosterone levels tend to be low in both men and women. This is often accompanied by reduced exercise performance, low libido, and poor memory. The normal level for a male is 50-210 pg/ml (174-729 pmol/L) and 1.0-8.5 pg/ml (3.5-29.5 pmol/L) for a female.
Note: Lab results can be skewed to the low side if one is on a low fat diet because testosterone is manufactured from much needed cholesterol in the body. A low testosterone level in men can also be caused by some inherited diseases (such as Klinefelter syndrome or Down syndrome), liver cirrhosis, prostate gland cancer treatment, chronic alcohol use, obesity, and chronic pain. In women, a low level of testosterone may be caused by an underactive pituitary gland, loss of ovary function through disease or surgery, Addison’s disease, and some medicines (such as corticosteroids or estrogen).
- Cortisol and DHEA ratio
Two key hormones regulating the metabolic cycle are cortisol and Dehydroepiandrosterone (DHEA). Cortisol is a hormone secreted by the adrenal glands to help the body in times of stress which can trigger the catabolic process. It performs a number of functions including the breakdown of muscle proteins, which causes an increase in glucose in the bloodstream to help the body attain the energy it needs in times of stress. Cortisol generally has a catabolic effect. DHEA usually has the opposite effect, since it’s an anabolic hormone and anabolism is the process that occurs when food converts into living tissue. When you are under chronic stress an imbalance occurs because the production of cortisol is increased and DHEA production slows down. This results in your body going into a catabolic state. The net result is cortisol dominance.
Both cortisol and DHEA (present in blood as DHEA-S) can be measured by routine laboratory testing. A blood cortisol/DHEA-S ratio of greater than 6 is an alert sign of catabolic state.
Raised ratios of cortisol to DHEA cause an increase in fat deposits, predominately in the midsection. This is the commonly referred to muffin top we see in people under stress or middle-aged people that are sedentary. It also impairs skin regeneration, which can cause wrinkles to develop. Protein breakdown due to stress can also accelerate the development of osteoarthritis and the bone loss that goes with it. It also extends the time it takes for someone to heal from an injury or trauma. Other physical conditions, which are related to a rise in cortisol to DHEA ratios, include depression, hypertension, ischemic heart disease and various types of cancer.
Unfortunately, the clinical correlation between laboratory tests of catabolic state markers is neither linear nor absolute. There is considerable personal variance as well as changes as the catabolism progresses. The absolute cortisol level, whether by blood or saliva, cannot be relied on as the sole indicator of catabolic state. Catabolic markers are helpful and serve as a reference point. They are best used in the context of close clinical correlation. For example, loss of body weight and muscle mass usually occurs gradually in patients with chronic conditions such as Adrenal Fatigue Syndrome. One can be in a catabolic state but the cortisol/DHEA ratio is under 6, for example. Again, a careful history and clinical symptoms remain the best tools in identifying catabolic state early on.
Anabolic Hormones — Wait a Minute!
Once the catabolic state is suspected, the conventional approach is to start immediately on anabolic hormones. This is especially true if the blood testosterone and DHEA are low. Unfortunately, this is one of the most common clinical mistakes one can make if advanced AFS is present.
Clinically, we see that the more advanced the AFS backdrop, the less such anabolic hormonal approaches will be tolerated. Some feel more energized, but only for a short time. Others may in fact feel jittery and anxious from the get go. Heart palpitations and panic attacks are common while adrenal crashes are triggered in others. This creates an atmosphere of the weaker the adrenals the higher the risk of a backfire.
The deranged autonomic nervous system (ANS) associated with advanced AFS may be a strong contributing factor to treatment failure. Those with advanced AFS typically are in a state of ANS overdrive. The sympathetic nervous system, along with its stimulatory hormone epinephrine (also called adrenaline) is typically in overdrive as an autonomic compensatory response by the body when it enters a flight-or-fight mode in its fight for survival brought on by perceived stress. The body is on full alert. Receptor sites are hypersensitized. The extracellular matrix is congested from cellular metabolites overload, while the liver is overburdened with resulting slow clearance. The result is a body saturated with unwanted metabolite that causes inflammation. Any anabolic agent that has intrinsic metabolic stimulatory properties tends to make the internal terrain even more hostile. These agents, while constructive for those who are not in advanced AFS, tend to behave paradoxically. Anxiety, panic attacks, jitteriness, a sense of wired and tired, insomnia, heart palpitations, and POTS-like symptoms are frequently reported. Adrenal fatigue may worsen as adrenal crashes are triggered by such anabolic therapeutic agents in a setting of catabolic state and concurrent advanced AFS.
Agents to be avoided unless clinically critical and conducted under supervision include testosterone, DHEA, pregnenolone, growth hormone, estrogen, thyroid, glandular such as adrenal cortex, and herbs such as rhodiola, ashwagandha, maca, ginseng, and green tea. Even vitamin C may not be tolerated while in the catabolic process.
Challenges of Catabolic Process Reversal in the Presence of Advanced AFS
A body in catabolic state with concurrent advanced AFS is usually not able to accept natural or synthetic anabolic compounds that have stimulatory properties. Use of any nutritional supplementation, even though intrinsically gentle by nature, needs to be carefully titrated to match the body’s state of function to be gently nurturing and supportive without triggering any crash. This is easier said than done because the AFS sufferer, when accompanied by catabolism, is typically in a fragile state, with little reserve remaining to cushion any change, whether it be good or bad. Many are already house bound and unable to work or maintain a normal social life. Adrenal crashes can be easily triggered.
Laboratory tests only give at best a rough picture and are neither specific nor sensitive enough to be relied upon heavily for day-to-day clinical decision-making. A detailed history by an experienced clinician is key. Yet, tremendous challenges face the clinician when designing a catabolic process/AFS recovery program. The sufferers are typically:
- Too weak to digest and tolerate any normal food
- Too fragile to accept any anabolic hormone
- Too prone to paradoxical reaction with supplements of any kind
- Their receptor sites are too sensitive and dosage becomes problematic
- Their liver is too congested, resulting in a high internal toxic load due to sluggish metabolic breakdown
- Their extracellular matrix is too polluted, resulting in a heightened sensitivity to food, drugs, and nutritional supplements
- Their reactive hypoglycemia makes dietary choices limited and difficult
- They have too much adrenaline flooding the body, leading to a lower threshold for adrenal crashes, heart palpations, and adrenergic POTS
- They have a sluggish assimilation rate across their GI tract, with reduced absorption and thus bioavailability of nutrients
- They are too weak to exercise, further worsening muscle wasting during inactivity
- They are too socially withdrawn to solicit emotional support and break the negative attitude cycle.
- Their thinking process is too slow often aggravated by brain fog.
- They are too weak to hold a full-time job, leading to financial hardship
- They are eager to get well, but have failed multiple times and lost patience, resulting in pent up frustration and anger towards health professionals
Given the above constraints, stabilizing and reverting the metabolic cycle from catabolism to neutral is a very challenging endeavor.
© Copyright 2016 Michael Lam, M.D. All Rights Reserved.