INFLAMMATION & DEPRESSION
THE MORE THINGS CHANGE, THE MORE THEY STAY THE SAME
- The April issue of the Indian Journal of Psychological Medicine (Is Depression an Inflammatory Disease?) attempts to answer this question right out of the chute by concluding, “There is evidence for higher baseline inflammation in depression…” How severe is this relationship? The same month’s issue of the Journal of Psychiatric Research gives us a glimpse with their study, Association Between C-Reactive Protein and Suicidal Behavior in an Adult Inpatient Population. Although it may not be the best blood marker for inflammation, C-Reactive Protein (CRP) is probably the most well known by the general public. “As CRP level increased, the probability of patients belonging to a suicide attempt group increased. We also observed a significant effect of depression in that depressed patients were more likely to have a suicide attempt when compared to patients with no depression. We replicated the association between a pro-inflammatory state and suicidal behavior in a sample of “real world” severely ill psychiatric inpatients.” This, folks, is why inflammation really is everything.
- A study from last week’s issue of the medical journal PLoS One (Risk of Diabetes in Older Adults with Co-Occurring Depressive Symptoms and Cardiometabolic Abnormalities) concluded, “High depressive symptoms and cardiometabolic abnormalities are independently associated with an increased risk of diabetes. Compared to the reference group, the hazard ratio for diabetes was 1.29 for those with high depressive symptoms only. It was 3.88 for those with cardiometabolic abnormalities only, and 5.56 for those with both high depressive symptoms and cardiometabolic abnormalities, after adjusting for socio-demographic, lifestyle and clinical variables. These findings suggest that those with high depressive symptoms and cardiometabolic abnormalities are at a particularly increased risk of type 2 diabetes.” What’s scary about this study is that OVER HALF the population has “cardiometabolic abnormalities” (CARDIOMETABOLIC SYNDROME — aka pre-diabetes). Some experts put this number closer to 75% for certain locales (e.g. “The South”).
- The International Neurology Journal (Pathophysiological Role of Neuroinflammation in Neurodegenerative Diseases and Psychiatric Disorders) stated just a couple of weeks ago that, “Brain diseases and disorders such as Alzheimer disease, Parkinson disease, depression, schizophrenia, autism, and addiction lead to reduced quality of daily life through abnormal thoughts, perceptions, emotional states, and behavior. Human and animal studies have supported a role of neuroinflammation in the etiology of these diseases. In the central nervous system, an increased inflammatory response is capable of activating microglial cells, leading to the release of pro-inflammatory cytokines including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. In turn, the pro-inflammatory cytokines aggravate and propagate neuroinflammation, degenerating healthy neurons and impairing brain functions.” The study goes on to talk more about the brain’s GLIAL CELLS, which we are also learning, are heavily involved in CHRONIC PAIN. By the way, I have posts on ALZHEIMER’S, PARKINSON’S, AUTISM, and SCHIZOPHRENIA on my site for those who are interested.
- DOPAMINE is one of the chief neurotransmitters in your body. Last month’s issue of Current Topics in Behavioral Neurosciences (The Role of Dopamine in Inflammation-Associated Depression: Mechanisms and Therapeutic Implications) sheds still more light on this topic by revealing that, “Studies investigating the impact of a variety of inflammatory stimuli on the brain and behavior have consistently reported evidence that inflammatory cytokines affect the basal ganglia and dopamine to mediate depressive symptoms related to motivation and motor activity. Findings have included inflammation-associated reductions in responses to hedonic reward, decreased dopamine and dopamine metabolites in cerebrospinal fluid, and decreased availability of striatal dopamine, all of which correlate with symptoms of anhedonia [the inability to experience pleasure from activities usually found enjoyable, e.g. exercise, hobbies, music, sexual activities], fatigue, and psychomotor retardation. Similar relationships between alterations in dopamine-relevant corticostriatal reward circuitry and symptoms of anhedonia and psychomotor slowing have also been observed in patients with major depression who exhibit increased peripheral cytokines and other inflammatory markers, such as C-reactive protein. Of note, these inflammation-associated depressive symptoms are often difficult to treat in patients with medical illnesses or major depression. Furthermore, a wealth of literature suggests that inflammation can decrease dopamine synthesis, packaging, and release, thus sabotaging or circumventing the efficacy of standard antidepressant treatments.” Did you catch the last sentence? Rampant inflammation is why research has proved that Antidepressant Medications are barely (if at all) better than placebo (HERE). How could they be? They don’t address Depression’s underlying cause. The study goes on to say that, “inflammation-related behavioral symptoms contribute to an inflammatory malaise.” An unfortunately accurate description of Depression.
- AUTOIMMUNE DISEASES (HERE is a list of the more common ones) are almost always associated with increased levels of Inflammation. A study from a week ago (Comorbidity in Psoriasis) published in a German journal I can neither spell nor pronounce said that, “Many epidemiological studies have shown that psoriasis is associated with psoriatic arthritis as well as cardiovascular and metabolic diseases. Furthermore, obesity and psychological diseases such as depression and anxiety disorders are linked with psoriasis.” Last week’s issue of Current Topics in Neurosciences (Depression in Autoimmune Diseases) took that a step further by talking about the relationship in general. “Up to 50% of patients with autoimmune diseases show an impairment of health-related quality of life and exhibit depression-like symptoms. The immune system not only leads to inflammation in affected organs, but also mediates behavior abnormalities including fatigue and depression-like symptoms.” If you are curious about your personal level of Inflammation, THIS POST is basically a self test.
- In yet another offering from last week’s “Inflammation / Depression” issue of Current Topics in Neurosciences (Evidence for Inflammation-Associated Depression), we see more on this unholy relationship. “Data to date suggest a bidirectional relationship between inflammation and depression wherein one process can drive the other. There is also evidence that this pro-inflammatory state is accompanied by aberrant inflammation-related processes including platelet activation factor hyperactivity, oxidative and nitrosative stress, and damage to mitochondria [can anyone say FIBROMYALGIA?]. These complex and interrelated mechanisms can collectively contribute to negative neurobiological outcomes that may, in part, underlie the etiopathology of depression.” The purpose of this study was to let readers know that using this information, any number of drugs are being developed to (supposedly / hopefully / maybe / probably not) solve the problem. Instead of new drugs, researchers writing in the August 2016 issue of the Journal of Affective Disorders (Statins for the Treatment of Depression…) are trying to teach an old dog a new trick. STATIN DRUGS are the latest medicine to be tested as a treatment for Depression.
- We should not be surprised that having an Inflammatory Disease makes you more likely to have more of the same (HERE is a list — a ten second browse of the post lets you know that many people have lots). A study in the April issue of Mediators of Inflammation (Emerging Comorbidities in Adult Asthma: Risks, Clinical Associations, and Mechanisms) bears this out. “Most studies with asthma have been performed in patients being otherwise healthy. However, in real life, comorbid diseases are very common in adult patients. We review here the emerging comorbid conditions to asthma such as obesity, metabolic syndrome, diabetes mellitus type 2 (DM2), and cardiac and psychiatric diseases. Their role as risk factors for incident asthma and whether they affect clinical asthma are evaluated. Obesity, independently or as a part of metabolic syndrome, DM2, and depression are risk factors for incident asthma. These emerging comorbidities often occur in the same multimorbid adult patient and may have in common metabolic pathways and inflammatory or other alterations such as early life exposures, systemic inflammation, inflammasome, adipokines, hyperglycemia, hyperinsulinemia, lung mechanics, mitochondrial dysfunction, disturbed nitric oxide metabolism, and leukotrienes.” In other words, IMPROPERLY CONTROLLED BLOOD SUGAR (whether your numbers look ‘OK’ or not) leads to some nasty health issues, including problems with the INFLAMMASOME. Oh; and look how the authors mention, “early life exposure“. They are talking here about the MICROBIOME and ANTIBIOTICS as related to the HYGIENE HYPOTHESIS. This is why I repeatedly warn my patients that besides the unbridled numbers of VACCINES being recommended today, one of the single worst things you can do for your children’s / infant’s health is give them antibiotics (HERE & HERE). A quick peek at the provided link proves that much — maybe even most — ASTHMA is preventable.
- Speaking of the Microbiome, the issue of Clinical Psychopharmacology and Neuroscience that came out just yesterday, carried a study called The Microbiome and Mental Health: Looking Back, Moving Forward with Lessons from Allergic Diseases. Spending a significant amount of time dealing with GUT HEALTH and DYSBIOSIS, the abstract concluded that, “Relationships between gastrointestinal viscera and human emotions have been documented by virtually all medical traditions known to date. In particular, we pay specific attention to how the hygiene hypothesis and emerging research on traditional dietary patterns has helped re-ignite interest in the use of microbes to support mental health. Impediments that could block translation of encouraging experimental studies include environmental forces that work toward dysbiosis, perhaps none more important than westernized dietary patterns. The microbiome is intimately connected to diet, nutrition, and other lifestyle variables; microbial-based psychopharmacology will need to consider this contextual application, otherwise the ceiling of clinical expectations will likely need to be lowered.” Do you catch what’s being said here? A failure to change your eating habits and move towards AN ANTI-INFLAMMATORY DIET means that you can essentially forget about truly solving your problem(s) — including Depression. Unfortunately, most doctors are not relating this to their patients (HERE).
I hope you are seeing how severe this issue of Inflammation really is, and that it can (will) affect you in ways that ten years ago you could never have even dreamed of. If you are serious about solving your inflammation-related health problem(s), I would suggest you at least take a look at THIS SHORT POST. Many people are charging a fortune for this sort of information, and I provide it to you free of charge. And if you are enjoying the free information, be sure to show us some love on FACEBOOK while you’re at it!